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Endothelial CEPT1 Promotes Angiogenesis Through PPARα and VEGF-A Signaling.

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Choline-ethanolamine phosphotransferase 1 (CEPT1) overexpression enhances endothelial cell function and promotes recovery after ischemic injury in diabetic mice. This suggests CEPT1 plays a compensatory role in vascular repair, particularly in diabetes-related peripheral artery disease.

Keywords:
angiogenesisendothelial cellsischemiaperipheral arterial diseasevascular endothelial growth factor A

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Area of Science:

  • Vascular Biology
  • Metabolic Diseases
  • Molecular Mechanisms of Angiogenesis

Background:

  • Choline-ethanolamine phosphotransferase 1 (CEPT1) is crucial for phospholipid synthesis and is affected by diabetes.
  • Endothelial cell-specific knockdown of CEPT1 impairs tissue recovery.
  • Hypothesis: CEPT1 overexpression promotes post-ischemic angiogenesis and recovery in diabetes.

Purpose of the Study:

  • To investigate the role of CEPT1 overexpression in promoting angiogenesis and recovery in a diabetic setting.
  • To evaluate CEPT1 levels in human peripheral arteries of patients with peripheral artery disease and diabetes.
  • To determine the molecular pathways influenced by CEPT1 in endothelial cells.

Main Methods:

  • Assessed CEPT1 content in human peripheral arteries from patients with peripheral artery disease and diabetes.
  • Generated a conditional endothelial cell-specific CEPT1-overexpressing mouse model (Cept1fl/fl Cre+).
  • Utilized unilateral hindlimb ischemia model in mice, followed by single-cell RNA sequencing and molecular pathway analysis of aortic and endothelial cells.

Main Results:

  • Human arterial intima showed elevated CEPT1, ACOX1, VEGF R2, p-Akt, and p-eNOS in patients with peripheral artery disease and diabetes.
  • Single-cell RNA sequencing revealed enrichment of wound healing, angiogenesis, sprouting, and cell migration pathways in CEPT1-overexpressing ECs.
  • Diabetic Cept1fl/fl Cre+ mice exhibited improved hindlimb perfusion and angiogenesis, with enhanced ex vivo capillary sprouting. CEPT1 overexpression increased EC migration, tubule formation, and proliferation, partly mediated by PPARα, Akt, and eNOS signaling.

Conclusions:

  • Overexpression of CEPT1 enhances endothelial cell function and post-ischemic recovery.
  • The pro-angiogenic effects of CEPT1 involve Akt/eNOS signaling and PPARα.
  • Elevated CEPT1 in diseased human arteries suggests a compensatory role in vascular repair following ischemic injury, especially in diabetes.