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Gene expression profiling of the RAS in myoblasts following differentiation and mechanical stretch
Author(s) -
Johnston Adam P,
Baker Jeff,
Parise Gianni
Publication year - 2008
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.22.1_supplement.1197.8
Subject(s) - downregulation and upregulation , c2c12 , angiotensin ii , angiotensin ii receptor type 1 , myocyte , gene expression , biology , muscle hypertrophy , microbiology and biotechnology , cellular differentiation , gene expression profiling , gene , receptor , angiotensin converting enzyme , gene family , endocrinology , medicine , genetics , myogenesis , blood pressure
Recent evidence, using animal models, suggests that angiotensin II can positively influence skeletal muscle hypertrophy. We conducted a genetic profile of RAS family members during C2C12 myoblast proliferation and differentiation. We also examined RAS family member gene expression following 4h of mechanical stretch. Both angiotensin II receptors (AT1 and AT2) were expressed in proliferating and differentiating myobasts and were significantly upregulated at day 1 of differentiation, while the AT2 receptor demonstrated a persistent upregulation at both day 1 and day 3 as compared to proliferation. Interestingly, angiotensiogen was transiently downregulated upon exposure to differentiation media but was significantly upregulated at day 7 of differentiation. Furthermore, angiotensin converting enzyme showed weak expression during proliferation but increased significantly upon differentiation across all time points. Immediately following mechanical stretch we observed a reduction in AT1 and AT2 gene expression. In addition we observed an increase in AT1 expression 4h post stretch. These results suggest that RAS family members may play a role in regulating myoblast differentiation. Furthermore, it appears that RAS family members are responsive to stretch‐induced stress.