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Macrophage PPAR‐γ in Post‐Myocardial Infarct remodeling
Author(s) -
Katwa Laxmansa C,
Nichols Marshall W,
Virag Jitka AI,
Carr Chris J,
Gould Amanda N,
Lust Robert M
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.599.15
Subject(s) - western blot , matrix metalloproteinase , macrophage , peroxisome proliferator activated receptor , chemistry , medicine , myocardial infarction , inflammation , endocrinology , knockout mouse , blot , receptor , biology , biochemistry , in vitro , gene
Macrophages play key role in initial tissue remodeling by engulfing debris and releasing cytokines at the site of injury. Currently, the contribution of macrophage PPARγ in response to myocardial infarction (MI) and post‐MI remodeling is unknown and the effect of early cytokine signals on the post‐MI expression of collagens, MMPs (Matrix metalloproteinases) and TIMPs (tissue inhibitors of MMP) is unclear. The study objective was to examine the role of macrophage PPARγ in post‐MI remodeling, particularly collagen I & III, MMP, and TIMP expression using macrophage specific PPARγ knockout (KO) and wild type (WT) mice. Protein and RNA were extracted from 28‐day post‐MI heart tissues from WT and PPARγ‐KO mice for western blot and real‐time PCR analysis. qPCR results showed a significant increase (p<0.05) in expression of collagens I and III, MMPs 9 and 13, and TIMPs 1 and 2 in the 28‐day post‐MI PPARγ‐KO model compared to the WTMI group. The level of MMP 2, although not significantly elevated, showed an increasing trend in the PPARγ‐KOMI compared to WTMI group. Western blot showed similar increasing trends in TIMP 1 and 2 expressions in the PPARγ‐KOMI group. Our results indicate that PPARγ could be influencing the initial signals that alter post‐MI remodeling by regulating the expression of collagens (I, III), MMP 9, TIMPs 1 and 2.