2022
DOI: 10.1016/j.jphs.2022.01.003
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Involvement of TREK1 channels in the proliferation of human hepatic stellate LX-2 cells

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Cited by 5 publications
(3 citation statements)
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“…In IPAH-PASMCs, increases in proliferation were reduced by a treatment with 300 μM quinine, a KCNK channel blocker ( 10 , 28 , 29 ), for 48 h (A 450 = 0.552 ± 0.032, n = 5, p = 0.008 vs. control, 1.057 ± 0.032, n = 5) ( Figure 4B ). A similar reduction was observed with 100 μM TPA, another KCNK channel blocker that is structurally different from quinine ( 29 32 ), for 48 h (0.703 ± 0.039, n = 5, p = 0.008 vs. control, 1.030 ± 0.013, n = 5) ( Figure 4C ). This result suggests that up-regulated KCNK channel function involved in the enhanced proliferation of IPAH-PASMCs.…”
Section: Resultssupporting
confidence: 75%
See 1 more Smart Citation
“…In IPAH-PASMCs, increases in proliferation were reduced by a treatment with 300 μM quinine, a KCNK channel blocker ( 10 , 28 , 29 ), for 48 h (A 450 = 0.552 ± 0.032, n = 5, p = 0.008 vs. control, 1.057 ± 0.032, n = 5) ( Figure 4B ). A similar reduction was observed with 100 μM TPA, another KCNK channel blocker that is structurally different from quinine ( 29 32 ), for 48 h (0.703 ± 0.039, n = 5, p = 0.008 vs. control, 1.030 ± 0.013, n = 5) ( Figure 4C ). This result suggests that up-regulated KCNK channel function involved in the enhanced proliferation of IPAH-PASMCs.…”
Section: Resultssupporting
confidence: 75%
“…In the present investigation, the KCNK channel blockers, quinine and TPA, blocked the proliferation and migration of IPAH-PASMCs. Previous studies reported that quinine blocked the KCNK1 and KCNK2 (also KCNK5, 6, 9, 16, and 18) channels ( 10 , 28 , 29 ), while TPA blocked the KCNK1 and KCNK2 (also KCNK4, 9, 10, 17, and 18) channels ( 29 32 ). These blockers were slightly less selective, but still inhibited the activities of KCNK1 and KCNK2 channels.…”
Section: Discussionmentioning
confidence: 97%
“…In addition, the inhibition of KCa3.1 has been shown to lead to cell apoptosis and increase the level of DNA damage, and also to stimulate the proliferation of hepatic stellate cells and aggravate liver fibrosis, which demonstrates that KCa3.1 channels exert a protective role in liver injury (33). The activity of two-pore domain K + (KCNK2) channels determines resting membrane potential and Ca 2+ levels, thereby fulfilling a role in extracellular matrix production and the cell proliferation of hepatic stellate cells, providing a potential therapeutic target for hepatic fibrosis (34).…”
Section: Role Of K + Channels In Regulating Metabolism Proliferation ...mentioning
confidence: 99%