Fig 1.
MAPK signaling is fully upregulated by MI injury in the hearts of 1-day-old pigs.
(A) The subpathways of MAPK signaling are displayed in a flow chart; genes that were expressed at significantly higher levels in the hearts of MI-P1 animals than in Age-matched normal -P1 hearts at P7 (i.e., early postnatal genes) or P28 (i.e., late postnatal genes) are displayed in a red box or in red text, respectively. (B) The expression of the initial signaling molecules (CSF1/CSF1R, CD14, TGFB) and the terminal effector molecules (JUND, ATF4, FOS, NFKB2 and RELB) of the MAPK signaling pathway was evaluated at the indicted time points in MI-P1 and Age-matched normal -P1 (CTL) hearts.
Fig 2.
Hippo signaling is fully upregulated by MI injury in the hearts of 1-day-old pigs.
(A) The subpathways of Hippo signaling are displayed in a flow chart; genes that were expressed at significantly higher levels in the hearts of MI-P1 animals than in Age-matched normal -P1 hearts at P7 (i.e., early postnatal genes) or P28 (i.e., late postnatal genes) are displayed in a red box or in red text, respectively. (B) The expression of an initial signaling molecule (TGFB1) and a terminal effector molecule (ITGB2) of the Hippo signaling pathway was evaluated at the indicted time points in MI-P1 and Age-matched normal -P1 (CTL) hearts.
Fig 3.
cAMP signaling is altered by MI injury in the hearts of 1-day-old pigs.
Two subpathways of cAMP signaling are displayed as flow charts. Genes that were expressed at significantly higher levels in the hearts of MI-P1 animals than in Age-matched normal -P1 hearts at P7 (i.e., early postnatal genes) or P28 (i.e., late postnatal genes) are displayed in a red box or in red text, respectively, and genes that were expressed at lower levels in MI-P1 than in Age-matched normal -P1 hearts at P28 are displayed in blue text.
Fig 4.
JAK/STAT signaling is fully upregulated by MI injury in the hearts of 1-day-old pigs.
(A) The subpathways of JAK/STAT signaling are displayed in a flow chart; genes that were expressed at significantly higher levels in the hearts of MI-P1 animals than in Age-matched normal -P1 hearts at P7 (i.e., early postnatal genes) or P28 (i.e., late postnatal genes) are displayed in a red box or in red text, respectively. (B) The expression of three terminal effector molecules (PIM1, MYC, and CCND3) of the JAK/STAT signaling pathway was evaluated at the indicted time points in MI-P1 and Age-matched normal -P1 (CTL) hearts.
Fig 5.
RAS signaling is fully upregulated by MI injury in the hearts of 1-day-old pigs.
The subpathways of RAS signaling are displayed in a flow chart; genes that were expressed at significantly higher levels in the hearts of MI-P1 animals than in Age-matched normal -P1 hearts at P7 (i.e., early postnatal genes) or P28 (i.e., late postnatal genes) are displayed in a red box or in red text, respectively.
Fig 6.
Western blotting. LAD ligation at P1 activates key cell proliferation signaling pathways and downstream components.
The expression of β-catenin, phosphorylated (Pho-) GSK 3α/β, total GSK 3α/β, Pho-Akt, total Akt, Pho-p42/44 MAPK, and total p42/44 MAPK was evaluated via Western blot. GAPDH levels were also evaluated to confirm equal loading. (A) Representative Western blotting of hearts from each time point/group; (B) Compiled Wetern blotting data, n = 3 hearts each bar. T-test (2 tails) with Bonferroni correction. *, p<0.05 between P28-MI vs P28-NL; #, p < 0.05 vs P7-MI; †, p<0.05 vs P7-NL. Total protein blots were the same original blots stripped and reprobed.