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miPEP31 inhibits the vascular smooth muscle cell proliferation via cooperation with transcription factor Trps1

Gonghao Jiang1, Xiangxiao Li1,2, Zilong Fang1

  • 1The Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|September 22, 2025
PubMed

Insights

miPEP31 inhibits vascular smooth muscle cell proliferation and protects against hypertension-induced vascular remodeling by suppressing miR-31 expression. This peptide shows therapeutic potential for hypertensive target organs.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Hypertension Research

Background:

  • Hypertension involves vascular remodeling driven by vascular smooth muscle cell (VSMC) proliferation.
  • MicroRNA-31 (miR-31) is implicated in VSMC proliferation and hypertensive vascular remodeling.
  • The precise role and mechanism of miPEP31, derived from pri-miRNA-31, in VSMC proliferation remain largely unknown.

Purpose of the Study:

  • To investigate the role of miPEP31 in VSMC proliferation.
  • To elucidate the underlying molecular mechanisms by which miPEP31 influences vascular remodeling.
  • To assess the therapeutic potential of miPEP31 in a mouse model of hypertension.

Main Methods:

  • Administration of synthetic miPEP31 and genetic deficiency models in Angiotensin II-infused mice.
  • Assessment of aortic structural changes (thickness, fibrosis, α-SMA staining).
  • Investigation of miPEP31's effect on PDGF-BB-induced VSMC proliferation and its nuclear localization.
  • Mechanistic studies involving Trps1 and miR-31 expression analysis.

Main Results:

  • miPEP31 administration mitigated Ang II-induced aortic thickening and fibrosis, while deficiency aggravated these changes.
  • miPEP31 inhibited PDGF-BB-induced VSMC proliferation and reduced Ang II-induced α-SMA staining.
  • miPEP31 localizes to the nucleus and acts as a transcriptional repressor, inhibiting miR-31 expression via cooperation with Trps1.
  • miPEP31 expression is endogenous in VSMCs.

Conclusions:

  • miPEP31 plays a protective role against Ang II-induced vascular remodeling by inhibiting VSMC proliferation.
  • miPEP31 functions as a transcriptional repressor, cooperating with Trps1 to suppress miR-31 expression.
  • These findings highlight miPEP31 as a potential therapeutic agent for hypertensive target organ damage.
Keywords:
Trps1hypertensionmiPEP31vascular remodelingvascular smooth muscle cell

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