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A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Role of src-suppressed C kinase substrate in rat pulmonary microvascular endothelial hyperpermeability stimulated by

Qing-Hai You1, Geng-Yun Sun, Nan Wang

  • 1Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|May 11, 2010
PubMed
Abstract

Insights

Src-suppressed C kinase substrate (SSeCKS) plays a role in inflammatory responses. This protein is involved in regulating endothelial cell permeability when exposed to inflammatory cytokines like interleukin-1β and tumor necrosis factor-α.

Area of Science:

  • Endothelial biology
  • Molecular and cellular physiology
  • Inflammation research

Background:

  • Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are key inflammatory cytokines.
  • Endothelial barrier function is crucial for regulating microvascular permeability.
  • Src-suppressed C kinase substrate (SSeCKS) is a protein kinase substrate with poorly understood roles in endothelial cells.

Purpose of the Study:

  • To investigate the role of SSeCKS in rat pulmonary microvascular endothelial cells (RPMVEC) permeability.
  • To determine if SSeCKS is involved in the endothelial response to IL-1β and TNF-α.

Main Methods:

  • Gene and protein expression of SSeCKS analyzed using RT-PCR and immunoblotting.
  • Protein kinase C (PKC) signaling pathway activation assessed.
  • Transendothelial electrical resistance (TER) and FITC-dextran flux (P(d)) measured across RPMVEC monolayers.
  • SSeCKS function studied using small interfering RNA (siRNA) in RPMVEC.

Main Results:

  • IL-1β and TNF-α activated PKC signaling and upregulated SSeCKS expression in RPMVEC.
  • Depletion of SSeCKS attenuated cytokine-induced decreases in TER and increases in P(d).
  • PKC inhibitors reduced cytokine-induced hyperpermeability and SSeCKS expression.

Conclusions:

  • SSeCKS is implicated in the endothelial hyperpermeability triggered by IL-1β and TNF-α during inflammation.
  • SSeCKS is a mediator in the inflammatory pathway affecting endothelial barrier function.

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