21 results on '"Biagio Palmisano"'
Search Results
2. THBS1 and THBS2 Enhance the In Vitro Proliferation, Adhesion, Migration and Invasion of Intrahepatic Cholangiocarcinoma Cells
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Eleonora Corbella, Claudia Fara, Francesca Covarelli, Veronica Porreca, Biagio Palmisano, Giuseppina Mignogna, Alessandro Corsi, Mara Riminucci, Bruno Maras, and Carmine Mancone
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intrahepatic cholangiocarcinoma ,tumor microenvironment ,THBS1 ,THBS2 ,angiogenesis ,lymphangiogenesis ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
In intrahepatic cholangiocarcinoma (iCCA), thrombospondin 1 (THBS1) and 2 (THBS2) are soluble mediators released in the tumor microenvironment (TME) that contribute to the metastatic spreading of iCCA cells via a lymphatic network by the trans-differentiation of vascular endothelial cells to a lymphatic-like phenotype. To study the direct role of THBS1 and THBS2 on the iCCA cells, well-established epithelial (HuCCT-1) and mesenchymal (CCLP1) iCCA cell lines were subjected to recombinant human THBS1 and THBS2 (rhTHBS1, rhTHBS2) for cellular function assays. Cell growth, cell adhesion, migration, and invasion were all enhanced in both CCLP1 and HuCCT-1 cells by the treatment with either rhTHBS1 or rhTHBS2, although they showed some variability in their intensity of speeding up cellular processes. rhTHBS2 was more intense in inducing invasiveness and in committing the HuCCT-1 cells to a mesenchymal-like phenotype and was therefore a stronger enhancer of the malignant behavior of iCCA cells compared to rhTHBS1. Our data extend the role of THBS1 and THBS2, which are not only able to hinder the vascular network and promote tumor-associated lymphangiogenesis but also exacerbate the malignant behavior of the iCCA cells.
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- 2024
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3. GsαR201C and estrogen reveal different subsets of bone marrow adiponectin expressing osteogenic cells
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Biagio Palmisano, Rossella Labella, Samantha Donsante, Cristina Remoli, Emanuela Spica, Ilenia Coletta, Giorgia Farinacci, Michele Dello Spedale Venti, Isabella Saggio, Marta Serafini, Pamela Gehron Robey, Alessandro Corsi, and Mara Riminucci
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Biology (General) ,QH301-705.5 ,Physiology ,QP1-981 - Abstract
Abstract The Gsα/cAMP signaling pathway mediates the effect of a variety of hormones and factors that regulate the homeostasis of the post-natal skeleton. Hence, the dysregulated activity of Gsα due to gain-of-function mutations (R201C/R201H) results in severe architectural and functional derangements of the entire bone/bone marrow organ. While the consequences of gain-of-function mutations of Gsα have been extensively investigated in osteoblasts and in bone marrow osteoprogenitor cells at various differentiation stages, their effect in adipogenically-committed bone marrow stromal cells has remained unaddressed. We generated a mouse model with expression of Gsα R201C driven by the Adiponectin (Adq) promoter. Adq-Gsα R201C mice developed a complex combination of metaphyseal, diaphyseal and cortical bone changes. In the metaphysis, Gsα R201C caused an early phase of bone resorption followed by bone deposition. Metaphyseal bone formation was sustained by cells that were traced by Adq-Cre and eventually resulted in a high trabecular bone mass phenotype. In the diaphysis, Gsα R201C , in combination with estrogen, triggered the osteogenic activity of Adq-Cre-targeted perivascular bone marrow stromal cells leading to intramedullary bone formation. Finally, consistent with the previously unnoticed presence of Adq-Cre-marked pericytes in intraosseous blood vessels, Gsα R201C caused the development of a lytic phenotype that affected both cortical (increased porosity) and trabecular (tunneling resorption) bone. These results provide the first evidence that the Adq-cell network in the skeleton not only regulates bone resorption but also contributes to bone formation, and that the Gsα/cAMP pathway is a major modulator of both functions.
