Mesangial proliferative glomerulonephritis: A glomerular disease or a non‐specific morphological change?

Arias, Luis Fernando; Taborda-Murillo, Alejandra

doi:10.1111/nep.13034

Cited by 4 publications

(4 citation statements)

References 1 publication

(1 reference statement)

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“…Mesangial proliferative glomerulonephritis (MsPGN) is an epidemic disease worldwide (1)(2)(3). The main pathological change in MsPGN is the lesion of mesangial cells (4,5). However, the depletion of podocytes in MsPGN is invariably recognized as the main cause of nephron loss, glomerulosclerosis and end-stage renal disease (ESRD), which are more serious (3,(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis

Wu¹,

Bai²,

Cui³

et al. 2020

Ann Transl Med

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Background: Mesangial proliferative glomerulonephritis (MsPGN) is an epidemic disease with increasing occurrence. As important as mesangial cells, podocytes are key innate cells for MsPGN prognosis and recovery. Renal progenitor cells, located at the urinary pole (UP) of Bowman's capsule (BC), could alleviate kidney injury through their capacity to differentiate into podocytes.Methods: Seventy-two male rats were categorized randomly into the sham (n=24), untreated Thy-1 (n=24) and losartan-treated (n=24) groups. We administered vehicle or losartan (50 mg/kg by gavage) daily to treat rats with anti-thy1.1 nephritis, an ideal model to simulate human MsPGN. Two weeks after the intravenous injection of antibody, urinary protein and blood samples were analyzed, pathological changes were examined, the number of podocytes was determined, and renal progenitor cells were studied.Results: Anti-thy1.1 nephritis was significantly alleviated after losartan treatment, as reported previously and as expected. Compared with the untreated Thy-1 group, the number of podocytes in the losartan group increased, and the area of renal progenitor cells significantly increased. The protein expression of components of the p-ERK pathway was determined during the development of renal progenitor cells differentiating into podocytes. Conclusions:The data in this paper show the direct glomerular cell action of angiotensin II receptor blocker (ARB) treatment in improving outcomes in anti-thy1.1 nephritis. The positive effects of ARB medication on anti-thy1.1 nephritis were due to an increase in the number of renal epithelial progenitor cells (defined as PECs that expressed only stem cell markers without podocyte proteins).

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Section: Introductionmentioning

confidence: 99%

Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis

Wu¹,

Bai²,

Cui³

et al. 2020

Ann Transl Med

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“…Mesangial proliferative glomerulonephritis (MPGN) does not represent a specific glomerulopathy. As a pathological description of a class of glomerular diseases with mesangial hyperplasia, it can occur in primary glomerulonephritis (IgA nephropathy, lupus nephritis, infectious glomerulonephritis, IgM nephropathy, etc) and systemic disease (kidney allograft, diabetes, immune complex deposition, etc) 27,28 . MPGN is one of the major factors of chronic kidney disease which leads to end‐stage renal disease.…”

Section: Discussionmentioning

confidence: 99%

“…As a pathological description of a class of glomerular diseases with mesangial hyperplasia, it can occur in primary glomerulonephritis (IgA nephropathy, lupus nephritis, infectious glomerulonephritis, IgM nephropathy, etc) and systemic disease (kidney allograft, diabetes, immune complex deposition, etc). 27,28 MPGN is one of the major factors of chronic kidney disease which leads to end-stage renal disease. Therefore, the study on its mechanism can provide new ideas for the treat- mesangial matrix accumulate, endothelial cells (ECs) proliferate increasingly.…”

Section: Discussionmentioning

confidence: 99%

Activated mesangial cells induce glomerular endothelial cells proliferation in rat anti‐Thy‐1 nephritis through VEGFA/VEGFR2 and Angpt2/Tie2 pathway

Zhao

Chen

et al. 2021

Cell Proliferation

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“…The World Health Organization Committee have defined MePGN as an essentially uniform increase in mesangial cells in more than 80% of the glomeruli [13]. Cell proliferation and fibrosis are typical signs of it and may ultimately result in end-stage renal disease.…”

Section: Discussionmentioning

confidence: 99%

Phosphoproteomic profile of peripheral blood mononuclear cells in mesangial proliferative glomerulonephritis patients

Zhang¹,

Sun²,

Li³

et al. 2020

Integr Mol Med

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To insight the pathogenesis of Mesangial proliferative glomerulonephritis (MsPGN), we investigated the phosphoproteomic profile of PBMCs from MsPGN patients and normal subjects by integrating TiO 2 enrichment technology, 2D nano-liter liquid chromatography and linear ion trap quadrupole mass spectrometry. We identified totally 693 differential phosphorylation sites and corresponded to 439 genes. Gene ontology (GO) analysis showed that protein or nucleic acid binding took up the largest proportion of molecular function, followed by nucleobase, nucleoside, nucleotide and nucleic acid metabolic process in the nucleus. KEGG Pathway analysis showed that most of differential gene enrich in mitogen-activated protein kinase (MAPK) signaling pathway and focal adhesion pathway. Gene network analysis showed that serine/arginine repetitive matrix (SRRM) 1, histone deacetylase (HDAC) 1 and protein kinase C delta (PRKED) were significantly regulators in the network. These results suggested that abnormal changes of protein phosphorylation modification may contribute to MsPGN, and may be derived from the dysregulation of MAPK signaling pathway and focal adhesion pathway. In these pathways, the differential genes SRRM1, HDAC1 and PRKCD with higher connection may be the promising biomarker for MsPGN.

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Mesangial proliferative glomerulonephritis: A glomerular disease or a non‐specific morphological change?

Cited by 4 publications

References 1 publication

Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis

Renal progenitor cells modulated by angiotensin II receptor blocker (ARB) medication and differentiation towards podocytes in anti-thy1.1 nephritis

Activated mesangial cells induce glomerular endothelial cells proliferation in rat anti‐Thy‐1 nephritis through VEGFA/VEGFR2 and Angpt2/Tie2 pathway

Phosphoproteomic profile of peripheral blood mononuclear cells in mesangial proliferative glomerulonephritis patients

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