scholarly journals Formaldehyde Induces Mesenteric Artery Relaxation via a Sensitive Transient Receptor Potential Ankyrin-1 (TRPA1) and Endothelium-Dependent Mechanism: Potential Role in Postprandial Hyperemia

2019 ◽  
Vol 10 ◽  
Author(s):  
L. Jin ◽  
G. Jagatheesan ◽  
L. Guo ◽  
M. Nystoriak ◽  
M. Malovichko ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
Potential Role ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor ◽  
Postprandial Hyperemia ◽  
Dependent Mechanism

scholarly journals TRPM7 Upregulate the Activity of SMAD1 through PLC Signaling Way to Promote Osteogenesis of hBMSCs

2020 ◽  
Vol 2020 ◽  
pp. 1-23
Author(s):  
Fanfan Hong ◽  
Shali Wu ◽  
Cui Zhang ◽  
Liang Li ◽  
Jianling Chen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Essential Role ◽  
Potential Role ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Kinase Domain ◽  
Osteogenic Induction ◽  
Transient Receptor

TRPM7 is a member of the transient receptor potential cation channel (TRP channel) subfamily M and possesses both an ion channel domain and a functional serine/threonine α-kinase domain. It has been proven to play an essential role in the osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs). However, the signaling pathway and molecular mechanism for TRPM7 in regulating osteogenic differentiation remain largely unknown. In this study, the potential role and mechanism of TRPM7 in the osteogenic differentiation of hBMSCs were investigated. The results showed that the expression of TRPM7 mRNA and protein increased, as did the osteogenic induction time. Upregulation or inhibition of TRPM7 could promote or inhibit the osteogenic differentiation of hBMSCs for 14 days. It was also found that the upregulation or inhibition of TRPM7 promoted or inhibited the activity of PLC and SMAD1, respectively, during osteogenic differentiation. PLC could promote osteogenic differentiation by upregulating the activity of SMAD1. However, inhibition of PLC alone could reduce the activity of SMAD1 but not inhibit completely the activation of SMAD1. Therefore, we inferred that it is an important signaling pathway for TRPM7 to upregulate the activity of SMAD1 through PLC and thereby promote the osteogenic differentiation of hBMSCs, but it is not a singular pathway. TRPM7 may also regulate the activation of SMAD1 through other ways, except for PLC, during osteogenic differentiation of hBMSCs.

scholarly journals Potential role of melastatin-related transient receptor potential cation channel subfamily M gene expression in the pathogenesis of urinary bladder cancer

2016 ◽  
Vol 12 (6) ◽  
pp. 5235-5239 ◽  
Author(s):  
Gülay Güleç Ceylan ◽  
Ebru Etem Önalan ◽  
Tuncay Kuloğlu ◽  
Gülten Aydoğ ◽  
İbrahim Keleş ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bladder Cancer ◽  
Urinary Bladder ◽  
Potential Role ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Urinary Bladder Cancer ◽  
M Gene ◽  
Transient Receptor

scholarly journals Potential role of transient receptor potential (TRP) channels in bladder cancer cells

2014 ◽  
Vol 64 (4) ◽  
pp. 305-314 ◽  
Author(s):  
Hideki Mizuno ◽  
Yoshiro Suzuki ◽  
Masaki Watanabe ◽  
Takaaki Sokabe ◽  
Tokunori Yamamoto ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Potential Role ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Bladder Cancer Cells ◽  
Transient Receptor

scholarly journals TRPC5 is required for the NO-dependent increase in dendritic Ca2+ and GABA release from chick retinal amacrine cells

2018 ◽  
Vol 119 (1) ◽  
pp. 262-273 ◽  
Author(s):  
J. Wesley Maddox ◽  
Nikka Khorsandi ◽  
Evanna Gleason
Keyword(s):  
Nitric Oxide ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Amacrine Cells ◽  
Gaba Release ◽  
Visual Signal ◽  
Inner Retina ◽  
Transient Receptor Potential Canonical ◽  
Transient Receptor ◽  
Dependent Mechanism

GABAergic signaling from amacrine cells (ACs) is a fundamental aspect of visual signal processing in the inner retina. We have previously shown that nitric oxide (NO) can elicit release of GABA independently from activation of voltage-gated Ca2+ channels in cultured retinal ACs. This voltage-independent quantal GABA release relies on a Ca2+ influx mechanism with pharmacological characteristics consistent with the involvement of the transient receptor potential canonical (TRPC) channels TRPC4 and/or TRPC5. To determine the identity of these channels, we evaluated the ability of NO to elevate dendritic Ca2+ and to stimulate GABA release from cultured ACs under conditions known to alter the function of TRPC4 and 5. We found that these effects of NO are phospholipase C dependent, have a biphasic dependence on La3+, and are unaffected by moderate concentrations of the TRPC4-selective antagonist ML204. Together, these results suggest that NO promotes GABA release by activating TRPC5 channels in AC dendrites. To confirm a role for TRPC5, we knocked down the expression of TRPC5 using CRISPR/Cas9-mediated gene knockdown and found that both the NO-dependent Ca2+ elevations and increase in GABA release are dependent on the expression of TRPC5. These results demonstrate a novel NO-dependent mechanism for regulating neurotransmitter output from retinal ACs. NEW & NOTEWORTHY Elucidating the mechanisms regulating GABAergic synaptic transmission in the inner retina is key to understanding the flexibility of retinal ganglion cell output. Here, we demonstrate that nitric oxide (NO) can activate a transient receptor potential canonical 5 (TRPC5)-mediated Ca2+ influx, which is sufficient to drive vesicular GABA release from retinal amacrine cells. This NO-dependent mechanism can bypass the need for depolarization and may have an important role in processing the visual signal by enhancing retinal amacrine cell GABAergic inhibitory output.

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