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- 2022
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4. An in vivo humanized model to study homing and sequestration of Plasmodium falciparum transmission stages in the bone marrow
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Samantha Donsante, Giulia Siciliano, Mariagrazia Ciardo, Biagio Palmisano, Valeria Messina, Valeria de Turris, Giorgia Farinacci, Marta Serafini, Francesco Silvestrini, Alessandro Corsi, Mara Riminucci, and Pietro Alano
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malaria ,Plasmodium falciparum ,gametocytes ,bone marrow ,ectopic ossicles ,skeletal stem cells ,Microbiology ,QR1-502 - Abstract
IntroductionRecent evidence suggests that the bone marrow (BM) plays a key role in the diffusion of P. falciparum malaria by providing a “niche” for the maturation of the parasite gametocytes, responsible for human-to-mosquito transmission. Suitable humanized in vivo models to study the mechanisms of the interplay between the parasite and the human BM components are still missing.MethodsWe report a novel experimental system based on the infusion of immature P. falciparum gametocytes into immunocompromised mice carrying chimeric ectopic ossicles whose stromal and bone compartments derive from human osteoprogenitor cells.ResultsWe demonstrate that immature gametocytes home within minutes to the ossicles and reach the extravascular regions, where they are retained in contact with different human BM stromal cell types.DiscussionOur model represents a powerful tool to study BM function and the interplay essential for parasite transmission in P. falciparum malaria and can be extended to study other infections in which the human BM plays a role.
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- 2023
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5. Morphological and Immunophenotypical Changes of Human Bone Marrow Adipocytes in Marrow Metastasis and Myelofibrosis
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Michele Dello Spedale Venti, Biagio Palmisano, Samantha Donsante, Giorgia Farinacci, Flavia Adotti, Ilenia Coletta, Marta Serafini, Alessandro Corsi, and Mara Riminucci
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bone marrow ,marrow metastasis ,myeloproliferative neoplasia ,myelofibrosis ,bone marrow adipose tissue ,bone marrow adipocytes ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
The bone marrow adipose tissue constitutes more than two-thirds of the bone marrow volume in adult life and is known to have unique metabolic and functional properties. In neoplastic disorders, bone marrow adipocytes (BMAds) contribute to create a favorable microenvironment to survival and proliferation of cancer cells. Many studies explored the molecular crosstalk between BMAds and neoplastic cells, predominantly in ex-vivo experimental systems or in animal models. However, little is known on the features of BMAds in the human neoplastic marrow. The aim of our study was to analyze the in situ changes in morphology and immunophenotype of BMAds in two different types of neoplastic marrow conditions. We selected a series of archival iliac crest and vertebral bone biopsies from patients with bone marrow metastasis (MET), patients with myeloproliferative neoplasia with grade-3 myelofibrosis (MPN-MF) and age-matched controls (CTR). We observed a significant reduction in the number of BMAds in MET and MPN-MF compared to CTR. Accordingly, in the same groups, we also detected a significant reduction in the mean cell diameter and area. Immunolocalization of different adipocyte markers showed that, compared to CTR, in both MET and MPN-MF the percentages of adiponectin- and phosphorylated hormone sensitive lipase-positive BMAds were significantly reduced and increased respectively. No statistically significant difference was found between MET and MPN-MF. Interestingly, in one MET sample, “remodeled” BMAds containing a large lipid vacuole and multiple, smaller and polarized lipid droplets were identified. In conclusion, our data show that in different types of marrow cancers, BMAds undergo significant quantitative and qualitative changes, which need to be further investigated in future studies.
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- 2022
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6. Nanostring technology on Fibrous Dysplasia bone biopsies. A pilot study suggesting different histology-related molecular profiles
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Agnese Persichetti, Edoardo Milanetti, Biagio Palmisano, Annamaria di Filippo, Emanuela Spica, Samantha Donsante, Ilenia Coletta, Michele Dello Spedali Venti, Ernesto Ippolito, Alessandro Corsi, Mara Riminucci, and Domenico Raimondo
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Fibrous Dysplasia ,Bone disease ,Bone biopsy ,Nanostring ,Diseases of the musculoskeletal system ,RC925-935 - Abstract
Identifying the molecular networks that underlie Fibrous Dysplasia (FD) is key to understand the pathogenesis of the disease, to refine current diagnostic approaches and to develop efficacious therapies. In this study, we used the NanoString nCounter Analysis System to investigate the gene signature of a series of nine Formalin Fixed Decalcified and Paraffin-Embedded (FFDPE) bone biopsies from seven FD patients.We analyzed the expression level of 770 genes. Unsupervised clustering analysis demonstrated partitioning into two clusters with distinct patterns of gene expression. Differentially expressed genes included growth factors, components of the Wnt signaling system, interleukins and some of their cognate receptors, ephrin ligands, matrix metalloproteinases, neurotrophins and genes encoding components of the cAMP-dependent protein kinase. Interestingly, two tissue samples obtained from the same skeletal site of one patient one year apart failed to segregate in the same cluster. Retrospective histological review of the samples revealed different microscopic aspects in the two groups.The results of our pilot study suggest that the genetic signature of FD is heterogeneous and varies according to the histology and, likely, to the age of the lesion. In addition, they show that the Nanostring technology is a valuable tool for molecular translational studies on archival FFDPE material in FD and other rare bone diseases.
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- 2022
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7. Next Generation Bone Marrow Adiposity Researchers: Report From the 1st BMAS Summer School 2021
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Rossella Labella, Sarah Little-Letsinger, Viktorjia Avilkina, Rita Sarkis, Michaela Tencerova, Annegreet Vlug, and Biagio Palmisano
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bone marrow adipose tissue (BMAT) ,bone marrow adiposity ,bone marrow adipocytes ,metabolism ,imaging technique ,BMSC – bone marrow stromal cells ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
The first International Summer School on Bone Marrow Adiposity was organized by members of Bone Marrow Adiposity Society and held virtually on September 6-8 2021. The goal of this meeting was to bring together young scientists interested in learning about bone marrow adipose tissue biology and pathology. Fifty-two researchers from different backgrounds and fields, ranging from bone physiopathology to adipose tissue biology and hematology, participated in the summer school. The meeting featured three keynote lectures on the fundamentals of bone marrow adiposity, three scientific workshops on technical considerations in studying bone marrow adiposity, and six motivational and career development lectures, spanning from scientific writing to academic career progression. Moreover, twenty-one participants presented their work in the form of posters. In this report we highlight key moments and lessons learned from the event.
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- 2022
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8. Angiotensin II Modulates Calcium/Phosphate Excretion in Experimental Model of Hypertension: Focus on Bone
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Giovanna Castoldi, Raffaella Carletti, Silvia Ippolito, Isabella Villa, Biagio Palmisano, Simona Bolamperti, Alessandro Rubinacci, Gianpaolo Zerbini, Michela Meani, Giovanni Zatti, and Cira R. T. di Gioia
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angiotensin II ,experimental hypertension ,bone ,rats ,Biology (General) ,QH301-705.5 - Abstract
A link between hypertension and long-term bone health has been suggested. The aim of this study was to investigate the effects of chronic angiotensin II administration on urinary calcium/phosphate excretion, bone mineral density, bone remodeling and osteoblast population in a well-established experimental model of hypertension, in the absence of possible confounding factors that could affect bone metabolism. Male Sprague–Dawley rats, divided in the following groups: (a) Angiotensin II (Ang II, 200 ng/kg/min, osmotic minipumps, sub cutis, n = 8); (b) Ang II+losartan (Los, 50 mg/kg/day, per os, n = 6); (c) control group (physiological saline, sub cutis, n = 9); and (d) control+losartan (n = 6) were treated for four weeks. During the experimental period, 24-hour diuresis, urinary calcium, phosphate and sodium excretion were measured prior to the treatment, at two weeks of treatment, and at the end of the treatment. Systolic blood pressure was measured by plethysmography technique (tail cuff method). At the end of the experimental protocol, the rats were euthanized and peripheral quantitative computed tomography at the proximal metaphysis and at the diaphysis of the tibiae and quantitative bone histomorphometry on distal femora were performed. Angiotensin II-dependent hypertension is associated with increased calcium and phosphate excretion. AT1 receptor blockade prevented the increase of blood pressure and phosphate excretion but did not affect the increase of calcium excretion. These changes took place without significantly affecting bone density, bone histology or osteoblast population. In conclusion, in our experimental conditions, angiotensin II-dependent hypertension gave rise to an increased urinary excretion of calcium and phosphate without affecting bone density.
