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Up-Regulation of Calcium Homeostasis Modulator-1 in Pulmonary Artery Smooth Muscle Cells with Idiopathic Pulmonary Arterial Hypertension
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A2098 - Up-Regulation of Calcium Homeostasis Modulator-1 in Pulmonary Artery Smooth Muscle Cells with Idiopathic Pulmonary Arterial Hypertension
Author Block: M. Rodriguez1, J. X. Yuan2; 1Medicine, University of Arizona, Tucson, AZ, United States, 2Department of Medicine, University of Arizona, Tucson, AZ, United States.
Upregulation of Calcium Homeostasis Modulator-1 in Pulmonary Artery Smooth Muscle Cells with Idiopathic Pulmonary Arterial Hypertension
Abstract
The pulmonary circulation is a low pressure and resistance system. Patients with pulmonary hypertension (PH) experience sustained pulmonary vasoconstriction and excessive vascular remodeling. This is a consequence of smooth muscle contraction in which many factors of the endothelium contribute to regulating. Similarly, a rise in cytosolic calcium concentration [Ca2+] in pulmonary artery smooth muscle cells is a major trigger for vasoconstriction. The upregulation or downregulation of ion channels and transporters along with adhesion molecules in intracellular signaling cascades are key to the remodeling of pulmonary vascular function and structure. The calcium homeostasis modulator 1 (CALHM1) is a receptor of channels that localizes in the plasma membrane and the endoplasmic reticulum (ER). CALHM1 has been known to reduce ER [Ca2+] uptake by decreasing both the transport capacity and the Ca2+ affinity of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) together suggesting that CALHM1 belongs to family of proteins that is similar to connexins and pannexins. Due to [Ca2+]cyt important role in PH, we investigate its expression levels in idiopathic pulmonary arterial hypertension (IPAH) related conditions compared to normal. Our current work shows that both CALHM1 and pannexin1 are upregulated in IPAH pulmonary artery smooth muscle cells (PASMCs) compared to normal PASMCs. Altogether this data demonstrates how the difference of expression of CALHM1 and pannexins provide a relevant link between Ca2+ homeostasis disruption in IPAH PASMCs. Furthermore, CALHM1 could be a key Ca2+ channel regulator in controlling cell proliferation/transition in IPAH.
Author Block: M. Rodriguez1, J. X. Yuan2; 1Medicine, University of Arizona, Tucson, AZ, United States, 2Department of Medicine, University of Arizona, Tucson, AZ, United States.
Upregulation of Calcium Homeostasis Modulator-1 in Pulmonary Artery Smooth Muscle Cells with Idiopathic Pulmonary Arterial Hypertension
Abstract
The pulmonary circulation is a low pressure and resistance system. Patients with pulmonary hypertension (PH) experience sustained pulmonary vasoconstriction and excessive vascular remodeling. This is a consequence of smooth muscle contraction in which many factors of the endothelium contribute to regulating. Similarly, a rise in cytosolic calcium concentration [Ca2+] in pulmonary artery smooth muscle cells is a major trigger for vasoconstriction. The upregulation or downregulation of ion channels and transporters along with adhesion molecules in intracellular signaling cascades are key to the remodeling of pulmonary vascular function and structure. The calcium homeostasis modulator 1 (CALHM1) is a receptor of channels that localizes in the plasma membrane and the endoplasmic reticulum (ER). CALHM1 has been known to reduce ER [Ca2+] uptake by decreasing both the transport capacity and the Ca2+ affinity of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) together suggesting that CALHM1 belongs to family of proteins that is similar to connexins and pannexins. Due to [Ca2+]cyt important role in PH, we investigate its expression levels in idiopathic pulmonary arterial hypertension (IPAH) related conditions compared to normal. Our current work shows that both CALHM1 and pannexin1 are upregulated in IPAH pulmonary artery smooth muscle cells (PASMCs) compared to normal PASMCs. Altogether this data demonstrates how the difference of expression of CALHM1 and pannexins provide a relevant link between Ca2+ homeostasis disruption in IPAH PASMCs. Furthermore, CALHM1 could be a key Ca2+ channel regulator in controlling cell proliferation/transition in IPAH.
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