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Protective effects of calcyclin-binding protein against pulmonary vascular remodeling in flow-associated pulmonary arterial hypertension
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Protective effects of calcyclin-binding protein against pulmonary vascular remodeling in flow-associated pulmonary arterial hypertension
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Protective effects of calcyclin-binding protein against pulmonary vascular remodeling in flow-associated pulmonary arterial hypertension
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Journal Article
Protective effects of calcyclin-binding protein against pulmonary vascular remodeling in flow-associated pulmonary arterial hypertension
2022
Overview
Background
Pulmonary arterial hypertension associated with congenital heart disease (CHD-PAH) is recognized as a cancer-like disease with a proliferative and pro-migratory phenotype in pulmonary artery smooth muscle cells (PASMCs). Calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP) has been implicated in the progression of various cancers; however, it has not been previously studied in the context of CHD-PAH. Here, we aimed to examine the function of CacyBP/SIP in CHD-PAH and explore its potential as a novel regulatory target for the disease.
Methods
The expression of CacyBP/SIP in PASMCs was evaluated both in the pulmonary arterioles of patients with CHD-PAH and in high-flow-induced PAH rats. The effects of CacyBP/SIP on pulmonary vascular remodeling and PASMC phenotypic switch, proliferation, and migration were investigated. LY294002 (MedChemExpress, NJ, USA) was used to block the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathway to explore changes in PASMC dysfunction induced by low CacyBP/SIP levels. Hemodynamics and pulmonary arterial remodeling were further explored in rats after short-interfering RNA-mediated decrease of CacyBP/SIP expression.
Results
CacyBP/SIP expression was markedly reduced both in the remodeled pulmonary arterioles of patients with CHD-PAH and in high-flow-induced PAH rats. Low CacyBP/SIP expression promoted hPASMC phenotypic switch, proliferation, and migration via PI3K/AKT pathway activation. Our results indicated that CacyBP/SIP protected against pulmonary vascular remodeling through amelioration of hPASMC dysfunction in CHD-PAH. Moreover, after inhibition of CacyBP/SIP expression in vivo, we observed increased right ventricular hypertrophy index, poor hemodynamics, and severe vascular remodeling.
Conclusions
CacyBP/SIP regulates hPASMC dysfunction, and its increased expression may ameliorate progression of CHD-PAH.
Publisher
BioMed Central,BioMed Central Ltd,Nature Publishing Group,BMC
Subject
1-Phosphatidylinositol 3-kinase
/ Animals
/ Calcium-Binding Proteins - genetics
/ Calcium-Binding Proteins - metabolism
/ Calcyclin-binding protein/Siah-1-interacting protein
/ Cancer
/ Complications and side effects
/ Familial Primary Pulmonary Hypertension
/ Hypertension, Pulmonary - prevention & control
/ Intracellular Signaling Peptides and Proteins - metabolism
/ Kinases
/ Lungs
/ Medicine
/ Muscles
/ Phosphatidylinositol 3-Kinases - metabolism
/ Pneumology/Respiratory System
/ Proteins
/ Proto-Oncogene Proteins c-akt - metabolism
/ Pulmonary Arterial Hypertension
/ Pulmonary Artery - metabolism
/ Pulmonary artery smooth muscle cells
/ Pulmonary vascular remodeling
/ Rats
/ Testing
