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Hypertrophic Changes (hypertrophic + change)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

miR133a regulates cardiomyocyte hypertrophy in diabetes

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 1 2010
Biao Feng
Abstract Background Diabetic cardiomyopathy, characterized by cardiac hypertrophy and contractile dysfunction, eventually leads to heart failure. We have previously shown that alterations of a number of key molecules are involved in producing cardiomyocyte hypertrophy in diabetes. The aim of the present study was to determine whether microRNAs (miRNA) play a role in mediating altered gene expression and structural/functional deficits in the heart in diabetes. Methods STZ-induced diabetic mice were haemodynamically investigated after 2 months of diabetes to establish the development of cardiomyopathy. The tissues were then examined for gene expression and microRNA analysis. We further investigated neonatal rat cardiomyocytes to identify the mechanisms of glucose-induced hypertrophy and the potential role of miR133a. Results Diabetic mice showed myocardial contractile dysfunction and augmented mRNA expression of atrial and brain natriuretic peptides (ANP, BNP), MEF2A and MEF2C, SGK1 and IGF1R compared to age- and sex-matched controls. Cardiac tissues from these mice showed alteration of multiple miRNAs by array analysis including miR133a, which was confirmed by RT-PCR. In vitro exposure of cardiomyocytes to high levels of glucose produced hypertrophic changes and reduced expression of miRNA133a. Finally, transfection of miR133a mimics prevented altered gene expression and hypertrophic changes. Conclusion Data from these studies demonstrate a novel glucose-induced mechanism regulating gene expression and cardiomyocyte hypertrophy in diabetes which is mediated through miR133a. Copyright © 2009 John Wiley & Sons, Ltd. [source]

L -Carnitine in the treatment of HIV-associated lipodystrophy syndrome

HIV MEDICINE, Issue 1 2001
S Mauss
Summary The objective of this pilot study was to assess the effect of L -carnitine on the course of the HIV-associated lipodystrophy syndrome. Twelve patients presenting with combined atrophic and hypertrophic changes of body fat were treated with L -carnitine 1000 mg bid for 3 months. No marked improvement of the body changes was observed. However a reduction in serum cholesterol levels, but not triglycerides, was noted. These preliminary data do not support the use of L -carnitine for the rapid reversal of advanced fat tissue alterations due to HIV-associated lipodystrophy. [source]

ERK-1/2 and p38 in the regulation of hypertrophic changes of normal articular cartilage chondrocytes induced by osteoarthritic subchondral osteoblasts

ARTHRITIS & RHEUMATISM, Issue 5 2010
Indira Prasadam
Objective Previous studies have shown the influence of subchondral bone osteoblasts (SBOs) on phenotypical changes of articular cartilage chondrocytes (ACCs) during the development of osteoarthritis (OA). The molecular mechanisms involved during this process remain elusive, in particular, the signal transduction pathways. The aim of this study was to investigate the in vitro effects of OA SBOs on the phenotypical changes in normal ACCs and to unveil the potential involvement of MAPK signaling pathways during this process. Methods Normal and arthritic cartilage and bone samples were collected for isolation of ACCs and SBOs. Direct and indirect coculture models were applied to study chondrocyte hypertrophy under the influence of OA SBOs. MAPKs in the regulation of the cell,cell interactions were monitored by phosphorylated antibodies and relevant inhibitors. Results OA SBOs led to increased hypertrophic gene expression and matrix calcification in ACCs by means of both direct and indirect cell,cell interactions. In this study, we demonstrated for the first time that OA SBOs suppressed p38 phosphorylation and induced ERK-1/2 signal phosphorylation in cocultured ACCs. The ERK-1/2 pathway inhibitor PD98059 significantly attenuated the hypertrophic changes induced by conditioned medium from OA SBOs, and the p38 inhibitor SB203580 resulted in the up-regulation of hypertrophic genes in ACCs. Conclusion The findings of this study suggest that the pathologic interaction of OA SBOs and ACCs is mediated via the activation of ERK-1/2 phosphorylation and deactivation of p38 phosphorylation, resulting in hypertrophic differentiation of ACCs. [source]