Fig. 7
- ID
- ZDB-FIG-180420-33
- Publication
- Dogra et al., 2017 - Opposite effects of Activin type 2 receptor ligands on cardiomyocyte proliferation during development and repair
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Mstnb and Inhbaa work through distinct Activin type 2 receptors to regulate CM proliferation. a?d RT-qPCR analysis for relative EGFP mRNA expression in 48 hpf Tg(ARE:EGFP) and Tg(12XSBE:EGFP) embryos injected with acvr2aa MO/mstnb-2A-H2B-mcherry mRNA, acvr2ab MO/mstnb-2A-H2B-mcherry mRNA, acvr2ba MO/mstnb-2A-H2B-mcherry mRNA, and acvr2bb MO/mstnb-2A-H2B-mcherry mRNA compared to control MO injected (n?=?2?×?10 embryos assessed as two biological and two technical replicates). e?h RT-qPCR analysis for relative EGFP mRNA expression in 48 hpf Tg(ARE:EGFP) and Tg(12XSBE:EGFP) embryos injected with acvr2ba MO/inhbaa-2A-H2B-mcherry mRNA, acvr2bb MO/inhbaa-2A-H2B-mcherry mRNA, acvr2aa MO/inhbaa-2A-H2B-mcherry mRNA, and acvr2ab MO/inhbaa-2A-H2B-mcherry mRNA compared to control MO-injected (n?=?2?×?10 embryos assessed as two biological and two technical replicates). i Experimental setup of injections, followed by EdU treatment and fixation. j?l Tg(myl7:nlsDsRedExpress) hearts of wild-type sibling, control MO-injected mstnb OE and acvr2bb MO-injected mstnb OE larvae at 72 hpf; ?-DsRed (red), EdU (green). White arrowheads point to proliferating CMs (EdU+/DsRed+). m Quantification of CM proliferation in wild-type sibling (n?=?7), control MO-injected mstnb OE (n?=?8) and acvr2bb MO-injected mstnb OE (n?=?8) ventricles at 72 hpf. n?p Tg(myl7:nlsDsRedExpress) hearts of wild-type sibling, control MO-injected inhbaa OE, and acvr2aa MO-injected inhbaa OE larvae at 72 hpf; ?-DsRed (red), EdU (green). q Quantification of CM proliferation in wild-type sibling (n?=?7), control MO-injected inhbaa OE (n?=?7) and acvr2aa MO-injected inhbaa OE (n?=?8) ventricles at 72 hpf. r Model of ligand-receptor relationship: Mstnb binds to Acvr2b, leading to the activation of Acvr1b/Tgfbr1, which promotes Smad2 and suppresses Smad3 activation. Inversely, Inhbaa binds to Acvr2a, recruiting Acvr1b/Acvr1c, thereby inducing Smad3 and suppressing Smad2 activation. This process is followed by the differential regulation of CM proliferation by Smad2 and Smad3. All cell counts were performed on non-overlapping confocal planes (thickness, 1?µm) (data are mean?±?s.e.m., ns: no significant changes observed, *P???0.05, **P???0.01, ***P???0.001 and ****P???0.0001?Student?s t test, two-tailed). Scale bars, 20?µm. vent., ventricle; atr., atrium |
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| Stage: | Protruding-mouth |