AI Article Synopsis
- Isolated KLF5, a transcription factor, is strongly induced in activated vascular smooth-muscle cells and fibroblasts.
- In KLF5-knockout mice, responses to stress were significantly reduced, showing less arterial-wall thickening and cardiac issues.
- KLF5 interacts with retinoic-acid receptor (RAR), with RAR ligands influencing KLF5's activity and cardiovascular responses, highlighting KLF5's role in stress-related cardiovascular remodeling.
Article Abstract
We recently isolated a Krüppel-like zinc-finger transcription factor 5 (KLF5; also known as BTEB2 and IKLF), which is markedly induced in activated vascular smooth-muscle cells and fibroblasts. Here we describe our analysis of the in vivo function of KLF5 using heterozygous KLF5-knockout mice (Klf5(+/-)). In response to external stress, Klf5(+/-) mice showed diminished levels of arterial-wall thickening, angiogenesis, cardiac hypertrophy and interstitial fibrosis. Also, angiotensin II induced expression of KLF5, which in turn activated platelet-derived growth factor-A (PDGF-A) and transforming growth factor-beta (TGF-beta) expression. In addition, we determined that KLF5 interacted with the retinoic-acid receptor (RAR), that synthetic RAR ligands modulated KLF5 transcriptional activity, and that in vivo administration of RAR ligands affected stress responses in the cardiovascular system in a KLF5-dependent manner. KLF5 thus seems to be a key element linking external stress and cardiovascular remodeling.
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