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https://www.readbyqxmd.com/read/28819298/transcriptome-based-network-analysis-reveals-renal-cell-type-specific-dysregulation-of-hypoxia-associated-transcripts
#1
Natallia Shved, Gregor Warsow, Felix Eichinger, David Hoogewijs, Simone Brandt, Peter Wild, Matthias Kretzler, Clemens D Cohen, Maja T Lindenmeyer
Accumulating evidence suggests that dysregulation of hypoxia-regulated transcriptional mechanisms is involved in development of chronic kidney diseases (CKD). However, it remains unclear how hypoxia-induced transcription factors (HIFs) and subsequent biological processes contribute to CKD development and progression. In our study, genome-wide expression profiles of more than 200 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium...
August 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28815607/a-3d-tri-culture-system-reveals-that-activin-receptor-like-kinase-5-and-connective-tissue-growth-factor-drive-human-glomerulosclerosis
#2
John P Waters, Yvonne C Richards, Jeremy N Skepper, Mark Southwood, Paul D Upton, Nicholas W Morrell, Jordan S Pober, John R Bradley
Glomerular scarring, known as glomerulosclerosis, occurs in many chronic kidney diseases and involves interaction between glomerular endothelial cells (GEC), podocytes and mesangial cells (MCs), leading to signals that promote extracellular matrix deposition and endothelial cell dysfunction and loss. We describe a 3D tri-culture system to model human glomerulosclerosis. In 3D monoculture, each cell type alters its phenotype in response to TGFβ, which has been implicated as an important mediator of glomerulosclerosis...
August 16, 2017: Journal of Pathology
https://www.readbyqxmd.com/read/28814739/re-characterization-of-the-glomerulopathy-in-cd2ap-deficient-mice-by-high-resolution-helium-ion-scanning-microscopy
#3
Kenji Tsuji, Teodor G Păunescu, Hani Suleiman, Dongping Xie, Fahmy A Mamuya, Jeffrey H Miner, Hua A Jenny Lu
Helium ion scanning microscopy (HIM) is a novel technology that directly visualizes the cell surface ultrastructure without surface coating. Despite its very high resolution, it has not been applied extensively to study biological or pathology samples. Here we report the application of this powerful technology to examine the three-dimensional ultrastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated protein (CD2AP) deficiency. HIM revealed the serial alteration of glomerular features including effacement and disorganization of the slit diaphragm, followed by foot process disappearance, flattening and fusion of major processes, and eventual transformation into a podocyte sheet as the disease progressed...
August 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28814668/injury-induced-actin-cytoskeleton-reorganization-in-podocytes-revealed-by-super-resolution-microscopy
#4
Hani Y Suleiman, Robyn Roth, Sanjay Jain, John E Heuser, Andrey S Shaw, Jeffrey H Miner
The architectural integrity of tissues requires complex interactions, both between cells and between cells and the extracellular matrix. Fundamental to cell and tissue homeostasis are the specific mechanical forces conveyed by the actomyosin cytoskeleton. Here we used super-resolution imaging methods to visualize the actin cytoskeleton in the kidney glomerulus, an organized collection of capillaries that filters the blood to make the primary urine. Our analysis of both mouse and human glomeruli reveals a network of myosin IIA-containing contractile actin cables within podocyte cell bodies and major processes at the outer aspects of the glomerular tuft...
August 17, 2017: JCI Insight
https://www.readbyqxmd.com/read/28814510/a-heterologous-model-of-thrombospondin-type-1-domain-containing-7a-associated-membranous-nephropathy
#5
Nicola M Tomas, Catherine Meyer-Schwesinger, Hanning von Spiegel, Ahmed M Kotb, Gunther Zahner, Elion Hoxha, Udo Helmchen, Nicole Endlich, Friedrich Koch-Nolte, Rolf A K Stahl
Thrombospondin type 1 domain-containing 7A (THSD7A) is a target for autoimmunity in patients with membranous nephropathy (MN). Circulating autoantibodies from patients with THSD7A-associated MN have been demonstrated to cause MN in mice. However, THSD7A-associated MN is a rare disease, preventing the use of patient antibodies for larger experimental procedures. Therefore, we generated antibodies against the human and mouse orthologs of THSD7A in rabbits by coimmunization with the respective cDNAs. Injection of these anti-THSD7A antibodies into mice induced a severe nephrotic syndrome with proteinuria, weight gain, and hyperlipidemia...
