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APJ Silencing Attenuates Apoptosis in H9c2 cells

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APJ Silencing Attenuates Apoptosis in H9c2 cells

Name:Personal
Ellen Thompson Role :Text(marcrelator)
creator

Name:Personal
Asli F. Ceylan Role :Text(marcrelator)
creator

Name:Personal
Jun Ren Role :Text(marcrelator)
creator

Name:Personal
Sreejayan Nair Role :Text(marcrelator)
creator

typeOfResource
text genre
Powerpoint/PDF
Origin Information Place
Laramie, Wyoming
University of Wyoming (keyDate="yes")
4/24/2010

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born digital

abstract
Obesity-related cardiovascular diseases have reached epidemic proportions in the United States. Studies have shown obesity may lead to hypertension, cardiac hypertrophy and compromised ventricular function. Apelin is a recently discovered protein involved in regulating cardiovascular, gastrointestinal and immune infections as well as in embryonic cardiovascular development and fluid homeostasis. It may prove therapeutic in preventing obesity-related diseases. This project aims to describe the signaling pathways involving apelin receptors (APJ) in insulin resistant mouse myocytes. Neonatal rat cardiac myocytes (H9c2 cells) were cultured and then insulin resistance was invoked by treatment with palmitic acid in both the presence and absence of APJ for varying time periods. The extent of phosphorylation and the concentration of proteins involved in the endoplasmic reticulum (ER) stress and apoptotic pathways were determined by Western blot analysis. Palmitic acid induced programmed cell death via ER stress. The absence of APJ improved cell survival. These results reveal that APJ plays an important role in palmitic acid induced apoptosis in H9c2 cells. note
From - Undergraduate Research Day 2010 - Celebration of Research - Abstracts
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Undergraduate Research Day

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Undergraduate Research Day 2010

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http://digital.uwyo.edu/copyright.htm
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http://hdl.handle.net/10176/wyu:621