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- 2022
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9. Reporting Guidelines, Review of Methodological Standards, and Challenges Toward Harmonization in Bone Marrow Adiposity Research. Report of the Methodologies Working Group of the International Bone Marrow Adiposity Society
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Josefine Tratwal, Rossella Labella, Nathalie Bravenboer, Greet Kerckhofs, Eleni Douni, Erica L. Scheller, Sammy Badr, Dimitrios C. Karampinos, Sarah Beck-Cormier, Biagio Palmisano, Antonella Poloni, Maria J. Moreno-Aliaga, Jackie Fretz, Matthew S. Rodeheffer, Parastoo Boroumand, Clifford J. Rosen, Mark C. Horowitz, Bram C. J. van der Eerden, Annegreet G. Veldhuis-Vlug, and Olaia Naveiras
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bone marrow adiposity ,bone marrow adipose tissue ,bone marrow fat ,marrow ,adipocyte ,standards ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
The interest in bone marrow adiposity (BMA) has increased over the last decade due to its association with, and potential role, in a range of diseases (osteoporosis, diabetes, anorexia, cancer) as well as treatments (corticosteroid, radiation, chemotherapy, thiazolidinediones). However, to advance the field of BMA research, standardization of methods is desirable to increase comparability of study outcomes and foster collaboration. Therefore, at the 2017 annual BMA meeting, the International Bone Marrow Adiposity Society (BMAS) founded a working group to evaluate methodologies in BMA research. All BMAS members could volunteer to participate. The working group members, who are all active preclinical or clinical BMA researchers, searched the literature for articles investigating BMA and discussed the results during personal and telephone conferences. According to the consensus opinion, both based on the review of the literature and on expert opinion, we describe existing methodologies and discuss the challenges and future directions for (1) histomorphometry of bone marrow adipocytes, (2) ex vivo BMA imaging, (3) in vivo BMA imaging, (4) cell isolation, culture, differentiation and in vitro modulation of primary bone marrow adipocytes and bone marrow stromal cell precursors, (5) lineage tracing and in vivo BMA modulation, and (6) BMA biobanking. We identify as accepted standards in BMA research: manual histomorphometry and osmium tetroxide 3D contrast-enhanced μCT for ex vivo quantification, specific MRI sequences (WFI and H-MRS) for in vivo studies, and RT-qPCR with a minimal four gene panel or lipid-based assays for in vitro quantification of bone marrow adipogenesis. Emerging techniques are described which may soon come to complement or substitute these gold standards. Known confounding factors and minimal reporting standards are presented, and their use is encouraged to facilitate comparison across studies. In conclusion, specific BMA methodologies have been developed. However, important challenges remain. In particular, we advocate for the harmonization of methodologies, the precise reporting of known confounding factors, and the identification of methods to modulate BMA independently from other tissues. Wider use of existing animal models with impaired BMA production (e.g., Pfrt−/−, KitW/W−v) and development of specific BMA deletion models would be highly desirable for this purpose.
