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Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Signal 2016 ; 28 (6): 688-98 Nephropedia Template TP
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Common pathways regulate Type III TGF? receptor?dependent cell invasion in epicardial and endocardial cells #MMPMID26970186
Clark CR; Robinson JY; Sanchez NS; Townsend TA; Arrieta JA; Merryman WD; Trykall DZ; Olivey HE; Hong CC; Barnett JV
Cell Signal 2016[Jun]; 28 (6): 688-98 PMID26970186show ga
Epithelial-Mesenchymal Transformation (EMT) and the subsequent invasion of epicardial and endocardial cells during cardiac development is critical to the development of the coronary vessels and heart valves. The transformed cells give rise to cardiac fibroblasts and vascular smooth muscle cells or valvular interstitial cells, respectively. The Type III Transforming Growth Factor ? (TGF?R3) receptor regulates EMT and cell invasion in both cell types, but the signaling mechanisms downstream of TGF?R3 are not well understood. Here we use epicardial and endocardial cells in in vitro cell invasion assays to identify common mechanisms downstream of TGF?R3 that regulate cell invasion. Inhibition of NF-?B activity blocked cell invasion in epicardial and endocardial cells. NF-?B signaling was found to be dysregulated in Tgfbr3?/? epicardial cells which also show impaired cell invasion in response to ligand. TGF?R3-dependent cell invasion is also dependent upon Activin Receptor-Like Kinase (ALK) 2, ALK3, and ALK5 activity. A TGF?R3 mutant that contains a threonine to alanine substitution at residue 841 (TGF?R3-T841A) induces ligand-independent cell invasion in both epicardial and endocardial cells in vitro. These findings reveal a role for NF-?B signaling in the regulation of epicardial and endocardial cell invasion and identify a mutation in TGF?R3 which stimulates ligand-independent signaling.