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Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2

Jing Zhang1, Limin Li1, Jing Li1

  • 1From the State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, School of Life Sciences, Nanjing University, Nanjing, Jiangsu, China (J.Z., L.L., J.L., C.-Y.Z., Y.Z., K.Z.); and Department of Biology, Center for Inflammation, Immunity and Infection, Georgia State University, Atlanta (Y.L.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|November 15, 2014
PubMed
Abstract

Insights

Protein tyrosine phosphatase 1B (PTP1B) inhibits diabetic wound healing by dephosphorylating VEGFR2. PTP1B inhibitors show potential as novel therapeutic tools for improving wound repair in diabetes.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Wound Healing Research

Background:

  • Diabetes mellitus is a leading cause of impaired wound healing.
  • The molecular mechanisms underlying diabetic wound complications are not fully understood.
  • Protein tyrosine phosphatase 1B (PTP1B) is implicated in metabolic regulation and cellular signaling.

Purpose of the Study:

  • To investigate the inhibitory role of PTP1B in diabetic wound healing.
  • To elucidate the molecular mechanisms by which PTP1B affects wound repair.
  • To evaluate the therapeutic potential of PTP1B inhibition for diabetic wounds.

Main Methods:

  • Comparative analysis of wound healing in PTP1B knockout, diabetic (ob/ob and streptozotocin-induced), and wild-type mice.
  • Assessment of PTP1B inhibitor efficacy in rescuing impaired wound healing.
  • In vitro studies on human microvascular endothelial cells (MVECs) to evaluate PTP1B's effect on proliferation, migration, and tube formation.
  • Investigation of PTP1B's downstream signaling pathways, focusing on vascular endothelial growth factor receptor 2 (VEGFR2) phosphorylation.

Main Results:

  • Diabetic conditions lead to upregulation and activation of PTP1B, inhibiting wound healing.
  • Administration of a PTP1B inhibitor successfully rescued impaired wound healing in diabetic mouse models.
  • PTP1B, upregulated by hyperglycemia, inhibits MVEC proliferation, migration, and tube formation.
  • PTP1B inhibition reverses these suppressive effects on MVECs.
  • Mechanism studies reveal PTP1B dephosphorylates VEGFR2, thereby suppressing endothelial cell function.

Conclusions:

  • PTP1B negatively regulates diabetic wound healing by dephosphorylating endothelial cell VEGFR2.
  • Targeting PTP1B with specific inhibitors presents a promising therapeutic strategy for enhancing diabetic wound repair.
Keywords:
PTP1B protein, humanangiogenesiseffecthyperglycemiareactive oxygen speciesvascular endothelial growth factor receptor-2, humanwound healing

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