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Stem cell factor is a potent endothelial permeability factor.

Ji Yeon Kim1, Jun-Sub Choi1, Sun-Hwa Song1

  • 1From the College of Pharmacy, Ajou University, Suwon, Korea (J.Y.K., S.-H.S., J.-E.I., K.K., S.K., W.S.); Department of Ophthalmology and Visual Science, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea (J.-S.C., C.-K.J.); Department of Molecular and Life Science, CHA University, Seoul, Korea (J.-M.K.); Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Gyeongnam, Korea (H.K.S.); and Drug Discovery Division, Korea Research Institute of Chemical Technology, Daejeon, Korea (B.H.L.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|May 3, 2014
PubMed
Summary
This summary is machine-generated.

Stem cell factor (SCF) disrupts vascular integrity by activating the cKit receptor in endothelial cells, leading to increased vascular leakage. Targeting SCF may offer a new therapy for hyperpermeable vascular diseases.

Keywords:
nitric oxide synthase type IIIstem cell factorvascular permeability

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Area of Science:

  • Endocrinology
  • Vascular Biology
  • Cell Signaling

Background:

  • Stem cell factor (SCF) is crucial for hematopoiesis, gametogenesis, and melanogenesis.
  • The role of SCF in regulating vascular integrity remained uninvestigated.

Purpose of the Study:

  • To elucidate the function of SCF in the regulation of vascular integrity.
  • To investigate the underlying molecular mechanisms of SCF-mediated vascular effects.

Main Methods:

  • Examined SCF binding and activation of the cKit receptor in endothelial cells.
  • Assessed the impact of SCF on vascular endothelial-cadherin internalization and dye extravasation.
  • Investigated the involvement of the phosphoinositide 3-kinase/Akt pathway and endothelial nitric oxide synthase (eNOS).
  • Utilized small interfering RNA (siRNA) knockdown and chemical inhibitors for eNOS and NO synthesis.
  • Employed eNOS knockout mice to confirm the role of NO.
  • Analyzed SCF and cKit expression in a mouse model of diabetic retinopathy.
  • Evaluated the therapeutic potential of anti-SCF neutralizing antibodies in vivo.

Main Results:

  • SCF activates cKit in endothelial cells, increasing vascular endothelial-cadherin internalization and dye extravasation.
  • SCF enhances endothelial NO production via the PI3K/Akt/eNOS pathway, contributing to vascular leakage.
  • Inhibition of eNOS or NO synthesis significantly reduced SCF-induced vascular permeability.
  • SCF-induced extravasation was abolished in eNOS knockout mice.
  • Elevated SCF and cKit expression was observed in the retinas of diabetic mice.
  • Anti-SCF treatment prevented vascular hyperpermeability in diabetic mouse retinas.

Conclusions:

  • SCF disrupts endothelial adherens junctions, promoting vascular leakage.
  • SCF-mediated vascular effects are dependent on eNOS-derived NO production.
  • Anti-SCF/cKit therapy shows promise for treating hyperpermeable vascular diseases.