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A repressor protein, Mnt, is a novel negative regulator of vascular smooth muscle cell hypertrophy by angiotensin II and neointimal hyperplasia by arterial injury

Authors
Journal
Atherosclerosis
0021-9150
Publisher
Elsevier
Volume
228
Issue
1
Identifiers
DOI: 10.1016/j.atherosclerosis.2013.02.033
Keywords
  • Transcriptional Repressor
  • Angioplasty
  • Gene Therapy
  • Restenosis
  • Signal Transduction
Disciplines
  • Biology
  • Medicine

Abstract

Abstract Objective The Max-interacting protein Mnt is a transcriptional repressor that can antagonize the transcriptional and proliferation-related activities of Myc. Here, we tested the hypothesis that Mnt is a negative regulator of pathological vascular remodeling. Methods Adenovirus encoding Mnt or control GFP was infected to cultured rat vascular smooth muscle cells (VSMC) and carotid arteries after a balloon angioplasty. Results In VSMC, adenoviral gene transfer of Mnt suppressed angiotensin II-induced protein expression of early growth response protein-1 (Egr1) and its promoter activation. Mnt adenovirus did not interfere with upstream signaling of angiotensin II. Angiotensin II-induced protein accumulation in VSMC was inhibited by Mnt adenovirus. Mnt adenovirus also inhibited platelet-derived growth factor-induced VSMC proliferation. Moreover, Mnt adenovirus prevented neointima formation in response to arterial injury. The adenoviral Mnt gene transfer also prevented Egr1 induction in neointima. Conclusion These data identify Mnt as a previously unrecognized negative regulator of pathological vascular remodeling.

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