King's College London

Research portal

The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia

Research output: Contribution to journalArticle

Standard

The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia. / Stiber, Jonathan A; Wu, Jiao-Hui; Zhang, Lisheng; Nepliouev, Igor; Zhang, Zhu-Shan; Bryson, Victoria G; Brian, Leigh; Bentley, Rex C; Gordon-Weeks, Phillip R; Rosenberg, Paul B; Freedman, Neil J.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, 24.03.2016.

Research output: Contribution to journalArticle

Harvard

Stiber, JA, Wu, J-H, Zhang, L, Nepliouev, I, Zhang, Z-S, Bryson, VG, Brian, L, Bentley, RC, Gordon-Weeks, PR, Rosenberg, PB & Freedman, NJ 2016, 'The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia', Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/ATVBAHA.115.306140

APA

Stiber, J. A., Wu, J-H., Zhang, L., Nepliouev, I., Zhang, Z-S., Bryson, V. G., Brian, L., Bentley, R. C., Gordon-Weeks, P. R., Rosenberg, P. B., & Freedman, N. J. (2016). The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/ATVBAHA.115.306140

Vancouver

Stiber JA, Wu J-H, Zhang L, Nepliouev I, Zhang Z-S, Bryson VG et al. The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia. Arteriosclerosis, Thrombosis, and Vascular Biology. 2016 Mar 24. https://doi.org/10.1161/ATVBAHA.115.306140

Author

Stiber, Jonathan A ; Wu, Jiao-Hui ; Zhang, Lisheng ; Nepliouev, Igor ; Zhang, Zhu-Shan ; Bryson, Victoria G ; Brian, Leigh ; Bentley, Rex C ; Gordon-Weeks, Phillip R ; Rosenberg, Paul B ; Freedman, Neil J. / The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2016.

Bibtex Download

@article{25bb7baeb2ca4928b39bc97946f5baa6,
title = "The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia",
abstract = "OBJECTIVE: Vascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper function of multiple TRP channels requires the scaffolding protein Homer 1, which associates with the actin-binding protein Drebrin. We found that SMC Drebrin expression is upregulated in atherosclerosis and in response to injury and investigated whether Drebrin inhibits SMC activation, either through regulation of TRP channel function via Homer or through a direct effect on the actin cytoskeleton.APPROACH AND RESULTS: Wild-type (WT) and congenic Dbn(-/+) mice were subjected to wire-mediated carotid endothelial denudation. Subsequent neointimal hyperplasia was 2.4±0.3-fold greater in Dbn(-/+) than in WT mice. Levels of globular actin were equivalent in Dbn(-/+) and WT SMCs, but there was a 2.4±0.5-fold decrease in filamentous actin in Dbn(-/+) SMCs compared with WT. Filamentous actin was restored to WT levels in Dbn(-/+) SMCs by adenoviral-mediated rescue expression of Drebrin. Compared with WT SMCs, Dbn(-/+) SMCs exhibited increased TRP channel activity in response to platelet-derived growth factor, increased migration assessed in Boyden chambers, and increased proliferation. Enhanced TRP channel activity and migration in Dbn(-/+) SMCs were normalized to WT levels by rescue expression of not only WT Drebrin but also a mutant Drebrin isoform that binds actin but fails to bind Homer.CONCLUSIONS: Drebrin reduces SMC activation through its interaction with the actin cytoskeleton but independently of its interaction with Homer scaffolds.",
author = "Stiber, {Jonathan A} and Jiao-Hui Wu and Lisheng Zhang and Igor Nepliouev and Zhu-Shan Zhang and Bryson, {Victoria G} and Leigh Brian and Bentley, {Rex C} and Gordon-Weeks, {Phillip R} and Rosenberg, {Paul B} and Freedman, {Neil J}",
note = "{\textcopyright} 2016 American Heart Association, Inc.",
year = "2016",
month = mar,
day = "24",
doi = "10.1161/ATVBAHA.115.306140",
language = "English",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - The Actin-Binding Protein Drebrin Inhibits Neointimal Hyperplasia

