Figure 1. Microarray-based expression analyses of the genes induced by MI and regulated by CaMKII in mouse hearts.

(A) Cardiac genes modulated by MI. cDNA microarray comparison of healthy versus infarcted hearts expressing scrambled control peptide (AC3-C) identified 128 induced and 28 repressed genes out of 8,600 represented on the microarrays. Up, upregulated; Dn, downregulated. (B) Infarcted hearts expressing CaMKII inhibitory peptide (AC3-I) in microarray analyses showed repression of 71 genes and induction of 36 genes when compared with infarcted control (AC3-C) hearts, indicating CaMKII-regulated genes. (C) CaMKII-regulated genes induced by MI. Venn diagram displaying the genes that were induced by MI in AC3-C hearts but were repressed in post-MI AC3-I hearts. A total of 54 (42%) MI-induced genes in AC3-C hearts were regulated by CaMKII. (D) Venn diagram showing the genes that are repressed upon MI and are regulated by CaMKII. A total of 11 (39%) MI-repressed genes in AC3-C hearts were regulated by CaMKII. (E) A subset of proinflammatory genes that were either upregulated in AC3-C hearts (red bars) or downregulated in AC3-C hearts after MI (green bars). In CaMKII-inhibited AC3-I hearts, the same genes displayed reduced expression (blue bars) or increased expression (purple bars), respectively. Adn, complement factor D; C4a, complement component 4A; C2, complement component 2; C1s, complement component 1, s subcomponent; Hmgn3, high mobility group nucleosomal binding domain 3; Cyp2f2, cytochrome P450, family 2, subfamily f, polypeptide 2; Stat1, signal transducer and activator of transcription 1; Pam, peptidylglycine alpha-amidating monooxygenase; Pttg1, pituitary tumor-transforming gene 1; Pdk4, pyruvate dehydrogenase kinase, isoenzyme 4; Ptgds, prostaglandin D2 synthase; Dtx2, deltex 2 homolog.