Abstract
Objective: To observe the pulmonary vascular remodeling in rats with pulmonary hypertension induced by hypoxia and hypercapnia, and to explore the role of endoplasmic reticulum stress in pulmonary hypertension. Methods: 1) 40 SD rats were randomly divided into four groups: normoxic control group (N), hypoxia hypercapnia group (HH), endoplasmic reticulum stress (ERS) inhibitor 4-phenyl butyric acid group (4-PBA), ERS pathway agonist tunicamycin group (TM). 2) The mean pulmonary arterial pressure (mPAP) and the right ventricular hypertrophy index (RV/(LV + S)) were measured in each group. 3) Identification of pulmonary artery smooth muscle cells (PASMCs) in each group by immunofluorescence α-SMA. 4) Morphological changes of lung tissue and pulmonary artery were observed by electron microscope. 5) The apoptotic index of PASMCs in each group was detected by TUNEL. 6) Reverse transcription polymerase chain reaction (RT-PCR) and Western Blot (WB) were used to detect the expression of ERS related protein and mRNA (GRP78, CHOP, JNK, Caspase-12) in each group. Results: 1) Compared with the N group, the mPAP, RV/(LV + S) and vascular wall area (WA)/total area (TA) value of HH group, 4-PBA group and TM group were increased (P P P P P P P P P P Conclusion: Hypoxia and hypercapnia induced pulmonary vascular remodeling may be related to the proliferation of PASMCs, and ERS related factors (JNK, Caspase12 and CHOP) are involved in the regulation of hypoxic hypercapnia.
Highlights
Pulmonary artery hypertension (PAH) is a kind of pulmonary vascular selective remodeling disease [1]
1) 40 SD rats were randomly divided into four groups: normoxic control group (N), hypoxia hypercapnia group (HH), endoplasmic reticulum stress (ERS) inhibitor 4-phenyl butyric acid group (4-PBA), endoplasmic stress (ERS) pathway agonist tunicamycin group (TM). 2) The mean pulmonary arterial pressure and the right ventricular hypertrophy index (RV/(LV + S)) were measured in each group
The latter three groups were placed in chamber of hypoxia hypercapnia, Oxygen concentration in the tank remained at 9% - 11%, and the concentration of carbon dioxide was maintained at 5% - 6% (Cabin water vapor was absorbed by anhydrous CaCl2, and excess carbon dioxide was absorbed by calcium hydroxide) for 24 days
Summary
Pulmonary artery hypertension (PAH) is a kind of pulmonary vascular selective remodeling disease [1]. Some studies have shown that a common feature of triggering or promoting PAH processes is endoplasmic stress (ERS) [2] [3]. Recent studies have shown that loss of function in BMPRII and the dysfunction of key protein transport can cause endoplasmic reticulum stress [7]. In these organelles, stress manifests as the accumulation of misfolding proteins, triggering an unfolded protein response (UPR). Under severe acute or chronic stress conditions, UPR directly drives mitochondria to cause apoptosis [9], and the rapid increase in GRP78 is considered to be the most sensitive sign of endoplasmic reticulum stress [10]
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