The activity of IKCa and BKCa channels contributes to insulin-mediated NO synthesis and vascular tone regulation in human umbilical vein

Rojas, Susana; Basualto, Emerita; Valdivia, Luz; Vallejos, Natalia; Ceballos, Karen; Peña, Emilio Duro; Rivas, Coralia I.; Nualart, Francisco; Guzmán-Gutiérrez, Enrique; Escudero, Carlos; Toledo, Fernando; Sobrevía, Luis; Cid, Marcela; González, Marcelo

doi:10.1016/j.niox.2020.03.004

Cited by 5 publications

(4 citation statements)

References 41 publications

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“…It modulates vasomotor and nerve excitability by regulating membrane potential and calcium signaling. [87][88][89] However, experiments performed by Cheng Du et al demonstrated that both BKCa mRNA and protein levels in PCa cells were increased compared with normal cells. BKCa overexpression strengthens the invasive ability of cancer cell.…”

Section: Ion Channel Proteins Take Part In Pca Migration Mediated By mentioning

confidence: 99%

<p>Role of αVβ3 in Prostate Cancer: Metastasis Initiator and Important Therapeutic Target</p>

Tang¹,

Xu²,

Zhang³

et al. 2020

OTT

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In prostate cancer, distant organ metastasis is the leading cause of patient death. Although the mechanism of malignant tumor metastasis is unclear, studies have confirmed that integrin αVβ3 plays an important role in this process. In prostate cancer, αVβ3 mediates adhesion, invasion, immune escape and neovascularization through interactions with different ligands. Among these ligands and in addition to proteins that are directly related to tumor invasion, other proteins that contain the RGD structure could also bind to αVβ3 and cause a number of biological effects. In this article, we summarized the ligand and downstream proteins related to αVβ3-mediated prostate cancer metastasis as well as some diagnostic and therapeutic measures targeting αVβ3.

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Section: Ion Channel Proteins Take Part In Pca Migration Mediated By mentioning

confidence: 99%

<p>Role of αVβ3 in Prostate Cancer: Metastasis Initiator and Important Therapeutic Target</p>

Tang¹,

Xu²,

Zhang³

et al. 2020

OTT

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“…In fact, insulin (10 nM) can directly activate native and recombinant BKCa currents in cell-attached patch-clamping experiments with a rapid effect that is MAPK-dependent when the hormone was added in the pipette [70]. There is evidence that insulin may induce endothelial cell hyperpolarization by modulating K channels activity [38,71]. The insulin-induced relaxation in human placental veins (~368 μm diameter), pre-constricted with U46619, is a mechanism dependent on the BKCa channel activity.…”

Section: Role Of Potassium Channels In Endothelial Functionmentioning

confidence: 99%

“…The effects of insulin on BKCa activity are associated with evidences that show that the constriction induced by U46619 and H 2 O 2 in placental vasculature is partially decreased with 10 nM insulin preincubation (10 min) in a mechanism totally dependent of BKCa activity [72]. Recently, it has been determined that insulin-mediated NO synthesis requires the participation of both IKCa/ BKCa channels and eNOS activity in HUVECs [71]. In the same cell type, insulin increased the open probability (NPo) of BKCa, associated with hyperpolarization in single cell analysis [69].…”

Section: Role Of Potassium Channels In Endothelial Functionmentioning

confidence: 99%

“…In human placental arteries, the relaxation induced by the NO donor, SNAP, is partially blocked by charybdotoxin (BKCa inhibitor) and almost totally blocked by charybdotoxin and ODQ (sGC inhibitor) [73]. Therefore, an extracellular stimulus that increases the NO availability activates a mechanism that involves sGC and BKCa activities [71]. These findings constitute evidence for postulating a new mechanism induced by insulin in human vasculature related with the physiological regulation of KCa activity for NO synthesis (Figure 4).…”

Section: Role Of Potassium Channels In Endothelial Functionmentioning

confidence: 99%

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L-Arginine/Nitric Oxide Pathway and KCa Channels in Endothelial Cells: A Mini-Review

González¹,

Rivas²

2020

Vascular Biology - Selection of Mechanisms and Clinical Applications

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The endothelium is an organ with a key role in the maintenance of cardiovascular health through the regulation of vascular tone, vascular resistance, blood flow, and arterial pressure. These functions are related with the synthesis and release of vasoactive molecules, mainly vasodilators like nitric oxide (NO) and endotheliumderived hyperpolarizing factor (EDHF). Both factors are released and diffused from endothelial cells to the smooth muscle cells, where there is a subsequent activation of signaling pathways that finally decrease the intracellular calcium to induce the vascular relaxation. The study of the molecular mechanisms that underlie the endothelial function still is in development, but from the evidence obtained from the endothelial cells in vitro studies are possible to partially describe the pathways to regulate the physiological endothelial function and the disturbances in pathological conditions. In this mini-review, we describe the main mechanisms for NO synthesis and the role of potassium channels related with EDHF. We include schemes and graphical summaries for better understanding of the molecular regulation of vascular tone in the human cardiovascular system.

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Physiological and Pathophysiological Role of Large-Conductance Calcium-Activated Potassium Channels (BKCa) in HUVECs and Placenta

Neira

Torres

et al. 2023

Advances in Experimental Medicine and Biology

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The activity of IKCa and BKCa channels contributes to insulin-mediated NO synthesis and vascular tone regulation in human umbilical vein

Cited by 5 publications

References 41 publications

<p>Role of αVβ3 in Prostate Cancer: Metastasis Initiator and Important Therapeutic Target</p>

<p>Role of αVβ3 in Prostate Cancer: Metastasis Initiator and Important Therapeutic Target</p>

L-Arginine/Nitric Oxide Pathway and KCa Channels in Endothelial Cells: A Mini-Review

Physiological and Pathophysiological Role of Large-Conductance Calcium-Activated Potassium Channels (BKCa) in HUVECs and Placenta

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