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1,179 results on '"Borén, Jan"'

3. Combined metabolic activators improve cognitive functions in Alzheimer’s disease patients: a randomised, double-blinded, placebo-controlled phase-II trial

Author

Yulug, Burak, Altay, Ozlem, Li, Xiangyu, Hanoglu, Lutfu, Cankaya, Seyda, Lam, Simon, Velioglu, Halil Aziz, Yang, Hong, Coskun, Ebru, Idil, Ezgi, Nogaylar, Rahim, Ozsimsek, Ahmet, Bayram, Cemil, Bolat, Ismail, Oner, Sena, Tozlu, Ozlem Ozdemir, Arslan, Mehmet Enes, Hacimuftuoglu, Ahmet, Yildirim, Serkan, Arif, Muhammad, Shoaie, Saeed, Zhang, Cheng, Nielsen, Jens, Turkez, Hasan, Borén, Jan, Uhlén, Mathias, and Mardinoglu, Adil

Published
2023
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10. Intussusceptive Angiogenesis in Human Metastatic Malignant Melanoma

Author

Pandita, Ankur, Ekstrand, Matias, Bjursten, Sara, Zhao, Zhiyuan, Fogelstrand, Per, Le Gal, Kristell, Ny, Lars, Bergo, Martin O, Karlsson, Joakim, Nilsson, Jonas A, Akyürek, Levent M, Levin, Malin C, Borén, Jan, Ewald, Andrew J, Mostov, Keith E, and Levin, Max

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Genetics, Biotechnology, 2.1 Biological and endogenous factors, Aetiology, Aged, Aged, 80 and over, Animals, Female, Heterografts, Humans, Male, Matrix Metalloproteinase 9, Melanoma, Mice, Middle Aged, Neovascularization, Pathologic, Skin Neoplasms, Medical and Health Sciences, Pathology, Biomedical and clinical sciences, Health sciences
Abstract

Angiogenesis supplies oxygen and nutrients to growing tumors. Inhibiting angiogenesis may stop tumor growth, but vascular endothelial growth factor inhibitors have limited effect in most tumors. This limited effect may be explained by an additional, less vascular endothelial growth factor-driven form of angiogenesis known as intussusceptive angiogenesis. The importance of intussusceptive angiogenesis in human tumors is not known. Epifluorescence and confocal microscopy was used to visualize intravascular pillars, the hallmark structure of intussusceptive angiogenesis, in tumors. Human malignant melanoma metastases, patient-derived melanoma xenografts in mice (PDX), and genetically engineered v-raf murine sarcoma viral oncogene homolog B1 (BRAF)-induced, phosphatase and TENsin homolog deleted on chromosome 10 (PTEN)-deficient (BPT) mice (BrafCA/+Ptenf/fTyr-Cre+/0-mice) were analyzed for pillars. Gene expression in human melanoma metastases and PDXs was analyzed by RNA sequencing. Matrix metalloproteinase 9 (MMP9) protein expression and T-cell and macrophage infiltration in tumor sections were determined with multiplex immunostaining. Intravascular pillars were detected in human metastases but rarely in PDXs and not in BPT mice. The expression of MMP9 mRNA was higher in human metastases compared with PDXs. High expression of MMP9 protein as well as infiltration of macrophages and T-cells were detected in proximity to intravascular pillars. MMP inhibition blocked formation of pillars, but not tubes or tip cells, in vitro. In conclusion, intussusceptive angiogenesis may contribute to the growth of human melanoma metastases. MMP inhibition blocked pillar formation in vitro and should be further investigated as a potential anti-angiogenic drug target in metastatic melanoma.

Published
2021

22. Metabolism of Triglyceride-Rich Lipoproteins

Author

Borén, Jan, Taskinen, Marja-Riitta, Barrett, James E., Editor-in-Chief, Flockerzi, Veit, Editorial Board Member, Frohman, Michael A., Editorial Board Member, Geppetti, Pierangelo, Editorial Board Member, Hofmann, Franz B., Editorial Board Member, Kuner, Rohini, Editorial Board Member, Michel, Martin C., Editorial Board Member, Page, Clive P., Editorial Board Member, Wang, KeWei, Editorial Board Member, von Eckardstein, Arnold, editor, and Binder, Christoph J., editor

Published
2022
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30. APRIL limits atherosclerosis by binding to heparan sulfate proteoglycans

