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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Main Authors: 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
Format: Article
Language:English
Published: Elsevier 2018-02-01
Series:Data in Brief
Online Access:http://www.sciencedirect.com/science/article/pii/S2352340917306571
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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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spelling 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