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TRPV1 agonism inhibits endothelial cell inflammation via activation of eNOS/NO pathway

Youping Wang1, Lin Cui1, Hui Xu2

  • 1Central Laboratory and Division of Cardiology, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, 450000, China.

Atherosclerosis
|March 22, 2017
PubMed
Abstract

Insights

Transient receptor potential vanilloid type 1 channel (TRPV1) activation in endothelial cells reduces inflammation via the eNOS/NO pathway. This mechanism protects against inflammatory responses, even in hypertensive conditions.

Area of Science:

  • Endothelial biology
  • Inflammation research
  • Cardiovascular science

Background:

  • Transient receptor potential vanilloid type 1 channel (TRPV1) is expressed in endothelial cells (ECs) and activates endothelial nitric oxide synthase (eNOS).
  • TRPV1 is implicated in attenuating inflammatory responses, but the underlying mechanisms are unclear.
  • This study investigates TRPV1's role in suppressing EC inflammatory responses via the eNOS/NO pathway.

Purpose of the Study:

  • To elucidate the mechanism by which TRPV1 activation suppresses endothelial cell inflammation.
  • To determine if the eNOS/NO pathway mediates the anti-inflammatory effects of TRPV1 in ECs.
  • To evaluate the protective effects of TRPV1 in ECs from hypertensive models.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) and renal microvascular endothelial cells (MVECs) from deoxycorticosterone (DOCA)-salt hypertensive mice were stimulated with lipopolysaccharide (LPS).
  • Cells were treated with capsaicin (CAP), a TRPV1 agonist, with or without inhibitors of TRPV1, NOS, or the PI3K/Akt pathway.
  • Nitric oxide (NO) metabolites, protein expression, inflammatory molecules, and monocyte adhesion were assessed.

Main Results:

  • CAP treatment increased NO production and eNOS phosphorylation (ser1177) in HUVECs.
  • CAP attenuated LPS-induced cytokine/chemokine production, adhesion molecule expression, NF-κB activation, and monocyte adhesion.
  • These TRPV1-mediated protective effects were abrogated by inhibiting TRPV1, NOS, or the PI3K/Akt pathway and were also observed in renal MVECs from hypertensive mice.

Conclusions:

  • TRPV1 activation suppresses endothelial cell inflammation through the Ca²⁺/PI3K/Akt/eNOS/NO pathway.
  • These protective effects of TRPV1 are demonstrated in ECs from salt-sensitive hypertensive mice.
  • TRPV1 represents a potential therapeutic target for mitigating endothelial inflammation in hypertension.
Keywords:
Endothelial cellEndothelial nitric oxide synthaseHypertensionInflammationNitric oxideTransient receptor potential vanilloid type 1 channel

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