TMCO1 is essential for ovarian follicle development by regulating ER Ca2+ store of granulosa cells

Sun, Zhiqiang; Zhang, Hui; Wang, Xi; Wang, Qiaochu; Zhang, Chuanchao; Wang, Jiuqiang; Wang, Yihan; An, Chaoqiang; Yang, Keyan; Wang, Yun; Gao, Fei; Guo, Caixia; Tang, Tie-Shan

doi:10.1038/s41418-018-0067-x

Cited by 64 publications

(40 citation statements)

References 45 publications

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“…The results demonstrated that TMCO1 had a relationship with A549 cells viability and migration. TMCO1, as a regulator of cellular calcium ions, was shown to affect numerous growth factors, which was in accordance with previous reports demonstrating that calcium ions participate in the regulation of numerous biological functions through complex networks (31,32). In the present study, immunostaining was performed to observe changes in the expression levels of associated proteins, which suggested that TMCO1 participated in A549 cell biological processes.…”

Section: Discussionsupporting

confidence: 91%

Mechanism of transmembrane and coiled‑coil domain 1 in the regulation of proliferation and migration of A549 cells

et al. 2020

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Bioinformatics analyses have shown that transmembrane and coiled-coil domain 1 (TMCO1) may be associated with lung adenocarcinoma. However, to the best of our knowledge, no current research has determined whether TMCO1 is involved in the development of lung adenocarcinoma. The present study aimed to identify the association between TMCO1 and lung adenocarcinoma. The present study demonstrated that the positive immunohistochemical staining of TMCO1 in lung adenocarcinoma tissues was significantly higher compared with paracarcinoma tissues. Additionally, knockdown of TMCO1 was demonstrated to downregulate B-cell lymphoma-2 protein expression levels and upregulate cysteinyl aspartate specific proteinase (caspase)-3 and caspase-9 protein expression levels in A549 cells. These changes resulted in decreased apoptosis of A549 cells uponTMCO1 downregulation. In addition, knockdown of TMCO1 decreased matrix metalloproteinase (MMP)-2 and MMP-9 expression levels. The expression of N-cadherin and vimentin also decreased. By contrast, the expression levels of E-cadherin protein increased. Knockdown of TMCO1 resulted in the inhibition of A549 cell migration. The results of the present study demonstrated that TMCO1 was associated with lung adenocarcinoma and that inhibition of TMCO1 expression levels negatively regulated the apoptosis and migration of lung adenocarcinoma cells. Therefore, the present study suggests the potential for TMCO1 to be used in the clinical treatment of lung adenocarcinoma.

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Section: Discussionsupporting

confidence: 91%

Mechanism of transmembrane and coiled‑coil domain 1 in the regulation of proliferation and migration of A549 cells

et al. 2020

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“…The results suggested that ER stress signaling pathway was involved in autoimmune‐induced POF mice. Studies have shown that the normal physiological function of GCs is dependent on the homeostatic maintenance of ER Ca 2+ store (Sun et al, ). Therefore, in the present study, the GCs apoptosis of POF mice may be triggered by the ER stress response.…”

Section: Discussionmentioning

confidence: 99%

“…As reported, pathogenesis of many autoimmune diseases is related to cell apoptosis caused by unfolded/misfolded proteins accumulation, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease (Hetz et al, 2013). Studies have confirmed that maintaining ER Ca 2+ homeostasis of GCs is important for ovarian follicle development (Sun et al, 2018). In addition, previous studies have shown that transplantation of hPMSCs improved the ovarian function of POF mice and reduced the expression of caspase-3 activation (Yin et al, 2018a).…”

Section: Introductionmentioning

confidence: 86%

Human placenta‐derived mesenchymal stem cells inhibit apoptosis of granulosa cells induced by IRE1α pathway in autoimmune POF mice

