Calpain mediated pulmonary vascular remodeling in hypoxia induced pulmonary hypertension

To explore the role of calpain in pulmonary vascular remodeling in hypoxia-induced pulmonary hypertension and the underlying mechanisms.
 Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary art...

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Veröffentlicht in:Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban 2016-09, Vol.41 (9), p.929
Hauptverfasser: Zhang, Weifang, Zhu, Tiantian, Xiong, Aizhen, Ge, Xiaoyue, Xu, Ruilai, Lu, Shegui, Hu, Changping
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container_issue 9
container_start_page 929
container_title Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban
container_volume 41
creator Zhang, Weifang
Zhu, Tiantian
Xiong, Aizhen
Ge, Xiaoyue
Xu, Ruilai
Lu, Shegui
Hu, Changping
description To explore the role of calpain in pulmonary vascular remodeling in hypoxia-induced pulmonary hypertension and the underlying mechanisms.
 Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored by a method with right external jugular vein cannula. Right ventricular hypertrophy index was presented as the ratio of right ventricular weight to left ventricular weight (left ventricle plus septum weight). Levels of calpain-1, -2 and -4 mRNA in pulmonary artery were determined by real-time PCR. Levels of calpain-1, -2 and -4 protein were determined by Western blot. Primary rat pulmonary arterial smooth muscle cells (PASMCs) were divided into 4 groups: a normoxia control group, a normoxia+MDL28170 group, a hypoxia group and a hypoxia+MDL28170 group. Cell proliferation was detected by MTS and flow cytometry. Levels of Ki-67 and proliferating cell nuclear antigen (PCNA) mRNA were
doi_str_mv 10.11817/j.issn.1672-7347.2016.09.007
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 Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored by a method with right external jugular vein cannula. Right ventricular hypertrophy index was presented as the ratio of right ventricular weight to left ventricular weight (left ventricle plus septum weight). Levels of calpain-1, -2 and -4 mRNA in pulmonary artery were determined by real-time PCR. Levels of calpain-1, -2 and -4 protein were determined by Western blot. Primary rat pulmonary arterial smooth muscle cells (PASMCs) were divided into 4 groups: a normoxia control group, a normoxia+MDL28170 group, a hypoxia group and a hypoxia+MDL28170 group. Cell proliferation was detected by MTS and flow cytometry. Levels of Ki-67 and proliferating cell nuclear antigen (PCNA) mRNA were</description><identifier>ISSN: 1672-7347</identifier><identifier>DOI: 10.11817/j.issn.1672-7347.2016.09.007</identifier><identifier>PMID: 27640791</identifier><language>chi</language><publisher>China</publisher><subject>Animals ; Calpain - genetics ; Calpain - physiology ; Cell Proliferation ; Dipeptides - physiology ; Hypertension, Pulmonary - chemically induced ; Hypertension, Pulmonary - genetics ; Hypertension, Pulmonary - physiopathology ; Hypertrophy, Right Ventricular ; Hypoxia ; Ki-67 Antigen - drug effects ; Myocytes, Smooth Muscle - physiology ; Proliferating Cell Nuclear Antigen - drug effects ; Pulmonary Artery ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Up-Regulation ; Vascular Remodeling - genetics ; Vascular Remodeling - physiology</subject><ispartof>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban, 2016-09, Vol.41 (9), p.929</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27640791$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Weifang</creatorcontrib><creatorcontrib>Zhu, Tiantian</creatorcontrib><creatorcontrib>Xiong, Aizhen</creatorcontrib><creatorcontrib>Ge, Xiaoyue</creatorcontrib><creatorcontrib>Xu, Ruilai</creatorcontrib><creatorcontrib>Lu, Shegui</creatorcontrib><creatorcontrib>Hu, Changping</creatorcontrib><title>Calpain mediated pulmonary vascular remodeling in hypoxia induced pulmonary hypertension</title><title>Zhong nan da xue xue bao. Journal of Central South University. Yi xue ban</title><addtitle>Zhong Nan Da Xue Xue Bao Yi Xue Ban</addtitle><description>To explore the role of calpain in pulmonary vascular remodeling in hypoxia-induced pulmonary hypertension and the underlying mechanisms.
 Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored by a method with right external jugular vein cannula. Right ventricular hypertrophy index was presented as the ratio of right ventricular weight to left ventricular weight (left ventricle plus septum weight). Levels of calpain-1, -2 and -4 mRNA in pulmonary artery were determined by real-time PCR. Levels of calpain-1, -2 and -4 protein were determined by Western blot. Primary rat pulmonary arterial smooth muscle cells (PASMCs) were divided into 4 groups: a normoxia control group, a normoxia+MDL28170 group, a hypoxia group and a hypoxia+MDL28170 group. Cell proliferation was detected by MTS and flow cytometry. 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 Sprague-Dawley rats were randomly divided into the hypoxia group and the normoxia control group. Right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP) were monitored by a method with right external jugular vein cannula. Right ventricular hypertrophy index was presented as the ratio of right ventricular weight to left ventricular weight (left ventricle plus septum weight). Levels of calpain-1, -2 and -4 mRNA in pulmonary artery were determined by real-time PCR. Levels of calpain-1, -2 and -4 protein were determined by Western blot. Primary rat pulmonary arterial smooth muscle cells (PASMCs) were divided into 4 groups: a normoxia control group, a normoxia+MDL28170 group, a hypoxia group and a hypoxia+MDL28170 group. Cell proliferation was detected by MTS and flow cytometry. Levels of Ki-67 and proliferating cell nuclear antigen (PCNA) mRNA were</abstract><cop>China</cop><pmid>27640791</pmid><doi>10.11817/j.issn.1672-7347.2016.09.007</doi></addata></record>
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subjects Animals
Calpain - genetics
Calpain - physiology
Cell Proliferation
Dipeptides - physiology
Hypertension, Pulmonary - chemically induced
Hypertension, Pulmonary - genetics
Hypertension, Pulmonary - physiopathology
Hypertrophy, Right Ventricular
Hypoxia
Ki-67 Antigen - drug effects
Myocytes, Smooth Muscle - physiology
Proliferating Cell Nuclear Antigen - drug effects
Pulmonary Artery
Rats
Rats, Sprague-Dawley
Real-Time Polymerase Chain Reaction
Up-Regulation
Vascular Remodeling - genetics
Vascular Remodeling - physiology
title Calpain mediated pulmonary vascular remodeling in hypoxia induced pulmonary hypertension
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