01 January 2015 by Kurt R Stenmark, Michael Yeager

Fibroblasts from the chronically hypoxic pulmonary artery express an "imprinted" pro-inflammatory phenotype

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Stenmark {KR},Yeager M,Riddle S,El Kasmi {KC},Frid {MG},Li M,{McKinsey} T.Targeting the adventitial microenvironment in pulmonary hypertension: A potential approach to therapy that considers epigenetic change. [Internet]. 2012 ;2:3. Available from:http://www.pulmonarycirculation.org/text.asp?2012/2/1/3/94817

Fibroblasts from the chronically hypoxic pulmonary artery express an "imprinted" pro-inflammatory phenotype. Fibroblasts derived from control and hypoxic pulmonary hypertensive calves were cultured and in the absence of any exogenous stimuli, the fibroblast from pulmonary hypertensive animals (PH-Fibs) exhibited a constitutively activated "imprinted" phenotype characterized by overexpression of cytokines, chemokines and adhesion molecules. This phenotype was confirmed at the mRNA level and at the protein level both in vivo and in vitro. At the protein level IL-1b, SDF-1, MCP-1, and VECAM are dramatically upregulated both in vivo and maintain this phenotype in vitro. Confirmation of MCP-1 and VECAM are shown in the bar graphs below.

 

Additional keywords: fibroblast,calf,inflammation,

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