Transmembrane protein 66 attenuates neointimal hyperplasia after carotid artery injury by SOCE inactivation

Yang,Jiong; Li,Shuang; Wang,Qiang; Yang,Dachun

doi:10.3892/mmr.2019.10328

Transmembrane protein 66 attenuates neointimal hyperplasia after carotid artery injury by SOCE inactivation

Authors:
- Jiong Yang
- Shuang Li
- Qiang Wang
- Dachun Yang
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Affiliations: Department of Cardiology, The General Hospital of Western Theater Command, Chengdu, Sichuan 610083, P.R. China
Published online on: June 4, 2019 https://doi.org/10.3892/mmr.2019.10328
Pages: 1436-1442

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Abstract

Neointimal hyperplasia could be one of the most important complications after balloon angioplasty. Since calcium signaling has several physiologic effects on the regulation of the proliferation and migration of vascular smooth muscle cells (VSMCs), it was hypothesized that transmembrane protein 66 (TMEM66), a store operated calcium entry (SOCE)‑associated regulatory factor, possesses vascular protection against balloon injury. The rat balloon‑induced carotid artery injury model was performed. Histological analysis was used to check neointimal hyperplasia. TMEM66 expression was measured by PCR and immunoblotting. The results revealed that TMEM66 was expressed in the medial and neointimal layers of the injured artery, and the expression of TMEM66 was markedly decreased. TMEM66 overexpression attenuated neointimal hyperplasia via VSMC proliferation/migration inhibition, and restored expression of VSMC phenotypic markers. Moreover, TMEM66 overexpression reduced the increased expression of Stim1 and Orai1 and PDGF‑BB treatment‑enhanced [Ca2+]i. In conclusion, TMEM66 protects against balloon injury‑induced neointimal hyperplasia, and may be a pharmacological target for the treatment of restenosis.

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