A study of peroxisome proliferator-activated receptor (PPAR) alpha in patients with ischemic heart disease and heal thy volunteers

Ischemic heart disease (IHD) is the most common cause of cardiovascular mortality in Malaysia and around the globe. New novel biomarker, Peroxisome Proliferator-Activated Receptors-Alpha (PPAR-a) was investigated in this study to give significant contribution to early detection of IHD. In this st...

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Bibliographic Details
Main Author: Fong Slew, Wai
Format: Monograph
Language:English
Published: Universiti Sains Malaysia 2008
Subjects:
Online Access:http://eprints.usm.my/48977/
http://eprints.usm.my/48977/1/FONG%20SIEW%20WAI%20-%2024%20pages.pdf
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Summary:Ischemic heart disease (IHD) is the most common cause of cardiovascular mortality in Malaysia and around the globe. New novel biomarker, Peroxisome Proliferator-Activated Receptors-Alpha (PPAR-a) was investigated in this study to give significant contribution to early detection of IHD. In this study, we investigated the mRNA expression and protein levels of both PPAR-a and C-Reactive Protein (CRP) genes in the peripheral blood of IHD patients (n=10) and apparently healthy volunteers (n=1 0). The mRNA levels of PPAR-a (native and truncated) and CRP were determined by reverse transcription-polymerase chain reaction. The protein expression was evaluated by Western blot and measured by Enzyme linked immunosorbent assay (ELISA). The CRP mRNA expression and serum levels increased significantly (p<0.05) in IHD patients compared to normal volunteers. There was presence of both native active and truncated inhibitory PPAR-a protein in human blood leukocytes. The mRNA expressions of both native and truncated variants of PPAR-a were lower (p <0.05) in IHD patients group than those in the normal volunteers group. However, there was no significant difference (p>0.05) in PPAR-a protein level between IHD patients and normal volunteers. These findings suggest that mRNA expression level of both PPAR-a variants is decreased in IHD patients. An over-expression of the truncated inhibitory isoform of PPAR-a protein may be involved in the pathogenesis of IHD. Further study will be conducted to elucidate this matter.