Activation of PKCα-cTnI pathway and ER stress in murine cardiomyocytes exposed to D39 or PLY.

<p>(<b>A</b>) Representative Western blots and (<b>B</b>) a band-quantification histogram showing the distribution of PKCα and PKCβII in the cytosol “C” and membrane “M” fractions of murine cardiomyocytes under untreated (UT), D39- and PLN-A-infection (1x10⁶ CFU) conditions (24 h post-infection). GAPDH and Pan-Cadherin were used as markers for “C” and “M” fractions, respectively. Data are presented as Mean±SD (n = 3). * <i>p</i><0.05. (<b>C</b>) and (<b>D</b>) Typical Western blots showing the effects of D39/PLN-A (1x10⁶ CFU) infection (C) and PLY/PdB (200 ng/g) i.v. injection (D) on the association of PKCα and PKCβII with the myofilament fraction of murine cardiomyocytes 24 h post injection. cTnI was used as an endogenous control (n = 3). (<b>E</b>) and (<b>F</b>) Typical Western blots illustrating the phosphorylation of cTnI at the S43 and T144 phosphorylation sites in murine cardiomyocytes following D39/PLN-A infection (E) and PLY/PdB injection (F) (24 h post injection). cTnI was used as an endogenous control (n = 3). (<b>G</b>) and (<b>H</b>) Typical Western blots showing activation of ER stress markers in murine cardiomyocytes at 24 h post-infection with D39/PLN-A (G) and PLY/PdB (H) (n = 3).