ArticleClinical and experimental medicine2014
AngII-induced glomerular mesangial cell proliferation inhibited by losartan via changes in intracellular calcium ion concentration.
Article in Clinical and experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 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
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons.International journal of molecular sciences · 2022Review
- The Effects of TRPC6 Knockout in Animal Models of Kidney Disease.Biomolecules · 2022Review
- Asian Pigeonwing Plants (Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Sauchinone Protects Renal Mesangial Cell Dysfunction against Angiotensin II by Improving Renal Fibrosis and Inflammation.International journal of molecular sciences · 2020Article
- MiR-29b expression is altered in crescent formation of HSPN and accelerates Ang II-induced mesangial cell activation.World journal of pediatrics : WJP · 2020Article
- Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement.Journal of diabetes research · 2020Review
- A NOX4/TRPC6 Pathway in Podocyte Calcium Regulation and Renal Damage in Diabetic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2018Article
- Angiotensin II-Induced Mesangial Cell Damaged Is Preceded by Cell Membrane Permeabilization Due to Upregulation of Non-Selective Channels.International journal of molecular sciences · 2018Article
- Role of adaptor protein p66Shc in renal pathologies.American journal of physiology. Renal physiology · 2018Review
- Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology.Antioxidants & redox signaling · 2016Review
- TRPC6 channel activation promotes neonatal glomerular mesangial cell apoptosis via calcineurin/NFAT and FasL/Fas signaling pathways.Scientific reports · 2016Article
- Effects of 1,25(OH)2D3 on proliferation and apoptosis of human glomerular mesangial cells.American journal of translational research · 2016Article
- Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the changes in intracellular [Ca(2+)](i) (intracellular calcium ion concentration) and TRPC6 (transient receptor potential channel 6) expression during angiotensin II (AngII)-induced glomerular mesangial cell (GMC) proliferation, as well as the inhibitory effect of losartan. GMC cultures were split into four groups treated for 24 h: Group N (blank control group), Group A (10(-7 )mol/L AngII), Group LT (10(-7 )mol/L AngII and 10(-5 )mol/L losartan), and Group Pred (10(-7 )mol/L AngII and 10(-5 )mol/L prednisone). GMCs proliferation was measured by the MTT and trypan blue assays. The distribution of TRPC6 was monitored by immunofluorescence, the expression of TRPC6 was detected by RT-PCR and Western blotting, and [Ca(2+)](i) was measured by laser scanning confocal microscopy. The results showed that the maximal proliferation of GMCs was induced by treatment with 10(-7 )mol/L AngII for 24 h. In Group A, the distribution of TRPC6 was not uniform in the cell membrane, there was increased accumulation of this protein within the cytoplasm, and the increased expression of TRPC6 and [Ca(2+)](i) was consistent with the proliferation of cells. In Group LT, losartan inhibited the proliferation of GMCs significantly, the levels of TRPC6 and [Ca(2+)](i) were diminished, and the distribution of TRPC6 was improved. Prednisone also significantly inhibited the proliferation of GMCs and had no effects on the expression of TRPC6 and [Ca(2+)](i) in Group Pred. These findings suggested that AngII could enhance the expression of TRPC6, increase [Ca(2+)](i,) and demonstrate a time-dose-response relationship with the proliferation of GMCs, while losartan reversed the effect of AngII on GMC proliferation.
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