Depot-specific regulation of adipose stem cell functions by local renin-angiotensin system
Obesity has became a worldwide health hazard, ranking the fifth for global deaths. Studies have shown that lipid accumulation in the visceral adipose tissue (VAT), but not subcutaneous adipose tissue (SAT), leads to obesity-related diseases which could be linked by the adipose renin-angiotensin syst...
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Format: | Final Year Project |
Language: | English |
Published: |
2014
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Online Access: | http://hdl.handle.net/10356/60258 |
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Institution: | Nanyang Technological University |
Language: | English |
Summary: | Obesity has became a worldwide health hazard, ranking the fifth for global deaths. Studies have shown that lipid accumulation in the visceral adipose tissue (VAT), but not subcutaneous adipose tissue (SAT), leads to obesity-related diseases which could be linked by the adipose renin-angiotensin system (aRAS). CD10 is recently found to be more highly expressed in subcutaneous adipose-derived stem cells (SC-ASCs), in comparison to visceral (VS) ASCs. However the functional relevance and underlying mechanism of CD10 in influencing adipogenesis in SC-ASCs is still unknown. We monitored adipogenesis in CD10-knockdown (KD) SC-ASCs, evaluated the expression of aRAS components throughout adipogenesis, and observed the effects of RAS antagonists. Oil Red O staining revealed that CD10-KD SC-ASCs had a significant reduction in adipogenesis. The qPCR data showed that majority of the aRAS components increased along with adipogenesis. Chemical treatments showed that angiotensin II receptors type 1 (AGTR1) antagonist (valsartan) increased adipogenesis for both depots, and angiotensin-converting enzyme (ACE) inhibitor (captopril) increased adipogenesis only for VS-ASCs. aRAS undoubtedly has a major role in influencing adipogenesis. Understanding the differences in aRAS components between SAT and VAT will certainly offer therapeutic benefits in the near future, especially for obesity and the related diseases. |
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