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Rap1 promotes proliferation and migration of vascular smooth muscle cell via the ERK pathway

Qin Li1, Yunfei Teng1, Jian Wang1

  • 1Department of Vascular Surgery, Union Hospital Affiliated with Tongji Medical College of Huazhong University of Science and Technology, China.

Pathology, Research and Practice
|May 24, 2018
PubMed
Abstract

Insights

Rap1 is crucial for vascular smooth muscle cell (VSMC) proliferation and migration via the ERK signaling pathway. This study details Rap1

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Rap1 is a key regulator in cellular signal transduction pathways, influencing cell proliferation and migration.
  • Rap1 plays a significant role in both physiological and pathological processes.

Purpose of the Study:

  • To elucidate the detailed mechanistic role of Rap1 in vascular smooth muscle cell (VSMC) proliferation and migration.

Main Methods:

  • VSMCs were transfected with vectors expressing Rap1V12 or Rap1GAP, or an empty vector.
  • Cell proliferation and migration were assessed using MTT assays and transwell analysis, respectively.
  • Western blotting was employed to detect the expression levels of ERK, phosphorylated-ERK, Rap1, Rap1GAP, and Rap1GTP.

Main Results:

  • Rap1V12 transfection significantly increased VSMC proliferation, migration, and the expression of Rap1, Rap1GAP, and phosphorylated-ERK (p-ERK).
  • Conversely, Rap1GAP transfection exhibited opposing effects on these cellular processes.
  • Pretreatment with Rap1 guanine exchange factor (Rap1GEF) activators (8CPT-2'OMe-cAMP, SDF-1) followed by transfection led to decreased expression of Rap1, Rap1GAP, and p-ERK.

Conclusions:

  • Rap1 is essential for regulating VSMC proliferation and migration.
  • The ERK signaling pathway is critically involved in mediating Rap1's effects on VSMCs.
  • These findings establish a novel mechanistic link between Rap1, ERK signaling, and VSMC function.
Keywords:
MigrationProliferationRap1Rap1-GAPVascular smooth muscle cell

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