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. 2009 Jun 5;13(8a):1513–1525. doi: 10.1111/j.1582-4934.2009.00798.x

Fig. 3.

Fig. 3

Fig. 3

Effects of TLR4 functional deficiency on ischemia-induced mitogen-activated protein kinases (MAPKs) and cardiac ER stress. Time course of p38 (A), JNK (B) and ERK (C) phosphorylation induced by in vivo regional ischemia or sham operation, in C3H/HeN and C3H/HeJ hearts. Immunoblots were performed with antibodies for phosphor-p38 (Thr180/Tyr182) (p-p38), total p38 (p38), phosphor-JNK (Thr183/Tyr185) (p-JNK), total JNK (JNK), phosphor-ERK (Thr202/Tyr204) (p-ERK) or total ERK (ERK). The graph shows phosphorylated p38 MAPK (A), phosphorylated JNK (B) and phosphorylated ERK (C) relative to the total amount of respective kinases. (D) The representative immunoblots show that ischemic stress (30 min.) stimulated the up-regulation of ER chaperons, Grp78/BiP and Gadd153/CHOP and ER integral membrane protein, IRE-1α. Immunoblots were performed with antibodies for Grp78/BiP, Gadd153/CHOP, IRE-1α or GAPDH. The graph shows the relative expression levels of Grp78/BiP, Gadd153/CHOP or IRE-1α to the GAPDH expression. Values are mean ± S.E.M. for five experiments. *P< 0.05 versus sham, †P< 0.05 versus C3H/HeN ischemic time-points, respectively.