Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro

Cessation of blood supply due to myocardial infarction (MI) leads to complicated pathological alteration in the affected regions. Cardiac stem cells (CSCs) migration plays a major role in promoting recovery of cardiac function and protecting cardiomyocytes in post-MI remodeling. Despite being the mo...

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Main Authors: Qing Gao, Maojuan Guo, Wenyun Zeng, Yijing Wang, Lin Yang, Xiaoli Pang, Huhu Li, Yanrong Suo, Xijuan Jiang, Chunquan Yu
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Stem Cells International
Online Access:http://dx.doi.org/10.1155/2015/836390
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author Qing Gao
Maojuan Guo
Wenyun Zeng
Yijing Wang
Lin Yang
Xiaoli Pang
Huhu Li
Yanrong Suo
Xijuan Jiang
Chunquan Yu
author_facet Qing Gao
Maojuan Guo
Wenyun Zeng
Yijing Wang
Lin Yang
Xiaoli Pang
Huhu Li
Yanrong Suo
Xijuan Jiang
Chunquan Yu
author_sort Qing Gao
collection DOAJ
description Cessation of blood supply due to myocardial infarction (MI) leads to complicated pathological alteration in the affected regions. Cardiac stem cells (CSCs) migration plays a major role in promoting recovery of cardiac function and protecting cardiomyocytes in post-MI remodeling. Despite being the most abundant cell type in the mammalian heart, cardiac fibroblasts (CFs) were underestimated in the mechanism of CSCs migration. Our objective in this study is therefore to investigate the migration related factors secreted by hypoxia CFs in vitro and the degree that they contribute to CSCs migration. We found that supernatant from hypoxia induced CFs could accelerate CSCs migration. Four migration-related cytokines were reported upregulated both in mRNA and protein levels. Upon adding antagonists of these cytokines, the number of migration cells significantly declined. When the cocktail antagonists of all above four cytokines were added, the migration cells number reduced to the minimum level. Besides, MMP-9 had an important effect on triggering CSCs migration. As shown in our results, MMP-9 induced CSCs migration and the underlying mechanism might involve TNF-α signaling which induced VEGF and MMP-9 expression.
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id doaj-art-29d43cf5cc3f4e739e640eb9e8464c28
institution Kabale University
issn 1687-966X
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language English
publishDate 2015-01-01
publisher Wiley
record_format Article
series Stem Cells International
spelling doaj-art-29d43cf5cc3f4e739e640eb9e8464c282025-08-20T03:54:37ZengWileyStem Cells International1687-966X1687-96782015-01-01201510.1155/2015/836390836390Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In VitroQing Gao0Maojuan Guo1Wenyun Zeng2Yijing Wang3Lin Yang4Xiaoli Pang5Huhu Li6Yanrong Suo7Xijuan Jiang8Chunquan Yu9School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, ChinaPeriodical Newsroom, Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaCessation of blood supply due to myocardial infarction (MI) leads to complicated pathological alteration in the affected regions. Cardiac stem cells (CSCs) migration plays a major role in promoting recovery of cardiac function and protecting cardiomyocytes in post-MI remodeling. Despite being the most abundant cell type in the mammalian heart, cardiac fibroblasts (CFs) were underestimated in the mechanism of CSCs migration. Our objective in this study is therefore to investigate the migration related factors secreted by hypoxia CFs in vitro and the degree that they contribute to CSCs migration. We found that supernatant from hypoxia induced CFs could accelerate CSCs migration. Four migration-related cytokines were reported upregulated both in mRNA and protein levels. Upon adding antagonists of these cytokines, the number of migration cells significantly declined. When the cocktail antagonists of all above four cytokines were added, the migration cells number reduced to the minimum level. Besides, MMP-9 had an important effect on triggering CSCs migration. As shown in our results, MMP-9 induced CSCs migration and the underlying mechanism might involve TNF-α signaling which induced VEGF and MMP-9 expression.http://dx.doi.org/10.1155/2015/836390
spellingShingle Qing Gao
Maojuan Guo
Wenyun Zeng
Yijing Wang
Lin Yang
Xiaoli Pang
Huhu Li
Yanrong Suo
Xijuan Jiang
Chunquan Yu
Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
Stem Cells International
title Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
title_full Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
title_fullStr Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
title_full_unstemmed Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
title_short Matrix Metalloproteinase 9 Secreted by Hypoxia Cardiac Fibroblasts Triggers Cardiac Stem Cell Migration In Vitro
title_sort matrix metalloproteinase 9 secreted by hypoxia cardiac fibroblasts triggers cardiac stem cell migration in vitro
url http://dx.doi.org/10.1155/2015/836390
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