Differential Role of TGF-β in Extracellular Matrix Regulation During Trypanosoma cruzi-Host Cell Interaction

Autor: Luis Felipe de Carvalho Ferreira, Claudia M. Calvet, Tatiana Araújo Silva, Mirian Claudia de Souza Pereira
Jazyk: angličtina
Rok vydání: 2019
Předmět:
Zdroj: International Journal of Molecular Sciences
Volume 20
Issue 19
International Journal of Molecular Sciences, Vol 20, Iss 19, p 4836 (2019)
ISSN: 1422-0067
DOI: 10.3390/ijms20194836
Popis: Transforming growth factor beta (TGF-&beta
) is a determinant for inflammation and fibrosis in cardiac and skeletal muscle in Chagas disease. To determine its regulatory mechanisms, we investigated the response of Trypanosoma cruzi-infected cardiomyocytes (CM), cardiac fibroblasts (CF), and L6E9 skeletal myoblasts to TGF-&beta
Cultures of CM, CF, and L6E9 were infected with T. cruzi (Y strain) and treated with TGF-&beta
(1&ndash
10 ng/mL, 1 h or 48 h). Fibronectin (FN) distribution was analyzed by immunofluorescence and Western blot (WB). Phosphorylated SMAD2 (PS2), phospho-p38 (p-p38), and phospho-c-Jun (p-c-Jun) signaling were evaluated by WB. CF and L6E9 showed an increase in FN from 1 ng/mL of TGF-&beta
while CM displayed FN modulation only after 10 ng/mL treatment. CF and L6E9 showed higher PS2 levels than CM, while p38 was less stimulated in CF than CM and L6E9. T. cruzi infection resulted in localized FN disorganization in CF and L6E9. T. cruzi induced an increase in FN in CF cultures, mainly in uninfected cells. Infected CF cultures treated with TGF-&beta
showed a reduction in PS2 and an increase in p-p38 and p-c-Jun levels. Our data suggest that p38 and c-Jun pathways may be participating in the fibrosis regulatory process mediated by TGF-&beta
after T. cruzi infection.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje