ResearchInhibition of proliferation of MCF-7 breast cancer cells by a blocker of Ca2+-permeable channel
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Loratadine, an antihistaminic drug, suppresses the proliferation of endometrial stromal cells by inhibition of TRPV2
2022, European Journal of PharmacologyValdecoxib blocks rat TRPV2 channels
2022, European Journal of PharmacologyRole of transient receptor potential vanilloid subtype 2 in lower oesophageal sphincter in rat acid reflux oesophagitis
2021, Journal of Pharmacological SciencesCitation Excerpt :There are several compounds targeting TRPV2 inhibition for therapy, such as lumin, probenecid, cannabidiol, and tranilast.36 Tranilast has been reported to be a blocker of TRPV2 Ca2+-activity37–39 and pharmacological evidence suggests that it is a TRPV2 antagonist in various disease models.36,37,40 In this study, body weight loss, and increase of erosive lesions and epithelial thickness in mucosa were attenuated by treatment with tranilast.
Transient receptor potential channel regulation by growth factors
2021, Biochimica et Biophysica Acta - Molecular Cell ResearchCitation Excerpt :In this study, it was shown that IGF-1 stimulation induced Ca2+ influx and membrane currents in CHO cells overexpressing TRPV2. An earlier study by the same group already identified that in MCF-7 breast cancer cells, IGF-1 dependent Ca2+ influx and proliferation could be diminished by tranilast, a TRPV2 inhibitor [50]. These findings were confirmed in a more recent study, in which it was demonstrated that in retinal pigment epithelial cells, incubation with IGF-1 increased current density of TRPV2 [51].
TRPV2 channel inhibitors attenuate fibroblast differentiation and contraction mediated by keratinocyte-derived TGF-β1 in an in vitro wound healing model of rats
2018, Journal of Dermatological ScienceCitation Excerpt :Stretch-triggered cation channels were shown to be blocked by the TRPV2 inhibitor tranilast in retinal arterioles [39]. Furthermore, several growth factors (insulin and insulin-like growth factor-1) and serum induced the translocation of TRPV2 from an intracellular compartment to the plasma membrane, which was inhibited by tranilast [23,24]. Therefore, it is possible that the initial gel contraction and growth factors could be triggers to activate TRPV2 channels expressed on fibroblasts and keratinocytes.