ArticleInternational journal of molecular sciences2018
Angiotensin II-Induced Mesangial Cell Damaged Is Preceded by Cell Membrane Permeabilization Due to Upregulation of Non-Selective Channels.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Connexin 43 and Pannexin 1 in Renal Cell Populations in Diabetic Kidney Disease.International journal of molecular sciences · 2026Article
- Pannexin channels in the kidney.American journal of physiology. Renal physiology · 2025Review
- Pharmacology of boldine: summary of the field and update on recent advances.Frontiers in pharmacology · 2024Review
- Activation of Pannexin-1 channels causes cell dysfunction and damage in mesangial cells derived from angiotensin II-exposed mice.Frontiers in cell and developmental biology · 2024Article
- Interaction of Angiotensin II AT1 Receptors with Purinergic P2X Receptors in Regulating Renal Afferent Arterioles in Angiotensin II-Dependent Hypertension.International journal of molecular sciences · 2023Review
- Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons.International journal of molecular sciences · 2022Review
- TNF-α Plus IL-1β Induces Opposite Regulation of Cx43 Hemichannels and Gap Junctions in Mesangial Cells through a RhoA/ROCK-Dependent Pathway.International journal of molecular sciences · 2022Article
- Possible role of pannexin 1 channels and purinergic receptors in the pathogenesis and mechanism of action of SARS-CoV-2 and therapeutic potential of targeting them in COVID-19.Life sciences · 2022Review
- Angiotensin II biphasically regulates cell differentiation in human iPSC-derived kidney organoids.American journal of physiology. Renal physiology · 2021Article
- Review
- Alteration of Cx37, Cx40, Cx43, Cx45, Panx1, and Renin Expression Patterns in Postnatal Kidneys of Dab1-/- (International journal of molecular sciences · 2021Article
- Role of a RhoA/ROCK-Dependent Pathway on Renal Connexin43 Regulation in the Angiotensin II-Induced Renal Damage.International journal of molecular sciences · 2019Article
- Integration of purinergic and angiotensin II receptor function in renal vascular responses and renal injury in angiotensin II-dependent hypertension.Purinergic signalling · 2019Review
- Constitutive SRC-mediated phosphorylation of pannexin 1 at tyrosine 198 occurs at the plasma membrane.The Journal of biological chemistry · 2019Article
- Involvement of Connexin Hemichannels in the Inflammatory Response of Chronic Diseases.International journal of molecular sciences · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 species (TBARS) and generated pro-inflammatory cytokines (ELISA; IL-1β and TNF-α). The membrane permeability increased progressively several hours before the latter outcome, which was a response prevented by Losartan, indicating the involvement of AT1 receptors. Western blot analysis showed that the amount of phosphorylated MYPT (a substrate of RhoA/ROCK) and Cx43 increased progressively and in parallel in cells treated with AngII, a response followed by an increase in the amount in Panx1 and P2X₇R. Greater membrane permeability was partially explained by opening of Cx43 hemichannels (Cx43 HCs) and Panx1 channels (Panx1 Chs), as well as P2X₇Rs activation by extracellular ATP, which was presumably released via Cx HCs and Panx1 Chs. Additionally, inhibition of RhoA/ROCK blocked the progressive increase in membrane permeability, and the remaining response was explained by the other non-selective channels. The rise of activity in the RhoA/ROCK-dependent pathway, as well as in Cx HCs, P2X₇R, and to a minor extent in Panx1 Chs led to higher amounts of TBARS and pro-inflammatory cytokines. We propose that AngII-induced mesangial cell damage could be effectively inhibited by concomitantly inhibiting the RhoA/ROCK-dependent pathway and one or more non-selective channel(s) activated through this pathway.
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