Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats
In the previous report, Meox1 was found to promote SMCs phenotypic modulation and injury-induced vascular remodeling by regulating the FAK-ERK1/2-autophagy signaling cascade (Wu et al., 2017) [1]. Here, we presented new original data on the involvement of Mesoderm/mesenchyme homeobox gene l (Meox1)...
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Elsevier
2018-02-01
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Series: | Data in Brief |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2352340917306571 |
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Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Bing Wu Lei Zhang Yun-He Zhu You-en Zhang Fei Zheng Jian-Ye Yang Ling-Yun Guo Xing-Yuan Li Lu Wang Jun-Ming Tang Shi-You Chen Jia-Ning Wang |
spellingShingle |
Bing Wu Lei Zhang Yun-He Zhu You-en Zhang Fei Zheng Jian-Ye Yang Ling-Yun Guo Xing-Yuan Li Lu Wang Jun-Ming Tang Shi-You Chen Jia-Ning Wang Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats Data in Brief |
author_facet |
Bing Wu Lei Zhang Yun-He Zhu You-en Zhang Fei Zheng Jian-Ye Yang Ling-Yun Guo Xing-Yuan Li Lu Wang Jun-Ming Tang Shi-You Chen Jia-Ning Wang |
author_sort |
Bing Wu |
title |
Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats |
title_short |
Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats |
title_full |
Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats |
title_fullStr |
Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats |
title_full_unstemmed |
Data on the involvement of Meox1 in balloon-injury-induced neointima formation of rats |
title_sort |
data on the involvement of meox1 in balloon-injury-induced neointima formation of rats |
publisher |
Elsevier |
series |
Data in Brief |
issn |
2352-3409 |
publishDate |
2018-02-01 |
description |
In the previous report, Meox1 was found to promote SMCs phenotypic modulation and injury-induced vascular remodeling by regulating the FAK-ERK1/2-autophagy signaling cascade (Wu et al., 2017) [1]. Here, we presented new original data on the involvement of Mesoderm/mesenchyme homeobox gene l (Meox1) in balloon-injury-induced neointima formation of rat. In rat carotid artery balloon injury model to induce vascular remodeling, Meox1 was induced in vascular smooth muscle cell (SMCs) of rat carotid arteries. Most proliferating cell nuclear antigen (PCNA)-positive cells also expressed Meox1. These data suggested that Meox1 may be involved in SMCs proliferation during injury-induced neointima formation. Furthermore, knocked down its expression in injured arteries by adenoviral delivery of Meox1 short hairpin RNA (shRNA) (shMeox1), neointima formation was significantly inhibited. Elastin staining also confirmed the reduction of neointima in Meox1 shRNA-transduced arteries. Moreover, knockdown of Meox1 decreased the collagen production/deposition that was significantly increased in neointima induced by balloon injury. Keywords: Meox1, SMCs, Balloon-injury, Neointimal formation |
url |
http://www.sciencedirect.com/science/article/pii/S2352340917306571 |
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doaj-bb2e065abad8426dbbc332860e990a702020-11-25T02:07:14ZengElsevierData in Brief2352-34092018-02-0116266270Data on the involvement of Meox1 in balloon-injury-induced neointima formation of ratsBing Wu0Lei Zhang1Yun-He Zhu2You-en Zhang3Fei Zheng4Jian-Ye Yang5Ling-Yun Guo6Xing-Yuan Li7Lu Wang8Jun-Ming Tang9Shi-You Chen10Jia-Ning Wang11Institute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaDepartment of Nuclear Medicine, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, ChinaDepartment of Physiology & Pharmacology, The University of Georgia, Athens, GA 30602, USAInstitute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China; Key Lab of Human Embryonic Stem Cell of Hubei Province and Department of Physiology, Hubei University of Medicine, Hubei 442000, China; Corresponding author at: Institute of Clinical Medicine and Department of Cardiology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, People's Republic of China. Fax: +86 719/8637792.In the previous report, Meox1 was found to promote SMCs phenotypic modulation and injury-induced vascular remodeling by regulating the FAK-ERK1/2-autophagy signaling cascade (Wu et al., 2017) [1]. Here, we presented new original data on the involvement of Mesoderm/mesenchyme homeobox gene l (Meox1) in balloon-injury-induced neointima formation of rat. In rat carotid artery balloon injury model to induce vascular remodeling, Meox1 was induced in vascular smooth muscle cell (SMCs) of rat carotid arteries. Most proliferating cell nuclear antigen (PCNA)-positive cells also expressed Meox1. These data suggested that Meox1 may be involved in SMCs proliferation during injury-induced neointima formation. Furthermore, knocked down its expression in injured arteries by adenoviral delivery of Meox1 short hairpin RNA (shRNA) (shMeox1), neointima formation was significantly inhibited. Elastin staining also confirmed the reduction of neointima in Meox1 shRNA-transduced arteries. Moreover, knockdown of Meox1 decreased the collagen production/deposition that was significantly increased in neointima induced by balloon injury. Keywords: Meox1, SMCs, Balloon-injury, Neointimal formationhttp://www.sciencedirect.com/science/article/pii/S2352340917306571 |