11 results on '"Yi Ping Li"'
Search Results
2. Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development
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Jingjing Ben, Yang Zhang, Haojie Liu, Lichan Yuan, Li Meng, Shuyu Guo, Junqing Ma, Na Zhao, Jieli Ni, and Yi-Ping Li
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0301 basic medicine ,Neural crest cells ,Craniofacial abnormality ,Medicine (miscellaneous) ,Biology ,Cell Line ,Myh9 ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Cell Movement ,medicine ,Animals ,Humans ,RNA, Messenger ,Craniofacial ,cell migration ,Pharmacology, Toxicology and Pharmaceutics (miscellaneous) ,Zebrafish ,beta Catenin ,craniofacial deformity ,Mice, Knockout ,Myosin Heavy Chains ,Gene Expression Regulation, Developmental ,Neural crest ,Cell Differentiation ,Cell migration ,Morphant ,Embryo, Mammalian ,medicine.disease ,biology.organism_classification ,Phenotype ,Cell biology ,HEK293 Cells ,030104 developmental biology ,Neural Crest ,Trio ,embryonic structures ,Knockout mouse ,030217 neurology & neurosurgery ,Signal Transduction ,Research Paper - Abstract
Trio is a unique member of the Rho-GEF family that has three catalytic domains and is vital for various cellular processes in both physiological and developmental settings. TRIO mutations in humans are involved in craniofacial abnormalities, in which patients present with mandibular retrusion. However, little is known about the molecular mechanisms of Trio in neural crest cell (NCC)-derived craniofacial development, and there is still a lack of direct evidence to assign a functional role to Trio in NCC-induced craniofacial abnormalities. Methods: In vivo, we used zebrafish and NCC-specific knockout mouse models to investigate the phenotype and dynamics of NCC development in Trio morphants. In vitro, iTRAQ, GST pull-down assays, and proximity ligation assay (PLA) were used to explore the role of Trio and its potential downstream mediators in NCC migration and differentiation. Results: In zebrafish and mouse models, disruption of Trio elicited a migration deficit and impaired the differentiation of NCC derivatives, leading to craniofacial growth deficiency and mandibular retrusion. Moreover, Trio positively regulated Myh9 expression and directly interacted with Myh9 to coregulate downstream cellular signaling in NCCs. We further demonstrated that disruption of Trio or Myh9 inhibited Rac1 and Cdc42 activity, specifically affecting the nuclear export of β-catenin and NCC polarization. Remarkably, craniofacial abnormalities caused by trio deficiency in zebrafish could be partially rescued by the injection of mRNA encoding myh9, ca-Rac1, or ca-Cdc42. Conclusions: Here, we identified that Trio, interacting mostly with Myh9, acts as a key regulator of NCC migration and differentiation during craniofacial development. Our results indicate that trio morphant zebrafish and Wnt1-cre;Triofl/fl mice offer potential model systems to facilitate the study of the pathogenic mechanisms of Trio mutations causing craniofacial abnormalities. more...
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- 2021
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3. TRAF Family Member-Associated NF-κB Activator (TANK) Induced by RANKL Negatively Regulates Osteoclasts Survival and Function
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Mengrui Wu, Yiping Wang, Lianfu Deng, Wei Chen, Yi-Ping Li
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Biology (General) ,QH301-705.5 - Abstract
Osteoclasts are the principle bone-resorbing cells. Precise control of balanced osteoclast activity is indispensable for bone homeostasis. Osteoclast activation mediated by RANK-TRAF6 axis has been clearly identified. However, a negative regulation-machinery in osteoclast remains unclear. TRAF family member-associated NF-κB activator (TANK) is induced by about 10 folds during osteoclastogenesis, according to a genome-wide analysis of gene expression before and after osteoclast maturation, and confirmed by western blot and quantitative RT-PCR. Bone marrow macrophages (BMMs) transduced with lentivirus carrying tank-shRNA were induced to form osteoclast in the presence of RANKL and M-CSF. Tank expression was downregulated by 90% by Tank-shRNA, which is confirmed by western blot. Compared with wild-type (WT) cells, osteoclastogenesis of Tank-silenced BMMs was increased, according to tartrate-resistant acid phosphatase (TRAP) stain on day 5 and day 7. Number of bone resorption pits by Tank-silenced osteoclasts was increased by 176% compared with WT cells, as shown by wheat germ agglutinin (WGA) stain and scanning electronic microscope (SEM) analysis. Survival rate of Tank-silenced mature osteoclast is also increased. However, acid production of Tank-knockdown cells was not changed compared with control cells. IκBα phosphorylation is increased in tank-silenced cells, indicating that TANK may negatively regulate NF-κB activity in osteoclast. In conclusion, Tank, whose expression is increased during osteoclastogenesis, inhibits osteoclast formation, activity and survival, by regulating NF-κB activity and c-FLIP expression. Tank enrolls itself in a negative feedback loop in bone resorption. These results may provide means for therapeutic intervention in diseases of excessive bone resorption. more...
