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The interaction between XBP1 and eNOS contributes to endothelial cell migration

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The interaction between XBP1 and eNOS contributes to endothelial cell migration. / Yang, Junyao; Xu, Jing; Danniel, Martin; Wang, Xiaocong; Wang, Wen; Zeng, Lingfang; Shen, Lisong.

In: Experimental Cell Research, 17.01.2018.

Research output: Contribution to journalArticle

Harvard

Yang, J, Xu, J, Danniel, M, Wang, X, Wang, W, Zeng, L & Shen, L 2018, 'The interaction between XBP1 and eNOS contributes to endothelial cell migration', Experimental Cell Research. https://doi.org/10.1016/j.yexcr.2018.01.016

APA

Yang, J., Xu, J., Danniel, M., Wang, X., Wang, W., Zeng, L., & Shen, L. (2018). The interaction between XBP1 and eNOS contributes to endothelial cell migration. Experimental Cell Research. https://doi.org/10.1016/j.yexcr.2018.01.016

Vancouver

Yang J, Xu J, Danniel M, Wang X, Wang W, Zeng L et al. The interaction between XBP1 and eNOS contributes to endothelial cell migration. Experimental Cell Research. 2018 Jan 17. https://doi.org/10.1016/j.yexcr.2018.01.016

Author

Yang, Junyao ; Xu, Jing ; Danniel, Martin ; Wang, Xiaocong ; Wang, Wen ; Zeng, Lingfang ; Shen, Lisong. / The interaction between XBP1 and eNOS contributes to endothelial cell migration. In: Experimental Cell Research. 2018.

Bibtex Download

@article{546402ef73b644e3bc0807780a0d1e06,
title = "The interaction between XBP1 and eNOS contributes to endothelial cell migration",
abstract = "The X-box binding protein 1 (XBP1) is a pivotal transcription factor in the endoplasmic reticulum stress response. Our previous studies have proven that XBP1 is involved in vascular endothelial growth factor (VEGF)-mediated endothelial cell (EC) proliferation and angiogenesis. In this study, we used EC monolayer wound healing, tube formation and transwell migration models to explorethe role of XBP1splicing in EC migration. We found that scratching on EC monolayer triggered XBP1splicing, which was attenuated by the presence of SU5416and LY294002, suggesting that VEGF signalling pathways may be involved. Over-expression of the spliced XBP1 (XBP1s) via Ad-XBP1sgene transfer increased while knockdown of IRE1αor XBP1by ShRNA lentivirus suppressed EC migration. Over-expression of XBP1s up-regulated the nitric oxide synthase 3 (NOS3)mRNA through the 3’UTR-mediated stabilization and increased eNOS protein translation. Further experiments demonstrated that miR-24 participated in the XBP1s-induced eNOSup-regulation and EC migration.Further co-IP and immunofluorescence staining assays revealed that protein kinase B (Akt), eNOS andXBP1s form a complex, resulting inAkt and eNOS nucleus relocation.These results suggest that XBP1 splicing can regulate eNOSexpression and cellular location, leading to EC migration and therefore contributing to wound healing and angiogenesis.",
keywords = "cell migration, endothelial cell, microRNA, nitric oxide synthase, X-box binding protein 1",
author = "Junyao Yang and Jing Xu and Martin Danniel and Xiaocong Wang and Wen Wang and Lingfang Zeng and Lisong Shen",
year = "2018",
month = "1",
day = "17",
doi = "10.1016/j.yexcr.2018.01.016",
language = "English",
journal = "Experimental Cell Research",
issn = "0014-4827",
publisher = "ACADEMIC PRESS INC",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - The interaction between XBP1 and eNOS contributes to endothelial cell migration

AU - Yang, Junyao

AU - Xu, Jing

AU - Danniel, Martin

AU - Wang, Xiaocong

AU - Wang, Wen

AU - Zeng, Lingfang

AU - Shen, Lisong

PY - 2018/1/17

Y1 - 2018/1/17

N2 - The X-box binding protein 1 (XBP1) is a pivotal transcription factor in the endoplasmic reticulum stress response. Our previous studies have proven that XBP1 is involved in vascular endothelial growth factor (VEGF)-mediated endothelial cell (EC) proliferation and angiogenesis. In this study, we used EC monolayer wound healing, tube formation and transwell migration models to explorethe role of XBP1splicing in EC migration. We found that scratching on EC monolayer triggered XBP1splicing, which was attenuated by the presence of SU5416and LY294002, suggesting that VEGF signalling pathways may be involved. Over-expression of the spliced XBP1 (XBP1s) via Ad-XBP1sgene transfer increased while knockdown of IRE1αor XBP1by ShRNA lentivirus suppressed EC migration. Over-expression of XBP1s up-regulated the nitric oxide synthase 3 (NOS3)mRNA through the 3’UTR-mediated stabilization and increased eNOS protein translation. Further experiments demonstrated that miR-24 participated in the XBP1s-induced eNOSup-regulation and EC migration.Further co-IP and immunofluorescence staining assays revealed that protein kinase B (Akt), eNOS andXBP1s form a complex, resulting inAkt and eNOS nucleus relocation.These results suggest that XBP1 splicing can regulate eNOSexpression and cellular location, leading to EC migration and therefore contributing to wound healing and angiogenesis.

AB - The X-box binding protein 1 (XBP1) is a pivotal transcription factor in the endoplasmic reticulum stress response. Our previous studies have proven that XBP1 is involved in vascular endothelial growth factor (VEGF)-mediated endothelial cell (EC) proliferation and angiogenesis. In this study, we used EC monolayer wound healing, tube formation and transwell migration models to explorethe role of XBP1splicing in EC migration. We found that scratching on EC monolayer triggered XBP1splicing, which was attenuated by the presence of SU5416and LY294002, suggesting that VEGF signalling pathways may be involved. Over-expression of the spliced XBP1 (XBP1s) via Ad-XBP1sgene transfer increased while knockdown of IRE1αor XBP1by ShRNA lentivirus suppressed EC migration. Over-expression of XBP1s up-regulated the nitric oxide synthase 3 (NOS3)mRNA through the 3’UTR-mediated stabilization and increased eNOS protein translation. Further experiments demonstrated that miR-24 participated in the XBP1s-induced eNOSup-regulation and EC migration.Further co-IP and immunofluorescence staining assays revealed that protein kinase B (Akt), eNOS andXBP1s form a complex, resulting inAkt and eNOS nucleus relocation.These results suggest that XBP1 splicing can regulate eNOSexpression and cellular location, leading to EC migration and therefore contributing to wound healing and angiogenesis.

KW - cell migration

KW - endothelial cell

KW - microRNA

KW - nitric oxide synthase

KW - X-box binding protein 1

U2 - 10.1016/j.yexcr.2018.01.016

DO - 10.1016/j.yexcr.2018.01.016

M3 - Article

JO - Experimental Cell Research

JF - Experimental Cell Research

SN - 0014-4827

ER -

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