An essential role for connexin43 gap junctions in mouse coronary artery development

• DOI: 10.1242/dev.129.8.2031
• Publication Date: 2021-04-23T20:33:15Z
• Authors: W. E. I. Li; K. Waldo; K. L. Linask; T. Chen; A. Wessels; M. S. Parmacek; M. L. Kirby; C. W. Lo
• Keywords: Coronary arteries; Knockout mouse

Connexin43 knockout mice die neonatally from conotruncal heart malformation and outflow obstruction. Previous studies have indicated the involvement of neural crest perturbations in these cardiac anomalies. We provide evidence for another extracardiac cell population, proepicardial cells. These cells give rise to vascular smooth muscle coronary arteries fibroblasts heart. observed abnormal presence fibroblast infundibular pouches connexin43 mouse In addition, exhibit a variety artery patterning defects previously described crest-ablated chick embryos, such as anomalous origin arteries, absent left or right artery, accessory arteries. However, we show that also express gap junctions abundantly. The are functionally well coupled, this coupling is significantly reduced with loss function. Further analysis revealed an elevation speed locomotion proliferation rate connexin43-deficient A parallel transgenic dominant negative inhibition targeted only showed none coupling, migration changes. obstruction, but no pouches. Together findings indicate important role patterning, probably involves discuss potential human cardiovascular anomalies involving