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Cellular and Molecular Mechanisms in Glomerulonephritis 2.0
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Cellular and Molecular Mechanisms in Glomerulonephritis 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 6635

Special Issue Editors

Prof. Dr. Elena Ranieri

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences, School of Medicine, University of Foggia, Viale Luigi Pinto, 1, Foggia, Italy
Interests: chronic and acute renal diseases; cytokines; intracellular signaling; kidney cancer; immunological responses; T cells; dendritic cells; autoimmunity; clinical and molecular pathology
Special Issues, Collections and Topics in MDPI journals
Dr. Giuseppe Stefano Netti

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences - Clinical Pathology Unit. University of Foggia, Foggia, Italy
Interests: kidney transplantation; renal disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “Cellular and Molecular Mechanisms in Glomerulonephritis 2.0”, will collect a selection of recent research topics and current review articles related to the role of “Cellular and Molecular Mechanisms in Primary and Secondary Glomerulonephritis” in order to update the current knowledge in this field. Original papers, up-to-date review articles, and commentaries are all welcome.

Extensive progress has been made in the understanding of the mechanisms underpinning renal diseases, and advances in this field will open the road to new therapeutic targets and better diagnostic and treatment approaches.

Glomerulonephritis (GN) refers to a group of heterogeneous diseases arising from inflammatory processes or metabolic diseases that affect the kidney. As a consequence, they are initiated mostly by local glomerular abnormalities, including genetic disease, with frequent involvement of renal tubulo-interstitium.

To date, GN remains a leading cause of end-stage renal disease (ESRD) and accounts for about 20% of chronic kidney disease (CKD) cases in most countries in the world. However, this percentage underestimates the real incidence of GN because of the commonly asymptomatic GN phenotype, incidentally diagnosed by abnormal urinary findings. In fact, GN is considered a public health issue, and during the past three decades, the incidence and prevalence of ESRD have risen progressively. In terms of numbers, by 2030, it is expected that the annual number of people with new onset of ESRD will exceed 450,000, and those receiving dialysis or who have had kidney transplants will exceed 2 million. Thus, more effort in research is needed to understand the causes and pathophysiology of GN in order to ameliorate the diagnosis and identify new therapeutic approaches.

Prof. Dr. Elena Ranieri
Dr. Giuseppe Stefano Netti
Guest Editors

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Published Papers (2 papers)

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Research

19 pages, 3708 KiB  
Article
Heparanase Increases Podocyte Survival and Autophagic Flux after Adriamycin-Induced Injury
by Hanan Abu-Tayeh Suleiman, Shereen Said, Haya Ali Saleh, Aviva Gamliel-Lazarovich, Eyas Haddad, Irina Minkov, Yaniv Zohar, Neta Ilan, Israel Vlodavsky, Zaid Abassi and Suheir Assady
Int. J. Mol. Sci. 2022, 23(20), 12691; https://doi.org/10.3390/ijms232012691 - 21 Oct 2022
Cited by 2 | Viewed by 2360
Abstract
The kidney glomerular filtration barrier (GFB) is enriched with heparan sulfate (HS) proteoglycans, which contribute to its permselectivity. The endoglycosidase heparanase cleaves HS and hence appears to be involved in the pathogenesis of kidney injury and glomerulonephritis. We have recently reported, nonetheless, that [...] Read more.
The kidney glomerular filtration barrier (GFB) is enriched with heparan sulfate (HS) proteoglycans, which contribute to its permselectivity. The endoglycosidase heparanase cleaves HS and hence appears to be involved in the pathogenesis of kidney injury and glomerulonephritis. We have recently reported, nonetheless, that heparanase overexpression preserved glomerular structure and kidney function in an experimental model of Adriamycin-induced nephropathy. To elucidate mechanisms underlying heparanase function in podocytes—key GFB cells, we utilized a human podocyte cell line and transgenic mice overexpressing heparanase. Notably, podocytes overexpressing heparanase (H) demonstrated significantly higher survival rates and viability after exposure to Adriamycin or hydrogen peroxide, compared with mock-infected (V) podocytes. Immunofluorescence staining of kidney cryo-sections and cultured H and V podocytes as well as immunoblotting of proteins extracted from cultured cells, revealed that exposure to toxic injury resulted in a significant increase in autophagic flux in H podocytes, which was reversed by the heparanase inhibitor, Roneparstat (SST0001). Heparanase overexpression was also associated with substantial transcriptional upregulation of autophagy genes BCN1, ATG5, and ATG12, following Adriamycin treatment. Moreover, cleaved caspase-3 was attenuated in H podocytes exposed to Adriamycin, indicating lower apoptotic cell death in H vs. V podocytes. Collectively, these findings suggest that in podocytes, elevated levels of heparanase promote cytoprotection. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Glomerulonephritis 2.0)
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12 pages, 3321 KiB  
Article
Imaging the Kidney with an Unconventional Scanning Electron Microscopy Technique: Analysis of the Subpodocyte Space in Diabetic Mice
by Sara Conti, Giuseppe Remuzzi, Ariela Benigni and Susanna Tomasoni
Int. J. Mol. Sci. 2022, 23(3), 1699; https://doi.org/10.3390/ijms23031699 - 1 Feb 2022
Cited by 6 | Viewed by 3053
Abstract
Transmission electron microscopy (TEM) remains the gold standard for renal histopathological diagnoses, given its higher resolving power, compared with light microscopy. However, it imposes several limitations on pathologists, including longer sample preparation time and a small observation area. To overcome these, we introduced [...] Read more.
Transmission electron microscopy (TEM) remains the gold standard for renal histopathological diagnoses, given its higher resolving power, compared with light microscopy. However, it imposes several limitations on pathologists, including longer sample preparation time and a small observation area. To overcome these, we introduced a scanning electron microscopy (SEM) technique for imaging resin-embedded semi-thin sections of renal tissue. We developed a rapid tissue preparation protocol for experimental models and human biopsies which, alongside SEM digital imaging acquisition of secondary electrons (SE–SEM), enables fast electron microscopy examination, with a resolution similar to that achieved by TEM. We used this unconventional SEM imaging approach to investigate the subpodocyte space (SPS) in BTBR ob/ob mice with type 2 diabetes. Analysis of semi-thin sections with secondary electrons revealed that the SPS had expanded in volume and covered large areas of the glomerular basement membrane, forming wide spaces between the podocyte body and the underlying filtering membrane. Our results show that SE–SEM is a valuable tool for imaging the kidney at the ultrastructural level, filling the magnification gap between light microscopy and TEM, and reveal that in diabetic mice, the SPS is larger than in normal controls, which is associated with podocyte damage and impaired kidney function. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Glomerulonephritis 2.0)
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