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- 2020
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10. Brief Report From the 3rd International Meeting on Bone Marrow Adiposity (BMA 2017)
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Alessandro Corsi, Biagio Palmisano, Josefine Tratwal, Mara Riminucci, and Olaia Naveiras
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bone marrow adiposity ,bone marrow adipocytes ,bone marrow ,bone marrow adiposity society (BMAS) ,bone ,bone marrow fat ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
The 3rd International Meeting on Bone Marrow Adiposity (BMA) was held at the Olympic Museum in Lausanne, Switzerland, on August 31st and September 1st, 2017. This brief monograph summarizes the scientific contents of the meeting and highlights the birth of the International Bone Marrow Adiposity Society (BMAS).
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- 2019
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11. From Stem Cells to Bone-Forming Cells
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Samantha Donsante, Biagio Palmisano, Marta Serafini, Pamela G. Robey, Alessandro Corsi, and Mara Riminucci
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osteoblasts ,skeletal stem cells ,bone ,bone marrow stromal cells ,skeletal biology ,Biology (General) ,QH301-705.5 ,Chemistry ,QD1-999 - Abstract
Bone formation starts near the end of the embryonic stage of development and continues throughout life during bone modeling and growth, remodeling, and when needed, regeneration. Bone-forming cells, traditionally termed osteoblasts, produce, assemble, and control the mineralization of the type I collagen-enriched bone matrix while participating in the regulation of other cell processes, such as osteoclastogenesis, and metabolic activities, such as phosphate homeostasis. Osteoblasts are generated by different cohorts of skeletal stem cells that arise from different embryonic specifications, which operate in the pre-natal and/or adult skeleton under the control of multiple regulators. In this review, we briefly define the cellular identity and function of osteoblasts and discuss the main populations of osteoprogenitor cells identified to date. We also provide examples of long-known and recently recognized regulatory pathways and mechanisms involved in the specification of the osteogenic lineage, as assessed by studies on mice models and human genetic skeletal diseases.
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- 2021
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12. 'Non-phosphaturic' variant of phosphaturic mesenchymal tumor of the middle ear expressing multiple phosphatonins
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Biagio Palmisano, Annalisa Pace, Luciano Colangelo, Roberta Polimeni, Chiara Sonato, Daniela Messineo, Salvatore Minisola, Giuseppe Magliulo, Mara Riminucci, and Alessandro Corsi
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non-phosphaturic variant ,Otorhinolaryngology ,FGF23 ,tumor-induced osteomalacia ,middle ear ,matrix extracellular phosphoglycoprotein ,FGF7 - Published
- 2023
13. Zoledronic Acid in a Mouse Model of Human Fibrous Dysplasia: Ineffectiveness on Tissue Pathology, Formation of 'Giant Osteoclasts' and Pathogenetic Implications
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Cristina Remoli, Annamaria Di Filippo, Emanuela Spica, Mara Riminucci, Francesca Fabretti, Alessandro Corsi, Michele Dello Spedale Venti, Marta Serafini, Ilenia Coletta, Rossella Labella, Biagio Palmisano, and Samantha Donsante
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Genetically modified mouse ,musculoskeletal diseases ,Pathology ,medicine.medical_specialty ,Nitrogen-containing bisphosphonates ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Osteoclasts ,Mice, Transgenic ,Bone tissue ,Fibrous dysplasia ,Giant Cells ,Zoledronic Acid ,Mice ,Endocrinology ,Osteoclast ,medicine ,Animals ,Orthopedics and Sports Medicine ,Original Research ,biology ,Diphosphonates ,business.industry ,Fibrous Dysplasia of Bone ,Bisphosphonate ,medicine.disease ,Disease Models, Animal ,Zoledronic acid ,medicine.anatomical_structure ,Denosumab ,RANKL ,Giant osteoclasts ,biology.protein ,denosumab ,fibrous dysplasia ,giant osteoclasts ,nitrogen-containing bisphosphonates ,zoledronic acid ,business ,medicine.drug - Abstract
We compared the effects of a nitrogen-containing bisphosphonate (N-BP), zoledronic acid (ZA), and an anti-mouse RANKL antibody (anti-mRANKL Ab) on the bone tissue pathology of a transgenic mouse model of human fibrous dysplasia (FD). For comparison, we also reviewed the histological samples of a child with McCune–Albright syndrome (MAS) treated with Pamidronate for 3 years. EF1α-GsαR201C mice with FD-like lesions in the tail vertebrae were treated with either 0.2 mg/kg of ZA at day 0, 7, and 14 or with 300 μg/mouse of anti-mRANKL Ab at day 0 and 21. All mice were monitored by Faxitron and histological analysis was performed at day 42. ZA did not affect the progression of the radiographic phenotype in EF1α-GsαR201C mice. FD-like lesions in the ZA group showed the persistence of osteoclasts, easily detectable osteoclast apoptotic activity and numerous “giant osteoclasts”. In contrast, in the anti-mRANKL Ab-treated mice, osteoclasts were markedly reduced/absent, the radiographic phenotype reverted and the FD-like lesions were extensively replaced by newly formed bone. Numerous “giant osteoclasts” were also detected in the samples of the child with MAS. This study supports the hypothesis that osteoclasts per se, independently of their resorptive activity, are essential for development and expansion of FD lesions.