Author

Tsiantoulas, Dimitrios, Eslami, Mahya, Obermayer, Georg, Clement, Marc, Smeets, Diede, Mayer, Florian J., Kiss, Máté G., Enders, Lennart, Weißer, Juliane, Göderle, Laura, Lambert, Jordi, Frommlet, Florian, Mueller, André, Hendrikx, Tim, Ozsvar-Kozma, Maria, Porsch, Florentina, Willen, Laure, Afonyushkin, Taras, Murphy, Jane E., Fogelstrand, Per, Donzé, Olivier, Pasterkamp, Gerard, Hoke, Matthias, Kubicek, Stefan, Jørgensen, Helle F., Danchin, Nicolas, Simon, Tabassome, Scharnagl, Hubert, März, Winfried, Borén, Jan, Hess, Henry, Mallat, Ziad, Schneider, Pascal, and Binder, Christoph J.

Published
2021
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32. Family-specific aggregation of lipid GWAS variants confers the susceptibility to familial hypercholesterolemia in a large Austrian family

Author

Nikkola, Elina, Ko, Arthur, Alvarez, Marcus, Cantor, Rita M, Garske, Kristina, Kim, Elliot, Gee, Stephanie, Rodriguez, Alejandra, Muxel, Reinhard, Matikainen, Niina, Söderlund, Sanni, Motazacker, Mahdi M, Borén, Jan, Lamina, Claudia, Kronenberg, Florian, Schneider, Wolfgang J, Palotie, Aarno, Laakso, Markku, Taskinen, Marja-Riitta, and Pajukanta, Päivi

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Digestive Diseases, Human Genome, Prevention, Genetics, Heart Disease, Cardiovascular, Atherosclerosis, Aetiology, 2.1 Biological and endogenous factors, Apolipoprotein B-100, Austria, Biomarkers, Cholesterol, DNA Mutational Analysis, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Heredity, Humans, Hyperlipoproteinemia Type II, Lipoprotein(a), Male, Middle Aged, Mutation, Pedigree, Phenotype, Polymorphism, Single Nucleotide, Receptors, LDL, Risk Factors, Exome Sequencing, Familial hypercholesterolemia, LDL cholesterol, Genetic risk score, Lipoprotein, Cardiorespiratory Medicine and Haematology, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

Background and aimsHypercholesterolemia confers susceptibility to cardiovascular disease (CVD). Both serum total cholesterol (TC) and LDL-cholesterol (LDL-C) exhibit a strong genetic component (heritability estimates 0.41-0.50). However, a large part of this heritability cannot be explained by the variants identified in recent extensive genome-wide association studies (GWAS) on lipids. Our aim was to find genetic causes leading to high LDL-C levels and ultimately CVD in a large Austrian family presenting with what appears to be autosomal dominant inheritance for familial hypercholesterolemia (FH).MethodsWe utilized linkage analysis followed by whole-exome sequencing and genetic risk score analysis using an Austrian multi-generational family with various dyslipidemias, including elevated TC and LDL-C, and one family branch with elevated lipoprotein (a) (Lp(a)).ResultsWe did not find evidence for genome-wide significant linkage for LDL-C or apparent causative variants in the known FH genes rather, we discovered a particular family-specific combination of nine GWAS LDL-C SNPs (p = 0.02 by permutation), and putative less severe familial hypercholesterolemia mutations in the LDLR and APOB genes in a subset of the affected family members. Separately, high Lp(a) levels observed in one branch of the family were explained primarily by the LPA locus, including short (

Published
2017

33. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

Author

Ference, Brian A, Ginsberg, Henry N, Graham, Ian, Ray, Kausik K, Packard, Chris J, Bruckert, Eric, Hegele, Robert A, Krauss, Ronald M, Raal, Frederick J, Schunkert, Heribert, Watts, Gerald F, Borén, Jan, Fazio, Sergio, Horton, Jay D, Masana, Luis, Nicholls, Stephen J, Nordestgaard, Børge G, van de Sluis, Bart, Taskinen, Marja-Riitta, Tokgözoğlu, Lale, Landmesser, Ulf, Laufs, Ulrich, Wiklund, Olov, Stock, Jane K, Chapman, M John, and Catapano, Alberico L

Subjects
Cardiovascular, Atherosclerosis, Clinical Trials and Supportive Activities, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Anticholesteremic Agents, Cholesterol, HDL, Cholesterol, LDL, Consensus, Epidemiologic Methods, Ezetimibe, Genetic Predisposition to Disease, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipidemias, Lipoproteins, LDL, PCSK9 Inhibitors, Cardiovascular disease, Causality, Clinical trials, Low-density lipoprotein, Mendelian randomization, PCSK9, Recommendations, Statin, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

AimsTo appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).Methods and resultsWe assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.ConclusionConsistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

Published
2017

34. CD38 as a therapeutic target in pediatric Burkitt’s Lymphoma: insights from a comparative approach (Running title: Targeting CD38 in pediatric Burkitt's Lymphoma)

Author

Kläsener, Kathrin, primary, Herrmann, Nadja, additional, Håversen, Liliana, additional, Sundell, Timothy, additional, Sundqvist, Martina, additional, Lundqvist, Christina, additional, Manna, Paul T., additional, Jonsson, Charlotte A., additional, Visentini, Marcella, additional, Sass, Diana Ljung, additional, McGrath, Sarah, additional, Grimstad, Kristoffer, additional, Aranburu, Alaitz, additional, Mellgren, Karin, additional, Fogelstrand, Linda, additional, Forsman, Huamei, additional, Ekwall, Olov, additional, Borén, Jan, additional, Gjertsson, Inger, additional, Reth, Michael, additional, Mårtensson, Inga-Lill, additional, and Camponeschi, Alessandro, additional

Published
2024
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37. Combined Metabolic Activators with Different NAD+ Precursors Improve Metabolic Functions in the Animal Models of Neurodegenerative Diseases.

Author

Altay, Ozlem, Yang, Hong, Yildirim, Serkan, Bayram, Cemil, Bolat, Ismail, Oner, Sena, Tozlu, Ozlem Ozdemir, Arslan, Mehmet Enes, Hacimuftuoglu, Ahmet, Shoaie, Saeed, Zhang, Cheng, Borén, Jan, Uhlén, Mathias, Turkez, Hasan, and Mardinoglu, Adil

Subjects
ALZHEIMER'S disease, PARKINSON'S disease, PATHOLOGICAL physiology, MITOCHONDRIAL pathology, ACETYLCYSTEINE, CALBINDIN, MOVEMENT disorders, METABOLIC disorders, DEACETYLATION
Abstract

Background: Mitochondrial dysfunction and metabolic abnormalities are acknowledged as significant factors in the onset of neurodegenerative disorders such as Parkinson's disease (PD) and Alzheimer's disease (AD). Our research has demonstrated that the use of combined metabolic activators (CMA) may alleviate metabolic dysfunctions and stimulate mitochondrial metabolism. Therefore, the use of CMA could potentially be an effective therapeutic strategy to slow down or halt the progression of PD and AD. CMAs include substances such as the glutathione precursors (L-serine and N-acetyl cysteine), the NAD+ precursor (nicotinamide riboside), and L-carnitine tartrate. Methods: Here, we tested the effect of two different formulations, including CMA1 (nicotinamide riboside, L-serine, N-acetyl cysteine, L-carnitine tartrate), and CMA2 (nicotinamide, L-serine, N-acetyl cysteine, L-carnitine tartrate), as well as their individual components, on the animal models of AD and PD. We assessed the brain and liver tissues for pathological changes and immunohistochemical markers. Additionally, in the case of PD, we performed behavioral tests and measured responses to apomorphine-induced rotations. Findings: Histological analysis showed that the administration of both CMA1 and CMA2 formulations led to improvements in hyperemia, degeneration, and necrosis in neurons for both AD and PD models. Moreover, the administration of CMA2 showed a superior effect compared to CMA1. This was further corroborated by immunohistochemical data, which indicated a reduction in immunoreactivity in the neurons. Additionally, notable metabolic enhancements in liver tissues were observed using both formulations. In PD rat models, the administration of both formulations positively influenced the behavioral functions of the animals. Interpretation: Our findings suggest that the administration of both CMA1 and CMA2 markedly enhanced metabolic and behavioral outcomes, aligning with neuro-histological observations. These findings underscore the promise of CMA2 administration as an effective therapeutic strategy for enhancing metabolic parameters and cognitive function in AD and PD patients. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM

Author

Nordestgaard, Børge G., Langlois, Michel R., Langsted, Anne, Chapman, M. John, Aakre, Kristin M., Baum, Hannsjörg, Borén, Jan, Bruckert, Eric, Catapano, Alberico, Cobbaert, Christa, Collinson, Paul, Descamps, Olivier S., Duff, Christopher J., von Eckardstein, Arnold, Hammerer-Lercher, Angelika, Kamstrup, Pia R., Kolovou, Genovefa, Kronenberg, Florian, Mora, Samia, Pulkki, Kari, Remaley, Alan T., Rifai, Nader, Ros, Emilio, Stankovic, Sanja, Stavljenic-Rukavina, Ana, Sypniewska, Grazyna, Watts, Gerald F., Wiklund, Olov, and Laitinen, Päivi

Published
2020
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44. Rare dyslipidaemias, from phenotype to genotype to management: a European Atherosclerosis Society task force consensus statement

Author

Hegele, Robert A, Borén, Jan, Ginsberg, Henry N, Arca, Marcello, Averna, Maurizio, Binder, Christoph J, Calabresi, Laura, Chapman, M John, Cuchel, Marina, von Eckardstein, Arnold, Frikke-Schmidt, Ruth, Gaudet, Daniel, Hovingh, G Kees, Kronenberg, Florian, Lütjohann, Dieter, Parhofer, Klaus G, Raal, Frederick J, Ray, Kausik K, Remaley, Alan T, Stock, Jane K, Stroes, Erik S, Tokgözoğlu, Lale, and Catapano, Alberico L

Published
2020
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45. Impact of proprotein convertase subtilisin/kexin type 9 inhibition with evolocumab on the postprandial responses of triglyceride-rich lipoproteins in type II diabetic subjects

Author

Taskinen, Marja-Riitta, Björnson, Elias, Andersson, Linda, Kahri, Juhani, Porthan, Kimmo, Matikainen, Niina, Söderlund, Sanni, Pietiläinen, Kirsi, Hakkarainen, Antti, Lundbom, Nina, Nilsson, Ralf, Ståhlman, Marcus, Adiels, Martin, Parini, Paolo, Packard, Chris, and Borén, Jan

Published
2020
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46. Liver receptor homolog‐1 is a critical determinant of methyl‐pool metabolism

Author

Wagner, Martin, Choi, Sungwoo, Panzitt, Katrin, Mamrosh, Jennifer L, Lee, Jae Man, Zaufel, Alex, Xiao, Rui, Wooton-Kee, Ruth, Ståhlman, Marcus, Newgard, Christopher B, Borén, Jan, and Moore, David D

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Liver Disease and Cirrhosis, Genetics, Digestive Diseases, Liver Disease, Nutrition, 2.1 Biological and endogenous factors, Aetiology, Oral and gastrointestinal, Good Health and Well Being, Animals, Liver, Male, Methylation, Mice, Mice, Knockout, Receptors, Cytoplasmic and Nuclear, Medical Biochemistry and Metabolomics, Immunology, Gastroenterology & Hepatology, Clinical sciences
Abstract

UnlabelledBalance of labile methyl groups (choline, methionine, betaine, and folate) is important for normal liver function. Quantitatively, a significant use of labile methyl groups is in the production of phosphatidylcholines (PCs), which are ligands for the nuclear liver receptor homolog-1 (LRH-1). We studied the role of LRH-1 in methyl-pool homeostasis and determined its metabolic effects using the methionine and choline-deficient (MCD) diet, which depletes methyl groups and results in a deleterious decrease in the PC-to-phosphatidylethanolamine ratio. We found that MCD diet-fed, liver-specific LRH-1 knockout mice (Lrh-1(-/-) ) do not show the expected decreased methyl-pool and PC/phosphatidylethanolamine ratio and are resistant to the hepatitis and fibrosis normally induced by the diet. Adaptive responses observed in wild-type mice on the MCD diet were also observed in Lrh-1(-/-) mice on a normal diet. This includes reduced expression of the highly active glycine-n-methyltransferase and the biliary phospholipid floppase multidrug-resistance protein 2 (Mdr2/Abcb4), resulting in reduced consumption of methyl groups and biliary PC secretion. In vitro studies confirm that Gnmt and Mdr2 are primary LRH-1 target genes. Additional similarities between hepatic gene expression profiles in MCD diet-fed wild-type and untreated Lrh-1(-/-) mice suggest that methyl-pool deficiency decreases LRH-1 activity, and this was confirmed by in vitro functional results in cells maintained in MCD medium.ConclusionLRH-1 is a novel transcriptional regulator of methyl-pool balance; when the methyl-pool is depleted, decreased LRH-1 transactivation suppresses expression of key genes to minimize loss of labile methyl groups. (Hepatology 2016;63:95-106).

Published
2016

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