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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: J Mol Cell Cardiol. 2008 May 20;45(2):193–197. doi: 10.1016/j.yjmcc.2008.05.005

Figure 1. KLF15 is an inhibitor of cardiac fibrosis and CTGF expression.

Figure 1

(A) CTGF expression from whole heart RNA extracts of KLF15 +/+ and −/− hearts. KLF15 −/− hearts exhibit exaggerated CTGF expression in response to pressure overload. (B) Representative example of Masson’s trichrome–stained left ventricular sections from KLF15 +/+ and −/− mouse hearts after 1 week AAC. (C) TGFβ1 downregulates KLF15 expression in NRVF. Isolated NRVF were serum starved for 48 hours and stimulated with TGFβ1 (10ng/mL, 6 hours). Total RNA was isolated and Northern analysis performed using indicated cDNA probes. (D) KLF15 inhibits basal and TGFβ1-induced CTGF expression. NRVF were starved for 24 hrs, infected with control adenovirus (Ad-GFP) or Ad-GFP-KLF15 for 24hrs, and treated with TGFb1 (10ng/ml, 6 hrs). Total RNA and protein were isolated for Northern and Western analysis for CTGF. (E) KLF15 inhibits CTGF promoter activity. NRVF were cotransfected with CTGF-promoter luciferase reporter, KLF15 expression plasmid or empty vector (pCDNA3.1). After transfection, cells were starved for 24hr and treated with TGFb1 (10ng/ml, 6 hrs). Cell lysates were assayed for luciferase activity, which was normalized to total protein content and expressed as fold-induction over empty-vector control ( n=6 per group).