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CRH/CRHR1 modulates cerebrovascular endothelial cell permeability in association with S1PR2 and S1PR3 under oxidative

Junyu Mu1, Yuhui Que1, Xu Li1

  • 1Department of pharmacology, Nanjing Medical University, Nanjing 210029, PR China.

Vascular Pharmacology
|November 15, 2021
PubMed

Insights

Corticotrophin-releasing hormone receptor 1 (CRHR1) activation reverses oxidative stress effects on brain endothelial cells. This involves sphingosine-1-phosphate receptors 2 and 3 (S1PR2/S1PR3), impacting vascular permeability and tight junctions.

Area of Science:

  • Neuroendocrinology
  • Vascular Biology
  • Cellular Physiology

Background:

  • Corticotrophin-releasing hormone (CRH) is implicated in vascular inflammation and permeability.
  • Previous work linked S1PR2 or CRHR1 blockade to inhibited H2O2-induced brain endothelial hyperpermeability.
  • The interplay between S1PRs and CRHR1 in oxidative stress-induced cerebrovascular changes remains unclear.

Purpose of the Study:

  • To investigate the linkage between sphingosine-1-phosphate receptors (S1PRs) and Corticotrophin-releasing hormone receptor 1 (CRHR1) in oxidative stress-induced cerebrovascular endothelial hyperpermeability.
  • To elucidate the roles of S1PR2 and S1PR3 in regulating endothelial monolayer permeability under oxidative stress.

Main Methods:

  • Utilized bEnd3 cell monolayers to assess endothelial permeability.
  • Investigated the effects of H2O2 exposure on cell permeability and tight junction protein (ZO-1) redistribution.
  • Examined the impact of S1PR2/S1PR3 blockade/silencing and CRHR1 activation on signaling pathways (p38, ERK, cPLA2 phosphorylation).

Main Results:

  • S1PR2 blockade reduced H2O2-induced hyperpermeability and ZO-1 redistribution, inhibiting p38, ERK, and cPLA2 phosphorylation.
  • S1PR3 suppression exacerbated H2O2-induced hyperpermeability and ZO-1 redistribution, increasing p38, ERK, and cPLA2 phosphorylation.
  • CRHR1 activation counteracted the effects of S1PR2 and S1PR3 modulation on endothelial permeability.

Conclusions:

  • CRHR1 activation can reverse the differential effects of S1PR2 and S1PR3 on endothelial monolayer permeability.
  • A functional link exists between CRHR1 and S1PR2/S1PR3 in managing endothelial barrier integrity during oxidative stress.
  • Findings suggest potential therapeutic targets for cerebrovascular disorders involving oxidative stress.

Keywords:
CRH/CRHR1Endothelial permeabilityOxidative stressS1PR2&S1PR3Tight junction protein ZO-1

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