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- 2020
14. Muscle-derived interleukin 6 increases exercise capacity by signaling in osteoblasts
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Helga Ellingsgaard, Paula Mera, Biagio Palmisano, Logan C Schulz, Gerard Karsenty, Juan Hidalgo, Jens C. Brüning, Julian Meyer Berger, Subrata Chowdhury, Vijay K. Yadav, and Parminder Singh
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0301 basic medicine ,medicine.medical_specialty ,medicine.medical_treatment ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Osteoclast ,Internal medicine ,medicine ,Animals ,Endocrine system ,Muscle, Skeletal ,Interleukin 6 ,Receptor ,Mice, Knockout ,Osteoblasts ,biology ,Interleukin-6 ,Catabolism ,business.industry ,Skeletal muscle ,General Medicine ,Macaca mulatta ,osteocalcin ,muscle ,bone ,osteoblasts ,osteoclasts ,030104 developmental biology ,medicine.anatomical_structure ,Cytokine ,Endocrinology ,030220 oncology & carcinogenesis ,Osteocalcin ,biology.protein ,Female ,business ,Signal Transduction ,Research Article - Abstract
Given the numerous health benefits of exercise, understanding how exercise capacity is regulated is a question of paramount importance. Circulating interleukin 6 (IL-6) levels surge during exercise and IL-6 favors exercise capacity. However, neither the cellular origin of circulating IL-6 during exercise nor the means by which this cytokine enhances exercise capacity has been formally established yet. Here we show through genetic means that the majority of circulating IL-6 detectable during exercise originates from muscle and that to increase exercise capacity, IL-6 must signal in osteoblasts to favor osteoclast differentiation and the release of bioactive osteocalcin in the general circulation. This explains why mice lacking the IL-6 receptor only in osteoblasts exhibit a deficit in exercise capacity of similar severity to the one seen in mice lacking muscle-derived IL-6 (mIL-6), and why this deficit is correctable by osteocalcin but not by IL-6. Furthermore, in agreement with the notion that IL-6 acts through osteocalcin, we demonstrate that mIL-6 promotes nutrient uptake and catabolism into myofibers during exercise in an osteocalcin-dependent manner. Finally, we show that the crosstalk between osteocalcin and IL-6 is conserved between rodents and humans. This study provides evidence that a muscle-bone-muscle endocrine axis is necessary to increase muscle function during exercise in rodents and humans.