August 16, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/28807596/the-role-of-angiotensin-ii-in-parietal-epithelial-cell-proliferation-and-crescent-formation-in-glomerular-diseases
#6
Paola Rizzo, Rubina Novelli, Cinzia Rota, Elena Gagliardini, Barbara Ruggiero, Daniela Rottoli, Ariela Benigni, Giuseppe Remuzzi
Crescentic glomerulonephritis (GN) is a devastating disease with rapidly progressive deterioration in kidney function, which, histologically, manifests as crescent formation in most glomeruli. We previously found that crescents derive from the aberrant proliferation and migration of parietal epithelial cells (PECs)/progenitor cells, and that the angiotensin (ang) II/ang II type-1 (AT1) receptor pathway may participate, together with the stromal cell-derived factor-1 (SDF-1)/CXCR4 axis, in the development of those lesions...
August 11, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28805828/mutations-in-keops-complex-genes-cause-nephrotic-syndrome-with-primary-microcephaly
#7
Daniela A Braun, Jia Rao, Geraldine Mollet, David Schapiro, Marie-Claire Daugeron, Weizhen Tan, Olivier Gribouval, Olivia Boyer, Patrick Revy, Tilman Jobst-Schwan, Johanna Magdalena Schmidt, Jennifer A Lawson, Denny Schanze, Shazia Ashraf, Jeremy F P Ullmann, Charlotte A Hoogstraten, Nathalie Boddaert, Bruno Collinet, Gaëlle Martin, Dominique Liger, Svjetlana Lovric, Monica Furlano, I Chiara Guerrera, Oraly Sanchez-Ferras, Jennifer F Hu, Anne-Claire Boschat, Sylvia Sanquer, Björn Menten, Sarah Vergult, Nina De Rocker, Merlin Airik, Tobias Hermle, Shirlee Shril, Eugen Widmeier, Heon Yung Gee, Won-Il Choi, Carolin E Sadowski, Werner L Pabst, Jillian K Warejko, Ankana Daga, Tamara Basta, Verena Matejas, Karin Scharmann, Sandra D Kienast, Babak Behnam, Brendan Beeson, Amber Begtrup, Malcolm Bruce, Gaik-Siew Ch'ng, Shuan-Pei Lin, Jui-Hsing Chang, Chao-Huei Chen, Megan T Cho, Patrick M Gaffney, Patrick E Gipson, Chyong-Hsin Hsu, Jameela A Kari, Yu-Yuan Ke, Cathy Kiraly-Borri, Wai-Ming Lai, Emmanuelle Lemyre, Rebecca Okashah Littlejohn, Amira Masri, Mastaneh Moghtaderi, Kazuyuki Nakamura, Fatih Ozaltin, Marleen Praet, Chitra Prasad, Agnieszka Prytula, Elizabeth R Roeder, Patrick Rump, Rhonda E Schnur, Takashi Shiihara, Manish D Sinha, Neveen A Soliman, Kenza Soulami, David A Sweetser, Wen-Hui Tsai, Jeng-Daw Tsai, Rezan Topaloglu, Udo Vester, David H Viskochil, Nithiwat Vatanavicharn, Jessica L Waxler, Klaas J Wierenga, Matthias T F Wolf, Sik-Nin Wong, Sebastian A Leidel, Gessica Truglio, Peter C Dedon, Annapurna Poduri, Shrikant Mane, Richard P Lifton, Maxime Bouchard, Peter Kannu, David Chitayat, Daniella Magen, Bert Callewaert, Herman van Tilbeurgh, Martin Zenker, Corinne Antignac, Friedhelm Hildebrandt
Galloway-Mowat syndrome (GAMOS) is an autosomal-recessive disease characterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain anomalies. Here we identified recessive mutations in OSGEP, TP53RK, TPRKB, and LAGE3, genes encoding the four subunits of the KEOPS complex, in 37 individuals from 32 families with GAMOS. CRISPR-Cas9 knockout in zebrafish and mice recapitulated the human phenotype of primary microcephaly and resulted in early lethality. Knockdown of OSGEP, TP53RK, or TPRKB inhibited cell proliferation, which human mutations did not rescue...
