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Krüppel-like factor (KLF) 5 mediates cyclin D1 expression and cell proliferation via interaction with c-Jun in Ang

Yu Liu1, Jin-kun Wen, Li-hua Dong

  • 1Department of Biochemistry and Molecular Biology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.

Acta Pharmacologica Sinica
|December 29, 2009
PubMed
Abstract

Insights

Krüppel-like factor 5 (KLF5) activates cyclin D1 in vascular smooth muscle cells (VSMC) proliferation. This occurs via interaction with c-Jun, downstream of ERK and p38 MAPK pathways, in response to Ang II.

Area of Science:

  • Molecular biology
  • Cell signaling
  • Cardiovascular research

Background:

  • Vascular smooth muscle cell (VSMC) proliferation is crucial in cardiovascular diseases.
  • Krüppel-like factor 5 (KLF5) is implicated in VSMC growth.
  • Understanding KLF5's role in cyclin D1 regulation is key.

Purpose of the Study:

  • To investigate the mechanism by which KLF5 activates cyclin D1 expression.
  • To elucidate the role of KLF5 in Angiotensin II (Ang II)-induced VSMC proliferation.

Main Methods:

  • Adenoviral vectors for KLF5 and c-Jun expression.
  • MTT assay and flow cytometry for cell growth analysis.
  • Luciferase and chromatin immunoprecipitation assays for gene regulation studies.

Main Results:

  • Ang II increased KLF5 expression and VSMC proliferation.
  • KLF5 activation by Ang II involves ERK and p38 MAPK pathways.
  • KLF5 and c-Jun interact to enhance cyclin D1 promoter activity.

Conclusions:

  • KLF5 is a downstream mediator of ERK/p38 MAPK signaling in Ang II-stimulated VSMCs.
  • KLF5, through interaction with c-Jun, drives cyclin D1 transcription.
  • This pathway is critical for Ang II-induced VSMC proliferation.

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