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- 2020
15. Gsα
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Biagio, Palmisano, Rossella, Labella, Samantha, Donsante, Cristina, Remoli, Emanuela, Spica, Ilenia, Coletta, Giorgia, Farinacci, Michele, Dello Spedale Venti, Isabella, Saggio, Marta, Serafini, Pamela Gehron, Robey, Alessandro, Corsi, and Mara, Riminucci
- Abstract
The Gsα/cAMP signaling pathway mediates the effect of a variety of hormones and factors that regulate the homeostasis of the post-natal skeleton. Hence, the dysregulated activity of Gsα due to gain-of-function mutations (R201C/R201H) results in severe architectural and functional derangements of the entire bone/bone marrow organ. While the consequences of gain-of-function mutations of Gsα have been extensively investigated in osteoblasts and in bone marrow osteoprogenitor cells at various differentiation stages, their effect in adipogenically-committed bone marrow stromal cells has remained unaddressed. We generated a mouse model with expression of Gsα
- Published
- 2021
16. Activated Gs⍺ pathway and estrogens reveal different subsets of adiponectin-expressing osteoprogenitors within bone marrow stroma
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Biagio Palmisano, Rossella Labella, Samantha Donsante, Ilenia Coletta, Giorgia Farinacci, Michele Dello Spedale Venti, Pamela Gehron Robey, Alessandro Corsi, and Mara Riminucci
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Endocrinology, Diabetes and Metabolism ,Orthopedics and Sports Medicine - Published
- 2022
17. Gene expression profiling in a mouse model of human Fibrous dysplasia reveals a role for matrix remodeling in the physiopathology of the disease
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Giorgia Farinacci, Biagio Palmisano, Ilenia Coletta, Samantha Donsante, Michele Dello Spedale Venti, Alessandro Corsi, Domenico Raimondo, and Mara Riminucci
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Endocrinology, Diabetes and Metabolism ,Orthopedics and Sports Medicine - Published
- 2022
18. From stem cells to bone-forming cells
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Marta Serafini, Samantha Donsante, Alessandro Corsi, Mara Riminucci, Biagio Palmisano, and Pamela Gehron Robey
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Lineage (genetic) ,Cell ,Review ,Biology ,bone ,Bone and Bones ,Catalysis ,Epigenesis, Genetic ,lcsh:Chemistry ,Inorganic Chemistry ,bone marrow stromal cells ,osteoblasts ,skeletal biology ,skeletal stem cells ,Osteogenesis ,medicine ,Animals ,Humans ,Physical and Theoretical Chemistry ,lcsh:QH301-705.5 ,Molecular Biology ,Spectroscopy ,Stem Cells ,Regeneration (biology) ,Organic Chemistry ,Embryonic Stage ,General Medicine ,Embryonic stem cell ,Computer Science Applications ,Cell biology ,medicine.anatomical_structure ,lcsh:Biology (General) ,lcsh:QD1-999 ,Bone forming ,Stem cell ,Function (biology) ,Signal Transduction - Abstract
Bone formation starts near the end of the embryonic stage of development and continues throughout life during bone modeling and growth, remodeling, and when needed, regeneration. Bone-forming cells, traditionally termed osteoblasts, produce, assemble, and control the mineralization of the type I collagen-enriched bone matrix while participating in the regulation of other cell processes, such as osteoclastogenesis, and metabolic activities, such as phosphate homeostasis. Osteoblasts are generated by different cohorts of skeletal stem cells that arise from different embryonic specifications, which operate in the pre-natal and/or adult skeleton under the control of multiple regulators. In this review, we briefly define the cellular identity and function of osteoblasts and discuss the main populations of osteoprogenitor cells identified to date. We also provide examples of long-known and recently recognized regulatory pathways and mechanisms involved in the specification of the osteogenic lineage, as assessed by studies on mice models and human genetic skeletal diseases.
- Published
- 2021
19. Validated Fall Risk Assessment Tools for Use with Older Adults: A Systematic Review
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Giovanni Galeoto, Roberta Mollica, Marcello Ruggieri, Valter Santilli, Biagio Palmisano, Anna Berardi, and Giancarlo Fratocchi
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Gerontology ,business.industry ,education ,Rehabilitation ,MEDLINE ,Adults ,aged ,fall risk assessment ,older ,systematic review ,validation questionnaire ,CINAHL ,PsycINFO ,03 medical and health sciences ,0302 clinical medicine ,Occupational Therapy ,Medicine ,030212 general & internal medicine ,Geriatrics and Gerontology ,business ,030217 neurology & neurosurgery ,Fall risk assessment - Abstract
Aims: to find and describe, through a systematic review, validated assessment tool that evaluate the fall risk in older adults. Methods: MEDLINE, PEDro, CINAHL, and PsycINFO were consulted and no r...
