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. Author manuscript; available in PMC: 2019 Apr 13.
Published in final edited form as: Circ Res. 2018 Mar 13;122(8):1052–1068. doi: 10.1161/CIRCRESAHA.117.312130

Figure 5. TXNDC5-dependent activation of hCF is associated with increased JNK, but not SMAD3 or ERK, activity.

Figure 5

(A) Overexpression of TXNDC5 in hCF was sufficient to trigger hCF activation (as reflected in increased αSMA and POSTN protein levels), and COL1A1 production. Phosphorylation of SMAD3 was not affected by ectopic TXNDC5 expression. (B) Forced expression of TXNDC5 led to significantly increased secretion of type 1 collagen (COL1A1) from hCF. (C) Knockdown of TXNDC5 in hCF abrogated TGFβ1-induced phosphorylation of JNK, but not of SMAD3 or ERK. Phosphorylated JNK, SMAD3 and ERK were expressed relative to total JNK, SMAD3 and ERK, respectively (#P<0.01, *P<0.001).