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      TRP Channels in Angiogenesis and Other Endothelial Functions

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          Abstract

          Angiogenesis is the growth of blood vessels mediated by proliferation, migration, and spatial organization of endothelial cells. This mechanism is regulated by a balance between stimulatory and inhibitory factors. Proangiogenic factors include a variety of VEGF family members, while thrombospondin and endostatin, among others, have been reported as suppressors of angiogenesis. Transient receptor potential (TRP) channels belong to a superfamily of cation-permeable channels that play a relevant role in a number of cellular functions mostly derived from their influence in intracellular Ca 2+ homeostasis. Endothelial cells express a variety of TRP channels, including members of the TRPC, TRPV, TRPP, TRPA, and TRPM families, which play a relevant role in a number of functions, including endothelium-induced vasodilation, vascular permeability as well as sensing hemodynamic and chemical changes. Furthermore, TRP channels have been reported to play an important role in angiogenesis. This review summarizes the current knowledge and limitations concerning the involvement of particular TRP channels in growth factor-induced angiogenesis.

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          TRP channels.

          Kartik Venkatachalam, Craig Montell (2007)
          The TRP (Transient Receptor Potential) superfamily of cation channels is remarkable in that it displays greater diversity in activation mechanisms and selectivities than any other group of ion channels. The domain organizations of some TRP proteins are also unusual, as they consist of linked channel and enzyme domains. A unifying theme in this group is that TRP proteins play critical roles in sensory physiology, which include contributions to vision, taste, olfaction, hearing, touch, and thermo- and osmosensation. In addition, TRP channels enable individual cells to sense changes in their local environment. Many TRP channels are activated by a variety of different stimuli and function as signal integrators. The TRP superfamily is divided into seven subfamilies: the five group 1 TRPs (TRPC, TRPV, TRPM, TRPN, and TRPA) and two group 2 subfamilies (TRPP and TRPML). TRP channels are important for human health as mutations in at least four TRP channels underlie disease.
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            Mechanisms and regulation of endothelial VEGF receptor signalling.

            Michael Simons, Emma Gordon, Lena Claesson-Welsh (2016)
            Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are uniquely required to balance the formation of new blood vessels with the maintenance and remodelling of existing ones, during development and in adult tissues. Recent advances have greatly expanded our understanding of the tight and multi-level regulation of VEGFR2 signalling, which is the primary focus of this Review. Important insights have been gained into the regulatory roles of VEGFR-interacting proteins (such as neuropilins, proteoglycans, integrins and protein tyrosine phosphatases); the dynamics of VEGFR2 endocytosis, trafficking and signalling; and the crosstalk between VEGF-induced signalling and other endothelial signalling cascades. A clear understanding of this multifaceted signalling web is key to successful therapeutic suppression or stimulation of vascular growth.
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              A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function.

              Stefan Feske, Yousang Gwack, Murali Prakriya … (2006)
              Antigen stimulation of immune cells triggers Ca2+ entry through Ca2+ release-activated Ca2+ (CRAC) channels, promoting the immune response to pathogens by activating the transcription factor NFAT. We have previously shown that cells from patients with one form of hereditary severe combined immune deficiency (SCID) syndrome are defective in store-operated Ca2+ entry and CRAC channel function. Here we identify the genetic defect in these patients, using a combination of two unbiased genome-wide approaches: a modified linkage analysis with single-nucleotide polymorphism arrays, and a Drosophila RNA interference screen designed to identify regulators of store-operated Ca2+ entry and NFAT nuclear import. Both approaches converged on a novel protein that we call Orai1, which contains four putative transmembrane segments. The SCID patients are homozygous for a single missense mutation in ORAI1, and expression of wild-type Orai1 in SCID T cells restores store-operated Ca2+ influx and the CRAC current (I(CRAC)). We propose that Orai1 is an essential component or regulator of the CRAC channel complex.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Physiol
                Journal ID (iso-abbrev): Front Physiol
                Journal ID (publisher-id): Front. Physiol.
                Title: Frontiers in Physiology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-042X
                Publication date (Electronic): 03 December 2018
                Publication date Collection: 2018
                Volume: 9
                Electronic Location Identifier: 1731
                Affiliations
                [1] 1Department of Medical Physiology and Biophysic, Institute of Biomedicine of Seville, University of Seville , Sevilla, Spain
                [2] 2CIBERCV , Madrid, Spain
                [3] 3Department of Animal Medicine, University of Extremadura , Cáceres, Spain
                [4] 4Department of Surgery, Uniformed Services University of the Health Sciences , Bethesda, MD, United States
                [5] 5INSERM U1029, University of Bordeaux , Bordeaux, France
                [6] 6Cell Physiology Research Group, Department of Physiology, University of Extremadura , Cáceres, Spain
                Author notes

                Edited by: Vijaya Iragavarapu-Charyulu, Florida Atlantic University, United States

                Reviewed by: Alexander Dietrich, Ludwig Maximilian University of Munich, Germany; Tim Murphy, University of New South Wales, Australia

                *Correspondence: Abdel-Majid Khatib majid.khatib@ 123456inserm.fr

                This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology

                †These authors have contributed equally to this work

                ‡These authors share senior authorship

                Article
                DOI: 10.3389/fphys.2018.01731
                PMC ID: 6287032
                PubMed ID: 30559679
                SO-VID: e2424eff-2389-4e51-9448-0f124970c7c1
                Copyright © Copyright © 2018 Smani, Gómez, Regodon, Woodard, Siegfried, Khatib and Rosado.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 23 June 2018
                Date accepted : 16 November 2018
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 129, Pages: 12, Words: 9896
                Funding
                Funded by: Ministerio de Economía y Competitividad, Gobierno de España 10.13039/501100010198
                Funded by: Consejería de Educación y Empleo, Junta de Extremadura 10.13039/501100008432
                Categories
                Subject: Physiology
                Subject: Review

                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: angiogenesis,endothelial cells,vegf,trp channels,trpc,trpv,trpm
                Data availability:
                ScienceOpen disciplines: Anatomy & Physiology
                Keywords: angiogenesis, endothelial cells, vegf, trp channels, trpc, trpv, trpm

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