Calcium Signaling in the Bronchopulmonary Dysplasia Rat Heart

Abstract

Bronchopulmonary dysplasia (BPD) is a chronic lung disease associated with premature birth. It is a significant contributor to perinatal morbidity and mortality. The disease results in disrupted alveolar and pulmonary vascular growth, and may lead to pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) during infancy. Although recent studies have shed light on the pathophysiology of BPD, much remains unknown about the long‐lasting effects of the disease into adulthood. Previous studies on heart failure, PH and RVH have shown that there are alterations in Ca2+ signaling proteins in the right heart myocardium. The objective of this study is to identify whether there are alterations in Ca2+ signaling protein expression in right ventricular (RV) myocytes in rats with BPD. We hypothesize that there is decreased expression of Ryanodine Receptor (RyR2), SERCA2A and L‐type Calcium Channel (LTCC), and an increased expression of protein kinase A (PKA), Na‐Ca exchanger (NCX) and phospholamban (PLN). A previously established rat model of BPD was used, where BPD rats were exposed to 85% O2 for 14 days and controls were exposed to 21% O2 for 14 days. 78 rat hearts in total were harvested during the study at p0, p7, p14, p21, p28, p56, p90, p180. Relative protein expression differences were determined using Western Blots with antibodies against key Ca2+ signaling proteins in control and BPD RV homogenate.