RGD Reference Report - Role of src-suppressed C kinase substrate in rat pulmonary microvascular endothelial hyperpermeability stimulated by inflammatory cytokines. - Rat Genome Database

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

Authors: You, Qing-Hai  Sun, Geng-Yun  Wang, Nan  Chen, Shan  Luo, Qing-Li 
Citation: You QH, etal., Inflamm Res. 2010 Nov;59(11):949-58. doi: 10.1007/s00011-010-0207-3. Epub 2010 May 8.
RGD ID: 14348957
Pubmed: PMID:20454828   (View Abstract at PubMed)
DOI: DOI:10.1007/s00011-010-0207-3   (Journal Full-text)


OBJECTIVE: The aim of the study was to investigate the role of src-suppressed C kinase substrate (SSeCKS) in the modulation of rat pulmonary microvascular endothelial cells (RPMVEC) permeability elicited by interleukin (IL)-1β and tumor necrosis factor (TNF)-α.
METHODS: The gene expression of SSeCKS was analyzed by reverse transcription-polymerase chain reaction. Immunoblotting was used to determine the SSeCKS protein expression and the activation of the protein kinase C (PKC) signaling pathway. A RPMVEC monolayer was constructed to determine changes of transendothelial electrical resistance (TER) and FITC-dextran flux (P (d)) across the monolayer. SSeCKS-specific small interfering RNA was transfected into RPMVEC.
RESULTS: IL-1β and TNF-α activated the PKC signaling pathway in RPMVEC, and up-regulated the gene and protein expression of SSeCKS. Depletion of endogenous SSeCKS in RPMVEC significantly attenuated cytokine-induced decrease in TER and increase in P (d), but not to the basal levels. PKC inhibitors also significantly decreased cytokine-induced hyperpermeability and SSeCKS expression.
CONCLUSIONS: SSeCKS is involved in the endothelial hyperpermeability induced by IL-1β and TNF-α in inflammatory process.



Gene Ontology Annotations    

Biological Process

Objects Annotated

Genes (Rattus norvegicus)
Akap12  (A-kinase anchoring protein 12)


Additional Information