TRP Channels in Angiogenesis and Other Endothelial Functions

Smani, Tarik; Gómez, L.; Regodón, S.; Woodard, Geoffrey E.; Siegfried, Géraldine; Khatib, Abdel‐Majid; Rosado, Juan A.

doi:10.3389/fphys.2018.01731

Cited by 67 publications

(82 citation statements)

References 130 publications

(148 reference statements)

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“…Furthermore, phosphatase and tensin homolog (PTEN) regulates TRPC6 activation and subsequent promotion of angiogenesis in primary human pulmonary artery endothelial cells (HPAEs) [118]. As several comprehensive reviews regarding TRP channels and angiogenesis have recently been published, we recommend the readers to turn to these for further information [119][120][121].…”

Section: Trpc Channels and Angiogenesismentioning

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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Section: Trpc Channels and Angiogenesismentioning

confidence: 99%

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

Asghar

Törnquist

2020

IJMS

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“…TRPC1 is a Ca2+-through pathway found in key metabolic organs and tissues, including hypothalamus, adipose tissue, and skeletal muscle. Deletion of TRPC1 may alter the regulation of cellular energy metabolism [36][37][38]. The TRPC1 promoter has 3 putative NF-κB binding sites.…”

Section: Discussionmentioning

confidence: 99%

The Effect and Mechanism of TRPC1, 3, and 6 on the Proliferation, Migration, and Lumen Formation of Retinal Vascular Endothelial Cells Induced by High Glucose

et al. 2020

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Objective: Transient receptor potential canonical (TRPC) channels are involved in neovascularization repairing after vascular injury in many tissues. However, whether TRPCs play a regulatory role in the development of diabetic retinopathy (DR) has rarely been reported. In the present study, we selected TRPC1, 3, and 6 to determine their roles and mechanism in human retina vascular endothelial cells (HREC) under high glucose (HG) conditions. Methods: HRECs were cultured in vitro under HG, hyper osmosis, and normal conditions. The expression of TRPC1, 3, and 6 in the cells at 24 and 48 h were detected by RT-polymerase chain reaction (PCR), Western blot and cell immunohistochemistry (IHC); In various concentrations, SKF96365 acted on HG cultured HRECs, the expression of vascular endothelial growth factor (VEGF) were detected by the same methods above; and the CCK-8, Transwell, cell scratch assay, and Matrigel assay were used to assess cell proliferation, migration, and lumen formation. Results: The RT-PCR, Western blot, and IHC results showed that TRPC1 expression was increased, and TRPC6 mRNA expression was increased under high-glucose conditions. SKF96365 acted on HG cultured HRECs that VEGF expression was significantly decreased. The CCK-8 assay, Transwell assay, cell scratch assay, and Matrigel assay showed that cell proliferation, migration, and lumen formation were downregulated by SKF96365. Conclusion: HG can induce increased expression of TRPC1 and 6 in HRECs. Inhibition of the TRPC pathway not only can decrease VEGF expression but also can prevent proliferation, migration, and lumen formation of HRECs induced by HG. Inhibition of TRPC channels is expected to become a drug target for

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“…High mRNA levels for TRPC1/4, TRPC6, TRPV2, TRPV4, TRPM4, and TRPM7 and the functional expression of TRPV2, TRPV4, TRPC6, and TRPM7 have been found in primary human endometrial stromal cells (hESC) [60]. Moreover, these channels were previously discovered to be somehow involved in several processes that regarded pathogenesis of endometriosis: TRPC1, TRPC4, and TRPV2 are involved in cell migration; TRPC4 in cell adhesion; and TRPM4, TRPM7, and TRPV2 have a crucial role in cell proliferation [47,[61][62][63]. Persoons et al [47] evaluated the expression profiles of TRP channels in endometrial biopsies from women with endometriosis taken at different times during the menstrual cycle.…”

Section: Transient Receptor Potential (Trp) Channels and Endometriosismentioning

confidence: 99%

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Riemma

Laganà

Schiattarella

et al. 2020

IJMS

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Background: Ion channels play a crucial role in many physiological processes. Several subtypes are expressed in the endometrium. Endometriosis is strictly correlated to estrogens and it is evident that expression and functionality of different ion channels are estrogen-dependent, fluctuating between the menstrual phases. However, their relationship with endometriosis is still unclear. Objective: To summarize the available literature data about the role of ion channels in the etiopathogenesis of endometriosis. Methods: A search on PubMed and Medline databases was performed from inception to November 2019. Results: Cystic fibrosis transmembrane conductance regulator (CFTR), transient receptor potentials (TRPs), aquaporins (AQPs), and chloride channel (ClC)-3 expression and activity were analyzed. CFTR expression changed during the menstrual phases and was enhanced in endometriosis samples; its overexpression promoted endometrial cell proliferation, migration, and invasion throughout nuclear factor kappa-light-chain-enhancer of activated B cells-urokinase plasminogen activator receptor (NFκB-uPAR) signaling pathway. No connection between TRPs and the pathogenesis of endometriosis was found. AQP5 activity was estrogen-increased and, through phosphatidylinositol-3-kinase and protein kinase B (PI3K/AKT), helped in vivo implantation of ectopic endometrium. In vitro, AQP9 participated in extracellular signal-regulated kinases/p38 mitogen-activated protein kinase (ERK/p38 MAPK) pathway and helped migration and invasion stimulating matrix metalloproteinase (MMP)2 and MMP9. ClC-3 was also overexpressed in ectopic endometrium and upregulated MMP9. Conclusion: Available evidence suggests a pivotal role of CFTR, AQPs, and ClC-3 in endometriosis etiopathogenesis. However, data obtained are not sufficient to establish a direct role of ion channels in the etiology of the disease. Further studies are needed to clarify this relationship.

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TRP Channels in Angiogenesis and Other Endothelial Functions

Cited by 67 publications

References 130 publications

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

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

The Effect and Mechanism of TRPC1, 3, and 6 on the Proliferation, Migration, and Lumen Formation of Retinal Vascular Endothelial Cells Induced by High Glucose

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

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