Trpc1

Nesin, Vasyl; Tsiokas, Leonidas

doi:10.1007/978-3-642-54215-2_2

Cited by 41 publications

(30 citation statements)

References 196 publications

(288 reference statements)

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“…It has been proposed that a number of TRP isoforms exhibit mechanosensitivity (TRPA1; TRPV1, 2, 4; TRPc1, 5, 6; TRPM3, 7; TRPP2) (31,32). Among these, TRPC1 was the first cloned TRP channel (33) and exhibited high mechanosensitivity in vertebrates (22). It is widely present in the heart, arteries, skeletal muscle and was reported to be plentifully expressed in airway epithelial cells and show a significant increase in patients with cOPd (18).…”

Section: Discussionmentioning

confidence: 99%

Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells

Wang

et al. 2020

Int J Mol Med

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Airway remodeling is a central event in the pathology of chronic obstructive pulmonary disease (cOPd) that leads to airway narrowing and subsequently, to increased mechanical pressure. High mechanical pressure can exacerbate airway remodeling. Thus, a treatment regimen aimed at disrupting this high-pressure airway remodeling vicious cycle may improve the prognosis of patients with cOPd. Recent studies have demonstrated that mechanical stress induces lung epithelial-mesenchymal transition (EMT), which is commonly present in airway epithelial cells of patients with cOPd. As TRPc1 functions as a mechanosensitive channel that mediates non-selective cation entry in response to increased membrane stretch, the present study investigated the role of TRPc1 in the occurrence of EMT induced by mechanical stress. In the present study, the expression of TRPc1 in the bronchial epithelium was examined in vivo by immunohistochemistry. In vitro, human bronchial epithelial (16HBE) cells were subjected to mechanical stretching for up to 48 h, and TRPc1 expression was then examined by RT-qPcR and western blot analysis. In addition, TRPc1 receptor function was assessed by ca 2+ imaging and siRNA transfection. EMT was identified using immunofluorescence, western blot analysis and RT-qPcR. It was found that TRPc1 expression was upregulated in patients with cOPd and in 16HBE cells subjected to mechanical stretch. The mechanical stress-induced activation of TRPc1 in 16HBE cells increased the intracellular calcium concentration and subsequently decreased the expression of cytokeratin 8 and E-cadherin, and increased the expression of α-smooth muscle actin, indicating the occurrence of EMT. On the whole, the findings of the present study demonstrate that TRPc1 plays a key role in the occurrence of EMT in human lung epithelial cells in response to mechanical stretch; thus, this protein may serve as a novel therapeutic target for progressive airway remodeling in cOPd.

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Section: Discussionmentioning

confidence: 99%

Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells

Wang

et al. 2020

Int J Mol Med

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“…TRPC1 has been established as a potent molecular component of SOCE in several distinct cell types [19,[45][46][47]. In addition, TRPC1 has been shown to function as a ROCE channel in several cell lines [48,49]. TRPC1 can make complexes with all other TRPC channels.…”

Section: Trpc1mentioning

confidence: 99%

“…Several TRPC channels are involved in regulating migration and invasion, and all are involved in enhancing proliferation of cancer cells [84][85][86]. TRPC1 channels are essential for the polarity and direction of migrating cells both in vitro and in vivo [49,51,52]. The directionality of migrating cells, as shown using renal transformed epithelial cells, was dependent on TRPC1 [87].…”

Section: Trpc Channels Migration and Invasionmentioning

confidence: 99%

Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion

Asghar

Törnquist

2020

IJMS

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Calcium (Ca2+) is perhaps the most versatile signaling molecule in cells. Ca2+ regulates a large number of key events in cells, ranging from gene transcription, motility, and contraction, to energy production and channel gating. To accomplish all these different functions, a multitude of channels, pumps, and transporters are necessary. A group of channels participating in these processes is the transient receptor potential (TRP) family of cation channels. These channels are divided into 29 subfamilies, and are differentially expressed in man, rodents, worms, and flies. One of these subfamilies is the transient receptor potential canonical (TRPC) family of channels. This ion channel family comprises of seven isoforms, labeled TRPC1–7. In man, six functional forms are expressed (TRPC1, TRPC3–7), whereas TRPC2 is a pseudogene; thus, not functionally expressed. In this review, we will describe the importance of the TRPC channels and their interacting molecular partners in the etiology of cancer, particularly in regard to regulating migration and invasion.

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“…The observed increase in nitric oxide production testifies to the protective role of TRPV4 [66]. Ca 2+ influx caused by TRPC1 activation regulates and stimulates cell proliferation, differentiation, secretion and migration, as well as modulates the expression of chemokines and cytokines, such as interleukin-13 (IL-13), matrix metalloproteinases-9 [29,30].…”

Section: Acidity Membrane Potential and Intracellular Calcium Ion Comentioning

confidence: 88%

“…TRPC channels are expressed in various tissues, but TRPC4 and TRPC5 are predominantly localized in the nervous system. TRPC1 channel activation is involved in the development of inflammation and airway remodeling [29,30]. In addition, bronchoconstriction and cough, which are characteristic of an asthmatic reaction, is mechanical stress to the airway that induces TRPC1 activation and promotes airway remodeling [31].…”

Section: Trpcmentioning

confidence: 99%

Dysfunction of transient receptor potential ion channels as an important pathophysiological mechanism in asthma

et al. 2020

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Asthma is a chronic heterogeneous disease characterized by chronic inflammation and bronchial hyperreactivity. Neurogenic inflammation is one of the important causes of hyperreactivity. Dysfunction of transient receptor potential (TRP) ion channels underlies the development of neurogenic inflammation, bronchial hyperreactivity and respiratory symptoms of asthma such as bronchospasm and cough. TRP channels are expressed in the respiratory tract. Their activation is mediated by endogenous and exogenous factors involved in the pathogenesis of asthma. The study of functioning and regulation of TRP channels is relevant, as they could be important therapeutic targets for asthma. The aim of the review is to summarize modern ideas about the mechanisms of functioning and regulation of members of the TRP channel superfamily, the role of which in lung pathology and physiology are the best studied.

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Trpc1

Cited by 41 publications

References 196 publications

Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells

Transient receptor potential canonical 1 channel mediates the mechanical stress‑induced epithelial‑mesenchymal transition of human bronchial epithelial (16HBE) cells

Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion

Dysfunction of transient receptor potential ion channels as an important pathophysiological mechanism in asthma

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