2018
DOI: 10.3390/ijms19040957
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Angiotensin II-Induced Mesangial Cell Damage Is Preceded by Cell Membrane Permeabilization Due to Upregulation of Non-Selective Channels

Abstract: Connexin43 (Cx43), pannexin1 (Panx1) and P2X7 receptor (P2X7R) are expressed in kidneys and are known to constitute a feedforward mechanism leading to inflammation in other tissues. However, the possible functional relationship between these membrane channels and their role in damaged renal cells remain unknown. In the present work, we found that MES-13 cells, from a cell line derived from mesangial cells, stimulated with angiotensin II (AngII) developed oxidative stress (OS, thiobarbituric acid reactive speci… Show more

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Cited by 21 publications
(54 citation statements)
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“…Their results indicated that activated RhoA/ ROCK signaling induced Cx43 degradation in GMCs cultured in high glucose depending on F-actin regulation that promoted the association between ZO-1 and Cx43, which possibly triggered Cx43 endocytosis, being these results beneficial to understanding of DN pathogenesis [56]. However, it is important to also consider that in a previous work, we demonstrated that in the glomerular cell line MES-13, AngII promotes a feedforward mechanism in which three non-selective channels (Cx HCs, pannexin1 channels and P2X7 receptors) maintain or even amplify inflammatory and oxidative responses, causing damage to kidney cells [57]. In this work, AngII-induced alterations in cell membrane permeability could lead to activation of several metabolic pathways including the RhoA/ROCK signaling pathway by the progressive increase in the amount of p-MYPT in MES-13 cells, which promote OS and generation of pro-inflammatory cytokines [57].…”
Section: Discussionmentioning
confidence: 68%
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“…Their results indicated that activated RhoA/ ROCK signaling induced Cx43 degradation in GMCs cultured in high glucose depending on F-actin regulation that promoted the association between ZO-1 and Cx43, which possibly triggered Cx43 endocytosis, being these results beneficial to understanding of DN pathogenesis [56]. However, it is important to also consider that in a previous work, we demonstrated that in the glomerular cell line MES-13, AngII promotes a feedforward mechanism in which three non-selective channels (Cx HCs, pannexin1 channels and P2X7 receptors) maintain or even amplify inflammatory and oxidative responses, causing damage to kidney cells [57]. In this work, AngII-induced alterations in cell membrane permeability could lead to activation of several metabolic pathways including the RhoA/ROCK signaling pathway by the progressive increase in the amount of p-MYPT in MES-13 cells, which promote OS and generation of pro-inflammatory cytokines [57].…”
Section: Discussionmentioning
confidence: 68%
“…A similar change occurs in GJs and Cx43 HCs in astrocytes subjected to hypoxia-reoxygenation and in the presence of a high concentration of extracellular glucose [28] and in mesangial cells exposed to high glucose and proinflammatory cytokines [29]. This opposed regulation of GJs and Cx43 HCs by pro-inflammatory factors also occur in cultures of proximal tubule cells treated with metabolic inhibitors or proinflammatory cytokines, where an increase in the activity of Cx HCs has been demonstrated [30,31].…”
Section: Introductionmentioning
confidence: 60%
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“…However, mice remained hypertensive. Collectively, these data suggest a role for CX37 and CX43 in Ang II‐induced renal damage (Gómez, Fernández, Velarde, & Sáez, ).…”
Section: Introductionmentioning
confidence: 85%