- Published
- 2012
4. TGF-β and BMP Signaling in Osteoblast Differentiation and Bone Formation
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Guiqian Chen, Chuxia Deng, Yi-Ping Li
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Biology (General) ,QH301-705.5 - Abstract
Transforming growth factor-beta (TGF-β)/bone morphogenic protein (BMP) signaling is involved in a vast majority of cellular processes and is fundamentally important throughout life. TGF-β/BMPs have widely recognized roles in bone formation during mammalian development and exhibit versatile regulatory functions in the body. Signaling transduction by TGF-β/BMPs is specifically through both canonical Smad-dependent pathways (TGF-β/BMP ligands, receptors and Smads) and non-canonical Smad-independent signaling pathway (e.g. p38 mitogen-activated protein kinase pathway, MAPK). Following TGF-β/BMP induction, both the Smad and p38 MAPK pathways converge at the Runx2 gene to control mesenchymal precursor cell differentiation. The coordinated activity of Runx2 and TGF-β/BMP-activated Smads is critical for formation of the skeleton. Recent advances in molecular and genetic studies using gene targeting in mice enable a better understanding of TGF-β/BMP signaling in bone and in the signaling networks underlying osteoblast differentiation and bone formation. This review summarizes the recent advances in our understanding of TGF-β/BMP signaling in bone from studies of genetic mouse models and human diseases caused by the disruption of TGF-β/BMP signaling. This review also highlights the different modes of cross-talk between TGF-β/BMP signaling and the signaling pathways of MAPK, Wnt, Hedgehog, Notch, and FGF in osteoblast differentiation and bone formation. more...
- Published
- 2012
5. Knockout and Double Knockout of Cathepsin K and Mmp9 reveals a novel function of Cathepsin K as a regulator of osteoclast gene expression and bone homeostasis.
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Guochun Zhu, Wei Chen, Chen-Yi Tang, McVicar, Abigail, Edwards, Diep, Jinwen Wang, McConnell, Matthew, Shuying Yang, Yang Li, Zhijie Chang, and Yi-Ping Li
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- 2022
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6. GPR125 positively regulates osteoclastogenesis potentially through AKT-NF-κB and MAPK signaling pathways.
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Chen-Yi Tang, He Wang, Yan Zhang, Zhongliang Wang, Guochun Zhu, McVicar, Abigail, Yi-Ping Li, and Wei Chen
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- 2022
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7. Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development.
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Shuyu Guo, Li Meng, Haojie Liu, Lichan Yuan, Na Zhao, Jieli Ni, Yang Zhang, Jingjing Ben, Yi-Ping Li, and Junqing Ma
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- 2021
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8. Chondrocyte-specific Knockout of Cbfβ Reveals the Indispensable Function of Cbfβ in Chondrocyte Maturation, Growth Plate Development and Trabecular Bone Formation in Mice
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Yun Lu, Rosa Serra, Wei Chen, Yiping Wang, Jian-Zhong Shao, Yi-Ping Li, Joel Jules, Mengrui Wu, Matthew McConnell, and Guochun Zhu
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medicine.medical_specialty ,Indian hedgehog ,Long bone ,Osteoporosis ,In Vitro Techniques ,Applied Microbiology and Biotechnology ,Core Binding Factor beta Subunit ,Chondrocyte ,Runx ,endochondral bone formation ,Mice ,03 medical and health sciences ,Chondrocytes ,0302 clinical medicine ,Osteogenesis ,Osteoclast ,Internal medicine ,medicine ,Animals ,Growth Plate ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,030304 developmental biology ,0303 health sciences ,biology ,Cbfβ ,Cartilage ,skeletal development ,Cell Biology ,Chondrogenesis ,biology.organism_classification ,medicine.disease ,RUNX2 ,chondrocyte proliferation and hypertrophy ,medicine.anatomical_structure ,Endocrinology ,Indian hedgehog (Ihh) ,030217 neurology & neurosurgery ,Research Paper ,Developmental Biology - Abstract
