Intracellular Ca2+ Dysregulation in Coronary Smooth Muscle Is Similar in Coronary Disease of Humans and Ossabaw Miniature Swine.
Jill K BadinCaleb EggenbergerStacey Dineen RodenbeckZubair A HashmiI-Wen WangJose P GarciaMouhamad AllooshMichael SturekPublished in: Journal of cardiovascular translational research (2021)
Intracellular free Ca2+ ([Ca2+]i) dysregulation occurs in coronary smooth muscle (CSM) in atherosclerotic coronary artery disease (CAD) of metabolic syndrome (MetS) swine. Our goal was to determine how CAD severity, arterial structure, and MetS risk factors associate with [Ca2+]i dysregulation in human CAD compared to changes in Ossabaw miniature swine. CSM cells were dispersed from coronary arteries of explanted hearts from transplant recipients and from lean and MetS swine with CAD. CSM [Ca2+]i elicited by Ca2+ influx and sarcoplasmic reticulum (SR) Ca2+ release and sequestration was measured with fura-2. Increased [Ca2+]i signaling was associated with advanced age and a greater media area in human CAD. Decreased [Ca2+]i signaling was associated with a greater number of risk factors and a higher plaque burden in human and swine CAD. Similar [Ca2+]i dysregulation exhibited in human and Ossabaw swine CSM provides strong evidence for the translational relevance of this large animal model.
Keyphrases
- coronary artery disease
- smooth muscle
- endothelial cells
- risk factors
- metabolic syndrome
- coronary artery
- protein kinase
- cardiovascular events
- percutaneous coronary intervention
- coronary artery bypass grafting
- induced pluripotent stem cells
- type iii
- aortic stenosis
- skeletal muscle
- induced apoptosis
- pluripotent stem cells
- bone mineral density
- left ventricular
- cell proliferation
- endoplasmic reticulum stress