Fig 1: SIRT1 deficiency blunts the induction of chemotaxis signaling in cardiomyocytes in vitro and in vivo. (A) The induction of chemotaxis genes in WT and SIRT1 KO cardiomyocytes. WT and SIRT1 KO mel1 hESCs were induced for cardiomyocyte differentiation, and total RNA was collected on D0, D8, D20 and D45, and processed for qPCR analysis of CCL2, CCR2, CCR4, CXCL12 and CXCR4 (n=3 independent lines/genotype, *P<0.05, Student's t-test, values represent mean±s.e.m.). (B,C) The expression of CCL2 and CCR4 is reduced in SIRT1 KO iCMs. D20 WT and SIRT1 KO iCMs were fixed and stained with anti-CCL2 and anti-ACTN2 antibodies (B), or anti-CCR4 and anti-ACTN2 antibodies (C). Scale bars: 25 µm. (D) Deletion of SIRT1 from E12.5 embryos results in reduction of CXCL12 and CCL12 expression in cardiomyocytes. Heart sections from E18.5 Flox and TiKO embryos were stained with anti-CXCL12 (left panels) or anti-CCL12 (right panels) antibodies. Scale bars: 25 µm.