Zhao

Wang

et al. 2019

Cell Biology International

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Previous studies have shown that the ovarian failure in autoimmune‐induced premature ovarian failure (POF) mice could be improved by the transplantation of human placenta‐derived mesenchymal stem cells (hPMSCs); however, the protective mechanism of hPMSCs transplantation on ovarian dysfunction remains unclear. Ovarian dysfunction is closely related to the apoptosis of granulosa cells (GCs). To determine the effects of hPMSCs transplantation on GCs apoptosis, an autoimmune POF mice model was established with zona pellucida glycoprotein 3 (ZP3) peptide. It is reported that the inositol‐requiring enzyme 1α (IRE1α) and its downstream molecules play a central role in the endoplasmic reticulum (ER) stress‐induced apoptosis pathway. So the aim of this study is to investigate whether hPMSCs transplantation attenuated GCs apoptosis via inhibiting ER stress IRE1α signaling pathway. The ovarian dysfunction, follicular dysplasia, and GCs apoptosis were observed in the POF mice. And the IRE1α pathway was activated in ovaries of POF mice, as demonstrated by, increased X‐box binding protein 1 (XBP1), up‐regulated 78 kDa glucose‐regulated protein (GRP78) and caspase‐12. Following transplantation of hPMSCs, the ovarian structure and function were significantly improved in POF mice. In addition, the GCs apoptosis was obviously attenuated and IRE1α pathway was significantly inhibited. Transplantation of hPMSCs suppressed GCs apoptosis‐induced by ER stress IRE1α signaling pathway in POF mice, which might contribute to the hPMSCs transplantation‐mediating ovarian function recovery.

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“…The physiological function of TMCO1 is not fully elucidated, whereas it has been reported that it plays a key role in the maintenance of calcium ion homeostasis within the ER [248,249]. Furthermore, it has been suggested that TMCO1 may constitute an important protein in tumor suppression as well as play a crucial role in cell cycle regulation within the ocular tissues [250,251].…”

Section: Tmco1mentioning

confidence: 99%

The Genetic and Endoplasmic Reticulum-Mediated Molecular Mechanisms of Primary Open-Angle Glaucoma

Rozpędek‐Kamińska

Wojtczak

Szaflik

et al. 2020

IJMS

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Glaucoma is a heterogenous, chronic, progressive group of eye diseases, which results in irreversible loss of vision. There are several types of glaucoma, whereas the primary open-angle glaucoma (POAG) constitutes the most common type of glaucoma, accounting for three-quarters of all glaucoma cases. The pathological mechanisms leading to POAG pathogenesis are multifactorial and still poorly understood, but it is commonly known that significantly elevated intraocular pressure (IOP) plays a crucial role in POAG pathogenesis. Besides, genetic predisposition and aggregation of abrogated proteins within the endoplasmic reticulum (ER) lumen and subsequent activation of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)-dependent unfolded protein response (UPR) signaling pathway may also constitute important factors for POAG pathogenesis at the molecular level. Glaucoma is commonly known as a ‘silent thief of sight’, as it remains asymptomatic until later stages, and thus its diagnosis is frequently delayed. Thereby, detailed knowledge about the glaucoma pathophysiology is necessary to develop both biochemical and genetic tests to improve its early diagnosis as well as develop a novel, ground-breaking treatment strategy, as currently used medical therapies against glaucoma are limited and may evoke numerous adverse side-effects in patients.

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TMCO1 is essential for ovarian follicle development by regulating ER Ca2+ store of granulosa cells

Cited by 64 publications

References 45 publications

Mechanism of transmembrane and coiled‑coil domain 1 in the regulation of proliferation and migration of A549 cells

Mechanism of transmembrane and coiled‑coil domain 1 in the regulation of proliferation and migration of A549 cells

Human placenta‐derived mesenchymal stem cells inhibit apoptosis of granulosa cells induced by IRE1α pathway in autoimmune POF mice

The Genetic and Endoplasmic Reticulum-Mediated Molecular Mechanisms of Primary Open-Angle Glaucoma

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