- Published
- 2018
20. RANKL Inhibition in Fibrous Dysplasia of Bone: A Preclinical Study in a Mouse Model of the Human Disease
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Samantha Donsante, Franco Marinozzi, Emanuela Spica, Alessandro Corsi, Alan Boyde, Rossella Labella, Fabiano Bini, Annamaria Di Filippo, Mara Riminucci, Biagio Palmisano, Domenico Raimondo, Cristina Remoli, and Pamela Gehron Robey
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musculoskeletal diseases ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Endocrinology, Diabetes and Metabolism ,Bone pathology ,030209 endocrinology & metabolism ,Mice, Transgenic ,Osteolysis ,Bone resorption ,Bone and Bones ,bone remodelling ,denosumab ,fibrous dysplasia ,RANKL ,GSα ,Bone remodeling ,03 medical and health sciences ,0302 clinical medicine ,Human disease ,Calcification, Physiologic ,Peptide Elongation Factor 1 ,GTP-Binding Protein alpha Subunits, Gs ,Medicine ,Animals ,Humans ,Orthopedics and Sports Medicine ,Bone pain ,biology ,business.industry ,Fibrous dysplasia ,RANK Ligand ,Fibrous Dysplasia of Bone ,medicine.disease ,Biomechanical Phenomena ,Rats ,Disease Models, Animal ,030104 developmental biology ,Denosumab ,Phenotype ,biology.protein ,Disease Progression ,Histopathology ,medicine.symptom ,business ,medicine.drug - Abstract
Fibrous dysplasia of bone/McCune-Albright syndrome (Polyostotic FD/MAS; OMIM#174800) is a crippling skeletal disease caused by gain-of-function mutations of Gs α. Enhanced bone resorption is a recurrent histological feature of FD and a major cause of fragility of affected bones. Previous work suggests that increased bone resorption in FD is driven by RANKL and some studies have shown that the anti-RANKL monoclonal antibody, denosumab, reduces bone turnover and bone pain in FD patients. However, the effect of RANKL inhibition on the histopathology of FD and its impact on the natural history of the disease remain to be assessed. In this study, we treated the EF1α-Gs αR201C mice, which develop an FD-like phenotype, with an anti-mouse RANKL monoclonal antibody. We found that the treatment induced marked radiographic and microscopic changes at affected skeletal sites in 2-month-old mice. The involved skeletal segments became sclerotic due to the deposition of new, highly mineralized bone within developing FD lesions and showed a higher mechanical resistance compared to affected segments from untreated transgenic mice. Similar changes were also detected in older mice with a full-blown skeletal phenotype. The administration of anti-mouse RANKL antibody arrested the growth of established lesions and, in young mice, prevented the appearance of new ones. However, after drug withdrawal, the newly formed bone was remodelled into FD tissue and the disease progression resumed in young mice. Taken together, our results show that the anti-RANKL antibody significantly affected the bone pathology and natural history of FD in the mouse. Pending further work on the prevention and management of relapse after treatment discontinuation, our preclinical study suggests that RANKL inhibition may be an effective therapeutic option for FD patients. © 2019 American Society for Bone and Mineral Research.
- Published
- 2019
21. Anti-RANKL treatment in a murine model of fibrous dysplasia
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Cristina Remoli, Alessandro Corsi, Pamela Gehron Robey, Mara Riminucci, Rossella Labella, Emanuela Spica, and Biagio Palmisano
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biology ,business.industry ,Fibrous dysplasia ,General Medicine ,medicine.disease ,030226 pharmacology & pharmacy ,03 medical and health sciences ,0302 clinical medicine ,RANKL ,Murine model ,medicine ,biology.protein ,Cancer research ,030212 general & internal medicine ,business - Published
- 2017
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