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Smith AH, Putta P, Driscoll EC, et al. Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury. JVS Vasc Sci. 2020;1:136-150doi: 10.1016/j.jvssci.2020.07.002.
Smith, A. H., Putta, P., Driscoll, E. C., Chaudhuri, P., Birnbaumer, L., Rosenbaum, M. A., & Graham, L. M. (2020). Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury. JVS-vascular science, 1136-150. https://doi.org/10.1016/j.jvssci.2020.07.002
Smith, Andrew H, et al. "Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury." JVS-vascular science vol. 1 (2020): 136-150. doi: https://doi.org/10.1016/j.jvssci.2020.07.002
Smith AH, Putta P, Driscoll EC, Chaudhuri P, Birnbaumer L, Rosenbaum MA, Graham LM. Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury. JVS Vasc Sci. 2020;1:136-150. doi: 10.1016/j.jvssci.2020.07.002. Epub 2020 Jul 28. PMID: 33554153; PMCID: PMC7861475.
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JVS Vasc Sci. 2020;1:136-150. doi: 10.1016/j.jvssci.2020.07.002. Epub 2020 Jul 28.

Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury.

JVS-vascular science

Andrew H Smith, Priya Putta, Erin C Driscoll, Pinaki Chaudhuri, Lutz Birnbaumer, Michael A Rosenbaum, Linda M Graham

Affiliations

  1. Department of Vascular Surgery, Cleveland Clinic, Cleveland.
  2. Department of Biomedical Engineering, Cleveland Clinic, Cleveland.
  3. Neurobiology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park.
  4. Institute of Biomedical Research (BIOMED), Catholic University of Argentina, Buenos Aires.
  5. Surgical Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland.

PMID: 33554153 PMCID: PMC7861475 DOI: 10.1016/j.jvssci.2020.07.002

Abstract

OBJECTIVE: Previous studies showed the benefit of canonical transient receptor potential 6 (TRPC6) channel deficiency in promoting endothelial healing of arterial injuries in hypercholesterolemic animals. Long-term studies utilizing a carotid wire-injury model were undertaken in wild-type (WT) and TRPC6

METHODS: The common carotid arteries (CCA) of WT and TRPC6

CONCLUSIONS: These results suggest that TRPC6 contributes to the restoration or maintenance of arterial SMC contractile phenotype following injury. Understanding the role of TRPC6 in phenotypic modulation may lead to mechanism-based therapies for attenuation of IH.

Keywords: Carotid injury; Intimal hyperplasia; Phenotypic modulation; Smooth muscle cells; TRPC6

Conflict of interest statement

Author conflict of interest: none. The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS-Vascular Science policy that requires reviewers to decline

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