Despite years of research into bone formation, the mechanisms by which transcription factors specify growth plate development and trabecular bone formation remain unclear and the role of hypertrophic chondrocytes in trabeculae morphogenesis is controversial. To study the role of Core binding factor beta (Cbfβ) in postnatal cartilage development and endochondral bone formation, we generated chondrocyte-specific Cbfβ-deficient mice (Cbfβf/fCol2α1-Cre mice) using floxed alleles of Cbfβ (Cbfβf/f) and Cre driven by the Collagen 2α1 promoter (Col2α1-Cre). Cbfβf/fCol2α1-Cre mice evaded developmental and newborn lethality to survive to adulthood and displayed severe skeletal malformation. Cbfβf/fCol2α1-Cre mice had dwarfism, hypoplastic skeletons, defective bone mineralization, shortened limbs, shortened sternum bodies, and un-calcified occipital bones and hyoid bones. In the long bone cartilage, the resting zone was elongated, and chondrocyte proliferation and hypertrophy were impaired in Cbfβf/fCol2α1-Cre mice, which led to deformation of the growth plates. Primary spongiosa formation was delayed, diaphysis was shortened and trabecular bone formation was almost absent in the mutant mice. In addition, lamellar bone formation in the secondary spongiosa was also impaired. However, osteoclast formation in the trabecular bone was not affected. Cbfβ deficiency led to down-regulation of chondrocyte-regulating genes [i.e, patched (Ptc1), Cyclin D1 and Indian hedgehog (Ihh)] in the cartilage. Interestingly, the expression of Runx2 and Runx3 was not changed in the cartilage of the mutants. Collectively, the results revealed that Cbfβ is crucial for postnatal skeletal development and endochondral bone formation through its function in growth plate development and chondrocyte proliferation and differentiation. This study also revealed that chondrocyte maturation, mediated by Cbfβ, was critical to trabecular bone morphogenesis. Significantly, these findings provide insight into the role of Cbfβ in postnatal skeletogenesis, which may assist in the development of new therapies for osteoporosis. more...
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- 2014
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9. Silencing of Atp6v1c1 Prevents Breast Cancer Growth and Bone Metastasis
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Wei Chen, Matthew McConnell, Qiang Zhao, Shengmei Feng, Qi Zhou, Lianfu Deng, Guochun Zhu, Yi-Ping Li, Mengrui Wu, Jinshen Wang, and Jin Qi
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Vacuolar Proton-Translocating ATPases ,Immunoblotting ,Atp6v1c1 (C1) ,V-ATPase ,Bone Neoplasms ,Breast Neoplasms ,lysosomal acidification ,Biology ,Applied Microbiology and Biotechnology ,Metastasis ,Mice ,03 medical and health sciences ,breast cancer ,0302 clinical medicine ,Breast cancer ,Cell Movement ,Cell Line, Tumor ,medicine ,Animals ,Neoplasm Invasiveness ,Gene Silencing ,Neoplasm Metastasis ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,Cell Proliferation ,DNA Primers ,030304 developmental biology ,0303 health sciences ,Matrigel ,Mammary tumor ,Reverse Transcriptase Polymerase Chain Reaction ,Cell growth ,Lentivirus ,Bone metastasis ,Cancer ,Cell Biology ,medicine.disease ,Immunohistochemistry ,3. Good health ,tumor bone metastasis ,Gene Knockdown Techniques ,030220 oncology & carcinogenesis ,Luminescent Measurements ,Cancer cell ,Cancer research ,Female ,RNA Interference ,Research Paper ,Developmental Biology - Abstract
Previous studies have shown that Atp6v1c1, a regulator of the assembly of the V0 and V1 domains of the V-ATPase complex, is up-regulated in metastatic oral tumors. Despite these studies, the function of Atp6v1c1 in tumor growth and metastasis is still unknown. Atp6v1c1's expression in metastatic oral squamous cell carcinoma indicates that Atp6v1c1 has an important function in cancer growth and metastasis. We hypothesized that elevated expression of Atp6v1c1 is essential to cancer growth and metastasis and that Atp6v1c1 promotes cancer growth and metastasis through activation of V-ATPase activity. To test this hypothesis, a Lentivirus-mediated RNAi knockdown approach was used to study the function of Atp6v1c1 in mouse 4T1 mammary tumor cell proliferation and migration in vitro and cancer growth and metastasis in vivo. Our data revealed that silencing of Atp6v1c1 in 4T1 cancer cells inhibited lysosomal acidification and severely impaired 4T1 cell growth, migration, and invasion through Matrigel in vitro. We also show that Atp6v1c1 knockdown with Lenti-c1s3, a lentivirus targeting Atp6v1c1 for shRNA mediated knockdown, can significantly inhibit 4T1 xenograft tumor growth, metastasis, and osteolytic lesions in vivo. Our study demonstrates that Atp6v1c1 may promote breast cancer growth and bone metastasis through regulation of lysosomal V-ATPase activity, indicating that Atp6v1c1 may be a viable target for breast cancer therapy and silencing of Atp6v1c1 may be an innovative therapeutic approach for the treatment and prevention of breast cancer growth and metastasis. more...
