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. 2016 Feb 12;310(8):H984–H994. doi: 10.1152/ajpheart.00879.2015

Fig. 6.

Fig. 6.

Activin-like kinase 2 (ALK2) is required for A2-induced cardiac hypertrophy. Tamoxifen (Tam) administration (30 mg·kg−1·day−1 ip) in α-MHC-MerCreMer (MCM)-ALK1flox/flox, MCM-ALK2flox/flox, and MCM-ALK3flox/flox mice for 5 days reduced mRNA levels of ALK1 (A), ALK2 (B), and ALK3 (C), respectively, in cardiomyocytes obtained from LV 5 wk after Tam injection (left). Before treatment with Tam and deletion of the floxed alleles, A2 administration in MCM-ALK1flox/flox (A), MCM-ALK2flox/flox (B), and MCM-ALK3flox/flox mice (C) increased the HW/TL and LVW/TL and increased IVS and PW thickness. A–C: A2 administration induced NPPB, NPPA, and Id1 expression in the LVs of these mice. After administration of Tam for 5 days to delete cardiac ALK1, ALK2, or ALK3, the effects of A2 on HW/TL and LVW/TL and IVS and PW thickness were inhibited in ALK2-deficient mice (B), but not in ALK1- (A) or ALK3-deficient animals (C). The effects of A2 on LV expression of NPPB, NPPA, and Id1 genes were inhibited in ALK2-deficient, but not ALK1- or ALK3-deficient mice. Values are means ± SE; n = 6–7 animals in each group. *P < 0.05, **P < 0.01, and ***P < 0.001 vs. corresponding saline or Veh treatment. †P < 0.05 vs. A2 + Veh treatment.