August 14, 2017: Nature Genetics
https://www.readbyqxmd.com/read/28804725/meprin-metalloprotease-deficiency-associated-with-higher-mortality-rates-and-more-severe-diabetic-kidney-injury-in-mice-with-stz-induced-type-1-diabetes
#8
John E Bylander, Faihaa Ahmed, Sabena M Conley, Jean-Marie Mwiza, Elimelda Moige Ongeri
Meprins are membrane-bound and secreted metalloproteinases consisting of α and/or β subunits that are highly expressed in kidney epithelial cells and are differentially expressed in podocytes and leukocytes (macrophages and monocytes). Several studies have implicated meprins in the progression of diabetic nephropathy (DN) and fibrosis-associated kidney disease. However, the mechanisms by which meprins modulate DN are not understood. To delineate the role of meprins in DN, we subjected meprin αβ knockout (αβKO) mice and their wild-type (WT) counterparts to streptozotocin-induced type 1 diabetes...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28803254/helicobacter-pylori-cytotoxin-associated-gene-a-impairs-the-filtration-barrier-function-of-podocytes-via-p38-mapk-signaling-pathway
#9
Man Yang, Ling Wang, Li-Jie Gu, Wei-Jie Yuan
Helicobacter pylori (Hp) specific antigens were found deposited in the glomeruli in some kidney diseases. However, the underlying molecular mechanisms remain to be elucidated. The aim of this study was to investigate the effect of cytotoxin associated gene A protein (CagA), a key virulence factor of Hp, on mouse podocytes. Cells were cultured and treated with recombinant CagA protein. The expression of the tight junction protein ZO-1 and p38 MAPK signaling pathway activation were measured with real-time RT-PCR and western blotting...
August 12, 2017: Acta Biochimica Polonica
https://www.readbyqxmd.com/read/28801123/a-new-mouse-model-of-apol1-associated-kidney-diseases-when-traffic-gets-snarled-the-podocyte-suffers
#10
EDITORIAL
John F O'Toole, Leslie A Bruggeman, John R Sedor
No abstract text is available yet for this article.
August 9, 2017: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/28796565/ultrastructural-changes-of-kidney-in-schistosoma-mansoni-infected-mice
#11
Refaat A Eid, Mubarak Al-Shraim, Fahmy El-Sayed, Khaled Radad
Schistosomiasis is the second threatening parasitic disease after malaria and among Schistosoma spp., Schistosoma mansoni (S. mansoni) affects about 100 million people in tropic regions in Africa and South America. The current study was carried out to investigate ultrastructural changes of the kidney in mice infected with cercariae of S. mansoni, in which 20 Swiss albino mice of 60-day-old were assigned into two groups (10 each). Control group received 1 ml normal saline by intraperitoneal route. Model group were intraperitoneally infected with 1 ml normal saline containing 40 cercariae of S...
August 10, 2017: Ultrastructural Pathology
https://www.readbyqxmd.com/read/28791309/research-progress-on-mechanism-of-podocyte-depletion-in-diabetic-nephropathy
#12
REVIEW
Haoran Dai, Qingquan Liu, Baoli Liu
Diabetic nephropathy (DN) together with glomerular hyperfiltration has been implicated in the development of diabetic microangiopathy in the initial stage of diabetic diseases. Increased amounts of urinary protein in DN may be associated with functional and morphological alterations of podocyte, mainly including podocyte hypertrophy, epithelial-mesenchymal transdifferentiation (EMT), podocyte detachment, and podocyte apoptosis. Accumulating studies have revealed that disruption in multiple renal signaling pathways had been critical in the progression of these pathological damages, such as adenosine monophosphate-activated kinase signaling pathways (AMPK), wnt/β-catenin signaling pathways, endoplasmic reticulum stress-related signaling pathways, mammalian target of rapamycin (mTOR)/autophagy pathway, and Rho GTPases...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28790860/the-level-of-urinary-semaphorin3a-is-associated-with-disease-activity-in-patients-with-minimal-change-nephrotic-syndrome
#13
Akiko Inoue-Torii, Shinji Kitamura, Jun Wada, Kenji Tsuji, Hirofumi Makino
Semaphorin3A is a secreted protein known to be involved in organogenesis, immune responses and cancer. In the kidney, semaphorin3A is expressed in the glomerular podocytes, distal tubules and collecting tubules, and believed to play a role in the regulation of the kidney development and function. We examined the serum and urinary semaphorin3A levels in 72 patients with renal disease and 5 healthy volunteers. The patients had been diagnosed with thin basement membrane disease (n=4), minimal change nephrotic syndrome (MCNS; n=22), IgA nephritis (n=21), membranous nephropathy (n=16) and focal segmental glomerular sclerosis (n=9)...
2017: International Journal of Nephrology and Renovascular Disease
https://www.readbyqxmd.com/read/28776307/genetic-basis-of-adult-onset-nephrotic-syndrome-and-focal-segmental-glomerulosclerosis
#14
REVIEW
Jian Liu, Weiming Wang
Nephrotic syndrome (NS) is one of the most common glomerular diseases with signs of nephrosis, heavy proteinuria, hypoalbuminemia, and edema. Dysfunction of glomerular filtration barrier causes protein loss through the kidneys. Focal segmental glomerulosclerosis (FSGS) accounts for nearly 20% of NS among children and adults. Adult-onset FSGS/NS is often associated with low response to steroid treatment and immunosuppressive medication and poor renal survival. Several genes involved in NS and FSGS have been identified by linkage analysis and next-generation sequencing...
August 3, 2017: Frontiers of Medicine
https://www.readbyqxmd.com/read/28775002/kindlin-2-association-with-rho-gdp-dissociation-inhibitor-%C3%AE-suppresses-rac1-activation-and-podocyte-injury
#15
Ying Sun, Chen Guo, Ping Ma, Yumei Lai, Fan Yang, Jun Cai, Zhehao Cheng, Kuo Zhang, Zhongzhen Liu, Yeteng Tian, Yue Sheng, Ruijun Tian, Yi Deng, Guozhi Xiao, Chuanyue Wu
Alteration of podocyte behavior is critically involved in the development and progression of many forms of human glomerular diseases. The molecular mechanisms that control podocyte behavior, however, are not well understood. Here, we investigated the role of Kindlin-2, a component of cell-matrix adhesions, in podocyte behavior in vivo Ablation of Kindlin-2 in podocytes resulted in alteration of actin cytoskeletal organization, reduction of the levels of slit diaphragm proteins, effacement of podocyte foot processes, and ultimately massive proteinuria and death due to kidney failure...
August 3, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/28761153/pla2r-binds-to-the-annexin-a2-s100a10-complex-in-human-podocytes
#16
Maryline Fresquet, Thomas A Jowitt, Edward A McKenzie, Matthew D Ball, Michael J Randles, Rachel Lennon, Paul E Brenchley
Phospholipase A2 receptor (PLA2R) is a member of the mannose receptor family found in podocytes in human kidney. PLA2R is the target of the autoimmune disease, membranous nephropathy, characterised by production of anti-PLA2R autoantibodies which bind to the podocyte. However the function of PLA2R in health and in disease remains unclear. To gain insight into the molecular mechanisms of PLA2R function, we searched for its endogenous binding partners. Proteomic analysis identified annexinA2 as a potential interactor with the extracellular domains of PLA2R...
July 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28757276/value-of-immunohistochemical-expression-of-podocalyxin-in-active-lupus-nephritis
#17
Maha Abdelmoneim Behairy, Marwa Mosaad Shakweer, Tamer Wahid El Said, Nermin Hassan ElGharbawy
Podocalyxin is an electronegative sialoglycoprotein that prevents the podocyte foot process from collapsing. The aim of this study was to detect an association between the glomerular immunohistochemical (IHC) expression of podocalyxin and the degree of podocyte effacement detected by electron microscopy, and to evaluate the role of podocalyxin IHC expression as a novel marker for disease activity in lupus nephritis (LN). METHODS: Thirty-two renal biopsies of active lupus nephritis patients were studied...
July 27, 2017: Nefrología: Publicación Oficial de la Sociedad Española Nefrologia
https://www.readbyqxmd.com/read/28756410/reduction-of-podocyte-globotriaosylceramide-content-in-adult-male-patients-with-fabry-disease-with-amenable-gla-mutations-following-6-months-of-migalastat-treatment
#18
Michael Mauer, Alexey Sokolovskiy, Jay A Barth, Jeffrey P Castelli, Hadis N Williams, Elfrida R Benjamin, Behzad Najafian
OBJECTIVE: Deficiency of α-galactosidase A (αGal-A) in Fabry disease leads to the accumulation mainly of globotriaosylceramide (GL3) in multiple renal cell types. Glomerular podocytes are relatively resistant to clearance of GL3 inclusions by enzyme replacement therapy (ERT). Migalastat, an orally bioavailable small molecule capable of chaperoning misfolded αGal-A to lysosomes, is approved in the European Union for the long-term treatment of patients with Fabry disease and amenable GLA (α-galactosidase A enzyme) mutations...
July 29, 2017: Journal of Medical Genetics
https://www.readbyqxmd.com/read/28754557/accelerated-podocyte-detachment-and-progressive%C3%A2-podocyte-loss-from-glomeruli-with%C3%A2-age%C3%A2-in-alport-syndrome
#19
Fangrui Ding, Larysa Wickman, Su Q Wang, Yanqin Zhang, Fang Wang, Farsad Afshinnia, Jeffrey Hodgin, Jie Ding, Roger C Wiggins
Podocyte depletion is a common mechanism driving progression in glomerular diseases. Alport Syndrome glomerulopathy, caused by defective α3α4α5 (IV) collagen heterotrimer production by podocytes, is associated with an increased rate of podocyte detachment detectable in urine and reduced glomerular podocyte number suggesting that defective podocyte adherence to the glomerular basement membrane might play a role in driving progression. Here a genetically phenotyped Alport Syndrome cohort of 95 individuals [urine study] and 41 archived biopsies [biopsy study] were used to test this hypothesis...
July 26, 2017: Kidney International
https://www.readbyqxmd.com/read/28754555/elastin-insufficiency-causes-hypertension-structural%C3%A2-defects-and-abnormal-remodeling-of%C3%A2-renal-vascular-signaling
#20
Elizabeth A Owens, Li Jie, Beverly A S Reyes, Elisabeth J Van Bockstaele, Patrick Osei-Owusu
Elastin deficiency causes vascular stiffening, a leading risk for hypertension and chronic kidney disease (CKD). The mechanisms mediating hypertension and/or CKD pathogenesis due to elastin deficiency are poorly understood. Using the elastin heterozygous (Eln+/-) mouse model, we tested whether renal dysfunction due to elastin deficiency occurs independently of and precedes the development of hypertension. We assessed blood pressure and renal hemodynamics in 30-day and 12-week-old male and female mice. At P30, blood pressure of Eln+/- mice was similar to wild-type controls; however, renal blood flow was lower, whereas renal vascular resistance was augmented at baseline in Eln+/- mice...
July 26, 2017: Kidney International
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