AU - Stiber, Jonathan A

AU - Wu, Jiao-Hui

AU - Zhang, Lisheng

AU - Nepliouev, Igor

AU - Zhang, Zhu-Shan

AU - Bryson, Victoria G

AU - Brian, Leigh

AU - Bentley, Rex C

AU - Gordon-Weeks, Phillip R

AU - Rosenberg, Paul B

AU - Freedman, Neil J

N1 - © 2016 American Heart Association, Inc.

PY - 2016/3/24

Y1 - 2016/3/24

N2 - OBJECTIVE: Vascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper function of multiple TRP channels requires the scaffolding protein Homer 1, which associates with the actin-binding protein Drebrin. We found that SMC Drebrin expression is upregulated in atherosclerosis and in response to injury and investigated whether Drebrin inhibits SMC activation, either through regulation of TRP channel function via Homer or through a direct effect on the actin cytoskeleton.APPROACH AND RESULTS: Wild-type (WT) and congenic Dbn(-/+) mice were subjected to wire-mediated carotid endothelial denudation. Subsequent neointimal hyperplasia was 2.4±0.3-fold greater in Dbn(-/+) than in WT mice. Levels of globular actin were equivalent in Dbn(-/+) and WT SMCs, but there was a 2.4±0.5-fold decrease in filamentous actin in Dbn(-/+) SMCs compared with WT. Filamentous actin was restored to WT levels in Dbn(-/+) SMCs by adenoviral-mediated rescue expression of Drebrin. Compared with WT SMCs, Dbn(-/+) SMCs exhibited increased TRP channel activity in response to platelet-derived growth factor, increased migration assessed in Boyden chambers, and increased proliferation. Enhanced TRP channel activity and migration in Dbn(-/+) SMCs were normalized to WT levels by rescue expression of not only WT Drebrin but also a mutant Drebrin isoform that binds actin but fails to bind Homer.CONCLUSIONS: Drebrin reduces SMC activation through its interaction with the actin cytoskeleton but independently of its interaction with Homer scaffolds.

AB - OBJECTIVE: Vascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper function of multiple TRP channels requires the scaffolding protein Homer 1, which associates with the actin-binding protein Drebrin. We found that SMC Drebrin expression is upregulated in atherosclerosis and in response to injury and investigated whether Drebrin inhibits SMC activation, either through regulation of TRP channel function via Homer or through a direct effect on the actin cytoskeleton.APPROACH AND RESULTS: Wild-type (WT) and congenic Dbn(-/+) mice were subjected to wire-mediated carotid endothelial denudation. Subsequent neointimal hyperplasia was 2.4±0.3-fold greater in Dbn(-/+) than in WT mice. Levels of globular actin were equivalent in Dbn(-/+) and WT SMCs, but there was a 2.4±0.5-fold decrease in filamentous actin in Dbn(-/+) SMCs compared with WT. Filamentous actin was restored to WT levels in Dbn(-/+) SMCs by adenoviral-mediated rescue expression of Drebrin. Compared with WT SMCs, Dbn(-/+) SMCs exhibited increased TRP channel activity in response to platelet-derived growth factor, increased migration assessed in Boyden chambers, and increased proliferation. Enhanced TRP channel activity and migration in Dbn(-/+) SMCs were normalized to WT levels by rescue expression of not only WT Drebrin but also a mutant Drebrin isoform that binds actin but fails to bind Homer.CONCLUSIONS: Drebrin reduces SMC activation through its interaction with the actin cytoskeleton but independently of its interaction with Homer scaffolds.

U2 - 10.1161/ATVBAHA.115.306140

DO - 10.1161/ATVBAHA.115.306140

M3 - Article

C2 - 27013612

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

ER -

View graph of relations

© 2018 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454