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Loss of Hand2 in a population of Periostin lineage cells results in pronounced bradycardia and neonatal death. | LitMetric

Loss of Hand2 in a population of Periostin lineage cells results in pronounced bradycardia and neonatal death.

Dev Biol

Riley Heart Research Center, Herman B Wells Center for Pediatric Research, Departments of Pediatrics and Medical and Molecular Genetics, Indiana University School of Medicine, 1044 West Walnut Street, Indianapolis, IN 46202-5225, USA. Electronic address:

Published: April 2014

The Periostin Cre (Postn-Cre) lineage includes endocardial and neural crest derived mesenchymal cells of the cardiac cushions, neural crest-derived components of the sympathetic and enteric nervous systems, and cardiac fibroblasts. In this study, we use the Postn-Cre transgenic allele to conditionally ablate Hand2 (H2CKO). We find that Postn-Cre H2CKOs die shortly after birth despite a lack of obvious cardiac structural defects. To ascertain the cause of death, we performed a detailed comparison of the Postn-Cre lineage and Hand2 expression at mid and late stages of embryonic development. Gene expression analyses demonstrate that Postn-Cre ablates Hand2 from the adrenal medulla as well as the sphenopalatine ganglia of the head. In both cases, Hand2 loss-of-function dramatically reduces expression of Dopamine Beta Hydroxylase (Dbh), a gene encoding a crucial catecholaminergic biosynthetic enzyme. Expression of the genes Tyrosine Hydroxylase (Th) and Phenylethanolamine N-methyltransferase (Pnmt), which also encode essential catecholaminergic enzymes, were severely reduced in postnatal adrenal glands. Electrocardiograms demonstrate that 3-day postnatal Postn-Cre H2CKO pups exhibit sinus bradycardia. In conjunction with the aforementioned gene expression analyses, these results strongly suggest that the observed postnatal lethality occurs due to a catecholamine deficiency and subsequent heart failure.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3990418PMC
http://dx.doi.org/10.1016/j.ydbio.2014.02.010DOI Listing

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