- Published
- 2013
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10. Anterior Visceral Endoderm SMAD4 Signaling Specifies Anterior Embryonic Patterning and Head Induction in Mice
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Cuiling Li, Yi-Ping Li, Xin-Yuan Fu, Chu-Xia Deng
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animal structures ,integumentary system ,lcsh:Biology (General) ,embryonic structures ,biological phenomena, cell phenomena, and immunity ,lcsh:QH301-705.5 ,digestive system diseases - Abstract
SMAD4 serves as a common mediator for signaling of TGF-β superfamily. Previous studies illustrated that SMAD4-null mice die at embryonic day 6.5 (E6.5) due to failure of mesoderm induction and extraembryonic defects; however, functions of SMAD4 in each germ layer remain elusive. To investigate this, we disrupted SMAD4 in the visceral endoderm and epiblast, respectively, using a Cre-loxP mediated approach. We showed that mutant embryos lack of SMAD4 in the visceral endoderm (Smad4Co/Co;TTR-Cre) died at E7.5-E9.5 without head-fold and anterior embryonic structures. We demonstrated that TGF-β regulates expression of several genes, such as Hex1, Cer1, and Lim1, in the anterior visceral endoderm (AVE), and the failure of anterior embryonic development in Smad4Co/Co;TTR-Cre embryos is accompanied by diminished expression of these genes. Consistent with this finding, SMAD4-deficient embryoid bodies showed impaired responsiveness to TGF-β-induced gene expression and morphological changes. On the other hand, embryos carrying Cre-loxP mediated disruption of SMAD4 in the epiblasts exhibited relatively normal mesoderm and head-fold induction although they all displayed profound patterning defects in the later stages of gastrulation. Cumulatively, our data indicate that SMAD4 signaling in the epiblasts is dispensable for mesoderm induction although it remains critical for head patterning, which is significantly different from SMAD4 signaling in the AVE, where it specifies anterior embryonic patterning and head induction. more...
- Published
- 2010
11. Anterior Visceral Endoderm SMAD4 Signaling Specifies Anterior Embryonic Patterning and Head Induction in Mice
- Author
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Yi-Ping Li, Chu-Xia Deng, Cuiling Li, and Xin-Yuan Fu
- Subjects
Mesoderm ,medicine.medical_specialty ,animal structures ,Embryonic Development ,Embryoid body ,Germ layer ,Biology ,SMAD4 ,Applied Microbiology and Biotechnology ,GDF1 ,Mice ,Pregnancy ,Transforming Growth Factor beta ,Internal medicine ,mesoderm patterning ,medicine ,Animals ,TGF-beta ,Molecular Biology ,In Situ Hybridization ,Ecology, Evolution, Behavior and Systematics ,Smad4 Protein ,AVE ,integumentary system ,Reverse Transcriptase Polymerase Chain Reaction ,epiblast ,Endoderm ,Gene Expression Regulation, Developmental ,Cell Biology ,Mice, Mutant Strains ,digestive system diseases ,Cell biology ,Gastrulation ,Viscera ,medicine.anatomical_structure ,Endocrinology ,Epiblast ,embryonic structures ,Female ,biological phenomena, cell phenomena, and immunity ,NODAL ,Head ,Research Paper ,Developmental Biology - Abstract
SMAD4 serves as a common mediator for signaling of TGF-β superfamily. Previous studies illustrated that SMAD4-null mice die at embryonic day 6.5 (E6.5) due to failure of mesoderm induction and extraembryonic defects; however, functions of SMAD4 in each germ layer remain elusive. To investigate this, we disrupted SMAD4 in the visceral endoderm and epiblast, respectively, using a Cre-loxP mediated approach. We showed that mutant embryos lack of SMAD4 in the visceral endoderm (Smad4(Co/Co);TTR-Cre) died at E7.5-E9.5 without head-fold and anterior embryonic structures. We demonstrated that TGF-β regulates expression of several genes, such as Hex1, Cer1, and Lim1, in the anterior visceral endoderm (AVE), and the failure of anterior embryonic development in Smad4(Co/Co);TTR-Cre embryos is accompanied by diminished expression of these genes. Consistent with this finding, SMAD4-deficient embryoid bodies showed impaired responsiveness to TGF-β-induced gene expression and morphological changes. On the other hand, embryos carrying Cre-loxP mediated disruption of SMAD4 in the epiblasts exhibited relatively normal mesoderm and head-fold induction although they all displayed profound patterning defects in the later stages of gastrulation. Cumulatively, our data indicate that SMAD4 signaling in the epiblasts is dispensable for mesoderm induction although it remains critical for head patterning, which is significantly different from SMAD4 signaling in the AVE, where it specifies anterior embryonic patterning and head induction. more...
- Published
- 2010
- Full Text
- View/download PDF
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