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RKIP negatively regulates the glucose induced angiogenesis and endothelial-mesenchymal transition in retinal

Le Feng1, Conghui Zhang1, Guodong Liu1

  • 1Department of Ophthalmology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai, 200072, China.

Experimental Eye Research
|October 27, 2019
PubMed

Insights

Raf kinase inhibitor protein (RKIP) negatively regulates diabetic retinopathy (DR) progression. Lower RKIP levels in the eye promote cell growth, migration, and blood vessel formation, contributing to DR development.

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetic retinopathy (DR) is a leading cause of blindness globally.
  • Reduced Raf kinase inhibitor protein (RKIP) levels are observed in proliferative diabetic retinopathy (PDR).
  • RKIP's role in PDR pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the functional role of RKIP in diabetic retinopathy.
  • To determine RKIP's effect on human retinal capillary endothelial cells (HRCECs) under high glucose conditions.
  • To elucidate RKIP's influence on cell viability, migration, angiogenesis, and endothelial-to-mesenchymal transition (EndMT).

Main Methods:

  • Stable RKIP overexpression (OE) and knockdown (KD) were established in HRCECs using lentivirus constructs.
  • Cells were exposed to high glucose conditions to mimic the diabetic environment.
  • Assays measured cell viability, migration, angiogenesis markers (CD31, vWF), and EndMT markers (α-SMA).

Main Results:

  • RKIP knockdown (KD) significantly increased glucose-induced HRCEC viability, migration, and angiogenesis.
  • RKIP overexpression (OE) significantly decreased glucose-induced HRCEC viability, migration, and angiogenesis.
  • RKIP KD upregulated CD31 and vWF while downregulating α-SMA; RKIP OE showed opposite effects under high glucose.

Conclusions:

  • RKIP acts as a negative regulator of glucose-induced cell viability, migration, angiogenesis, and EndMT in HRCECs.
  • The observed downregulation of RKIP in PDR patients may contribute to the development and progression of diabetic retinopathy.
  • Targeting RKIP could offer a potential therapeutic strategy for managing diabetic retinopathy.
Keywords:
AngiogenesisCell viabilityDiabetic retinopathyEndothelial to mesenchymal transitionMigrationRaf kinase inhibitor protein

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