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Title: Preconditioning with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway

Abstract

Nitric oxide (NO) signaling pathways are important in both the maintenance of vascular homeostasis and disease progression. Overproduction of NO has been associated with ischemia/reperfusion (I/R) injury. Growing evidences suggest that NO preconditioning has cytoprotective effects against I/R injury. However, the mechanism with which NO mediates these effects remains to be elucidated. The purpose of this study was to examine the mechanism of how NO preconditioning inhibits subsequent NO-induced apoptosis in vascular smooth muscle cells (VSMC), specifically focusing on heme oxygenase-1 (HO-1). According to our data, sodium nitroprusside (SNP) increased HO-1 expression in a concentration dependent manner. Preconditioning with low concentration SNP (0.3 mM) inhibited subsequent high concentration SNP (1.5 mM)-induced apoptosis, and this effect was reversed by the HO-1 inhibitor SnPP. Low concentration SNP-mediated protection involved p38 kinase inactivation and increased Bcl-2 expression. Furthermore, mitochondrial membrane potential was concomitantly increased with decreased expressions of Bax, Apaf-1, and activity of caspase-3, which was reversed by SnPP treatment. Our results show that low concentration SNP preconditioning suppresses subsequent high concentration SNP-induced apoptosis by inhibiting p38 kinase and mitochondrial death pathway via HO-1-dependent mechanisms in VSMC.

Authors:
 [1];  [1];  [2];  [1];  [1];  [1];  [1]
  1. Division of Cardiovascular Diseases, Center for Biomedical Sciences, National Institutes of Health, Nokbun-dong, Eunpyung-gu, Seoul 122-701 (Korea, Republic of)
  2. BK21 Project of Medicinal Science, Yonsei University (Korea, Republic of)
Publication Date:
OSTI Identifier:
20850491
Resource Type:
Journal Article
Journal Name:
Toxicology and Applied Pharmacology
Additional Journal Information:
Journal Volume: 217; Journal Issue: 2; Other Information: DOI: 10.1016/j.taap.2006.08.010; PII: S0041-008X(06)00300-0; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; DEATH; HEME; HOMEOSTASIS; INACTIVATION; INJURIES; ISCHEMIA; MEMBRANES; MUSCLES; NITRIC OXIDE; SODIUM

Citation Formats

Kwak, Hyun-Jeong, Park, Kyoung-Mi, Lee, Seahyoung, Lim, Hyun-Joung, Go, Sang-Hee, Eom, Sang-Mi, and Park, Hyun-Young. Preconditioning with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway. United States: N. p., 2006. Web. doi:10.1016/j.taap.2006.08.010.
Kwak, Hyun-Jeong, Park, Kyoung-Mi, Lee, Seahyoung, Lim, Hyun-Joung, Go, Sang-Hee, Eom, Sang-Mi, & Park, Hyun-Young. Preconditioning with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway. United States. https://doi.org/10.1016/j.taap.2006.08.010
Kwak, Hyun-Jeong, Park, Kyoung-Mi, Lee, Seahyoung, Lim, Hyun-Joung, Go, Sang-Hee, Eom, Sang-Mi, and Park, Hyun-Young. Fri . "Preconditioning with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway". United States. https://doi.org/10.1016/j.taap.2006.08.010.
@article{osti_20850491,
title = {Preconditioning with low concentration NO attenuates subsequent NO-induced apoptosis in vascular smooth muscle cells via HO-1-dependent mitochondrial death pathway},
author = {Kwak, Hyun-Jeong and Park, Kyoung-Mi and Lee, Seahyoung and Lim, Hyun-Joung and Go, Sang-Hee and Eom, Sang-Mi and Park, Hyun-Young},
abstractNote = {Nitric oxide (NO) signaling pathways are important in both the maintenance of vascular homeostasis and disease progression. Overproduction of NO has been associated with ischemia/reperfusion (I/R) injury. Growing evidences suggest that NO preconditioning has cytoprotective effects against I/R injury. However, the mechanism with which NO mediates these effects remains to be elucidated. The purpose of this study was to examine the mechanism of how NO preconditioning inhibits subsequent NO-induced apoptosis in vascular smooth muscle cells (VSMC), specifically focusing on heme oxygenase-1 (HO-1). According to our data, sodium nitroprusside (SNP) increased HO-1 expression in a concentration dependent manner. Preconditioning with low concentration SNP (0.3 mM) inhibited subsequent high concentration SNP (1.5 mM)-induced apoptosis, and this effect was reversed by the HO-1 inhibitor SnPP. Low concentration SNP-mediated protection involved p38 kinase inactivation and increased Bcl-2 expression. Furthermore, mitochondrial membrane potential was concomitantly increased with decreased expressions of Bax, Apaf-1, and activity of caspase-3, which was reversed by SnPP treatment. Our results show that low concentration SNP preconditioning suppresses subsequent high concentration SNP-induced apoptosis by inhibiting p38 kinase and mitochondrial death pathway via HO-1-dependent mechanisms in VSMC.},
doi = {10.1016/j.taap.2006.08.010},
url = {https://www.osti.gov/biblio/20850491}, journal = {Toxicology and Applied Pharmacology},
issn = {0041-008X},
number = 2,
volume = 217,
place = {United States},
year = {2006},
month = {12}
}