Transient Receptor Potential Canonical Channels Are Required for in Vitro Endothelial Tube Formation

Antigny, Fabrice; Girardin, Nathalie; Frieden, Maud

doi:10.1074/jbc.m111.295733

Cited by 90 publications

(73 citation statements)

References 41 publications

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“…Moreover, TRPC3 supports both spontaneous and histamine-evoked Ca 2+ oscillations arising, respectively, during and after EC tubule formation [224] . Finally, TRPC3-mediated Ca 2+ inflow may stimulate flow-dependent endothelium-dependent vasodilation [238] .…”

Section: Moccia F Et Al Camentioning

confidence: 77%

“…First, the blend of endothelial ion channels, transporters and receptors may vary with species, age, sex, hormonal status, vascular bed, and blood vessel diameter. This issue has been further stressed by the recent finding that Stim1 and Orai1 control in vitro tubulogenesis in HUVECs [206] , but not in the HUV-derived EC line, EA.hy926 [224] . As a consequence, the information on the Ca 2+ machinery acquired on animal or cell line models cannot undergo a straightforward clinical translation, but must be confirmed in humans and in the vascular region implicated in the disease under investigation.…”

Section: Resultsmentioning

confidence: 99%

“…Similarly, AngII upregulates TRPC1 levels in an NF-κB-dependent manner in ECs [223] . Finally, TRPC1 may be involved in endothelial tube formation both in vitro [224] and in vivo [225] . The expression of TRPC1 in vascular ECs may be increased by high glucose levels, with a consequent increase in the amplitude of agonistinduced Ca 2+ influx and a dramatic impact on endothelial function in diabetic patients [209] .…”

Section: +(Wb Ihc) +(Wb Ihc) +(Wb Ihc)mentioning

confidence: 99%

“…Therefore, TRPC4 might serve as an agonistrecruited SOC during endothelial cell-cycle transitions from a proliferating to a quiescent phenotype [265] . Whether TRPC4 contributes to the repetitive Ca 2+ spikes arising in HUVECs both before (spontaneous) and after (histamine-evoked) tubule formation in a store-dependent or independent manner has yet to be elucidated [224] . A single nucleotide polymorphism in the TRPC4 gene has been associated with protection from myocardial infarction and results in a larger current density when the mis-sense channel is expressed in heterologous cell systems [266] .…”

Section: +(Rt-pcr)mentioning

confidence: 99%

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Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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Section: Moccia F Et Al Camentioning

confidence: 77%

Section: Resultsmentioning

confidence: 99%

Section: +(Wb Ihc) +(Wb Ihc) +(Wb Ihc)mentioning

confidence: 99%

Section: +(Rt-pcr)mentioning

confidence: 99%

See 2 more Smart Citations

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

View full text Add to dashboard Cite

show abstract

“…Interestingly, STIM1, as well as TRPC1 and TRPC4 knockdown, inhibits tube formation in both HUVEC and EA.hy926 cells [52].…”

Section: Transient Receptor Potential Proteins and Stim1-orai1 Complexmentioning

confidence: 96%

Functional properties of ion channels and transporters in tumour vascularization

Fiorio

Munaron

2014

Phil. Trans. R. Soc. B

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Vascularization is crucial for solid tumour growth and invasion, providing metabolic support and sustaining metastatic dissemination. It is now accepted that ion channels and transporters play a significant role in driving the cancer growth at all stages. They may represent novel therapeutic, diagnostic and prognostic targets for anti-cancer therapies. On the other hand, although the expression and role of ion channels and transporters in the vascular endothelium is well recognized and subject of recent reviews, only recently has their involvement in tumour vascularization been recognized. Here, we review the current literature on ion channels and transporters directly involved in the angiogenic process. Particular interest will be focused on tumour angiogenesis in vivo as well as in the different steps that drive this process in vitro , such as endothelial cell proliferation, migration, adhesion and tubulogenesis. Moreover, we compare the ‘transportome’ system of tumour vascular network with the physiological one.

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MicroRNA‐185 inhibits angiogenesis in human microvascular endothelial cells through targeting stromal interaction molecule 1

Hou

Liu

Zhu

et al. 2016

Cell Biology International

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Angiogenesis is a vital biological mechanism representing the adaptive response to a variety of pathological stimuli such as hypoxia. It is regulated by several pro-angiogenic and anti-angiogenic microRNAs. Studies have demonstrated an altered microRNA-185 (miR-185) expression in endothelial cells under hypoxic conditions; however, its role in angiogenesis has not been elucidated. We investigated the role of miR-185 in angiogenesis and found that miR-185 had an inhibitory effect on cell proliferation, migration, and tube formation. Stromal interaction molecule 1 (STIM1) appeared to be a direct target of miR-185 by computational prediction; this was confirmed by luciferase reporter assay. Silencing of the STIM1 gene was found to mimic miR-185-mediated inhibition of angiogenesis. STIM1 overexpression eliminated the anti-angiogenic effect of miR-185. Our study results suggest a direct interaction between miR-185 and STIM1 mRNA in microvascular endothelial cells. MicroRNA-185 acted as a negative regulator of angiogenesis in microvascular endothelial cells through downregulation of the STIM1 protein.

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Transient Receptor Potential Canonical Channels Are Required for in Vitro Endothelial Tube Formation

Cited by 90 publications

References 41 publications

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Functional properties of ion channels and transporters in tumour vascularization

MicroRNA‐185 inhibits angiogenesis in human microvascular endothelial cells through targeting stromal interaction molecule 1

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Transient Receptor Potential Canonical Channels Are Required for in Vitro Endothelial Tube Formation

Cited by 90 publications

References 41 publications

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Functional properties of ion channels and transporters in tumour vascularization

MicroRNA‐185 inhibits angiogenesis in human microvascular endothelial cells through targeting stromal interaction molecule 1

Contact Info

Product

Resources

About

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters