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Podocyte disease

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https://www.readbyqxmd.com/read/27920156/nf%C3%AE%C2%BAb-induced-periostin-activates-integrin-%C3%AE-3-signaling-to-promote-renal-injury-in-gn
#1
Niki Prakoura, Panagiotis Kavvadas, Raphaёl Kormann, Jean-Claude Dussaule, Christos E Chadjichristos, Christos Chatziantoniou
De novo expression in the kidney of periostin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal disease. In this study, we investigated the mechanism(s) of induction and the role of periostin in renal disease. Using a combination of bioinformatics, reporter assay, and chromatin immunoprecipitation analyses, we found that NFκB and other proinflammatory transcription factors induce periostin expression in vitro and that binding of these factors on the periostin promoter is enriched in glomeruli during experimental GN...
December 5, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27918307/vegf-regulates-local-inhibitory-complement-proteins-in-the-eye-and-kidney
#2
Lindsay S Keir, Rachel Firth, Lyndsey Aponik, Daniel Feitelberg, Susumu Sakimoto, Edith Aguilar, Gavin I Welsh, Anna Richards, Yoshihiko Usui, Simon C Satchell, Valeryia Kuzmuk, Richard J Coward, Jonathan Goult, Katherine R Bull, Ruchi Sharma, Kapil Bharti, Peter D Westenskow, Iacovos P Michael, Moin A Saleem, Martin Friedlander
Outer retinal and renal glomerular functions rely on specialized vasculature maintained by VEGF that is produced by neighboring epithelial cells, the retinal pigment epithelium (RPE) and podocytes, respectively. Dysregulation of RPE- and podocyte-derived VEGF is associated with neovascularization in wet age-related macular degeneration (ARMD), choriocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA). Since complement activation and genetic variants in inhibitory complement factor H (CFH) are also features of both ARMD and TMA, we hypothesized that VEGF and CFH interact...
December 5, 2016: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/27913625/absence-of-mir-146a-in-podocytes-increases-risk-of-diabetic-glomerulopathy-via-upregulation-of-erbb4-and-notch-1
#3
Ha Won Lee, Samia Q Khan, Shehryar Khaliqdina, Mehmet M Altintas, Florian Grahammer, Jimmy L Zhao, Kwihey Koh, Nicholas J Tardi, Mohd Hafeez Faridi, Terese Geraghty, David J Cimbaluk, Katalin Susztak, Luis F Moita, David Baltimore, Pierre-Louis Tharaux, Tobias B Huber, Matthias Kretzler, Markus Bitzer, Jochen Reiser, Vineet Gupta
Podocyte injury is an early event in diabetic kidney disease and is a hallmark of glomerulopathy. MicroRNA-146a (miR-146a) is highly expressed in many cell types under homeostatic conditions, and plays an important anti-inflammatory role in myeloid cells. However, its role in podocytes is unclear. Here, we show that miR-146a expression levels decrease in the glomeruli of patients with type 2 diabetes (T2D), which correlates with increased albuminuria and glomerular damage. MiR-146a levels are also significantly reduced in the glomeruli of albuminuric BTBR ob/ob mice, indicating its significant role in maintaining podocyte health...
December 2, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27907022/nicotine-induces-podocyte-apoptosis-through-increasing-oxidative-stress
#4
Xiqian Lan, Rivka Lederman, Judith M Eng, Seyedeh Shadafarin Marashi Shoshtari, Moin A Saleem, Ashwani Malhotra, Pravin C Singhal
BACKGROUND: Cigarette smoking plays an important role in the progression of chronic kidney disease (CKD). Nicotine, one of the major components of cigarette smoking, has been demonstrated to increase proliferation of renal mesangial cells. In this study, we examined the effect of nicotine on podocyte injury. METHODS: To determine the expression of nicotinic acetylcholine receptors (nAChR subunits) in podocytes, cDNAs and cell lysate of cultured human podocytes were used for the expression of nAChR mRNAs and proteins, respectively; and mouse renal cortical sections were subjected to immunofluorescant staining...
2016: PloS One
https://www.readbyqxmd.com/read/27899487/glomerular-endothelial-mitochondrial-dysfunction-is-essential-and-characteristic-of-diabetic-kidney-disease-susceptibility
#5
Ilse Daehn, Haiying Qi, Gabriella Casalena, Shaolin Shi, Liping Yu, Kerstin Ebefors, Yezhou Sun, Weijia Zhang, Vivette D'Agati, Detlef Schlondorff, Börje Haraldsson, Erwin Böttinger
The molecular signaling mechanisms between glomerular cell types during initiation/progression of diabetic kidney disease (DKD) remain poorly understood. We compared the early transcriptome profile between DKD resistant C57BL/6J (B6) and DKD susceptible DBA/2J (D2) glomeruli, and demonstrated a significant down regulation of essential mitochondrial genes in glomeruli from diabetic D2 mice, but not in B6 with comparable hyperglycemia. Diabetic D2 mice manifested increased mtDNA lesions (8-oxoG), exclusively localized to glomerular endothelial cells after 3 weeks of diabetes and these accumulated over time as well as increased urine secretion of 8-oxodG...
November 29, 2016: Diabetes
https://www.readbyqxmd.com/read/27895156/sildenafil-prevents-podocyte-injury-via-ppar-%C3%AE-mediated-trpc6-inhibition
#6
Ramon Sonneveld, Joost G Hoenderop, Andrea M Isidori, Carole Henique, Henry B Dijkman, Jo H Berden, Pierre-Louis Tharaux, Johan van der Vlag, Tom Nijenhuis
Transient receptor potential channel C6 (TRPC6) gain-of-function mutations and increased TRPC6 expression in podocytes induce glomerular injury and proteinuria. Sildenafil reduces TRPC6 expression and activity in nonrenal cell types, although the mechanism is unknown. Peroxisome proliferator-activated receptor γ (PPAR-γ) is a downstream target of sildenafil in the cyclic guanosine monophosphate (cGMP)-activated protein kinase G (PKG) axis. PPAR-γ agonists, like pioglitazone, appear antiproteinuric. We hypothesized that sildenafil inhibits TRPC6 expression in podocytes through PPAR-γ-dependent mechanisms, thereby counteracting podocyte injury and proteinuria...
November 28, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27888806/decreased-dach1-expression-in-glomerulopathy-is-associated-with-disease-progression-and-severity
#7
Qing-Quan Liu, Ya-Qun Zhou, Hui-Quan Liu, Wen-Hui Qiu, Hui Liu, Ting-Yang Hu, Qing Xu, Yong-Man Lv, Kong-Ming Wu
Cell fate determination factor dachshund1 (DACH1) is a chromosome-associated protein that regulates cellular differentiation throughout development. Recent genome-wide association studies have show that missense mutation in DACH1 leads to hereditary renal hypodysplasia. Renal DACH1 expression can be used to estimate glomerular filtration rate (eGFR). We firstly characterized the function of DACH1 in normal and diseased renal tissue using immunohistochemistry to assess DACH1 in human renal biopsy specimens from 40 immunoglobulin A nephropathy (IgAN) patients, 20 idiopathic membranous nephropathy (IMN) patients, and 15 minimal change disease (MCD) patients...
November 19, 2016: Oncotarget
https://www.readbyqxmd.com/read/27885584/wt1-and-nphs2-gene-mutation-analysis-and-clinical-management-of-steroid-resistant-nephrotic-syndrome
#8
Aravind Selvin Kumar Ramanathan, Murali Vijayan, Srilakshmi Rajagopal, Padmaraj Rajendiran, Prabha Senguttuvan
Nephrotic syndrome (NS) is a kidney disease predominantly present in children with idiopathic condition; final stage of the disease progresses into end-stage renal disease. Generally, NS is treated using standard steroid therapy, however; most of the children are steroid sensitive and about 15-20% are non-responders (SRNS). Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1). The mutation in podocyte genes is associated with SRNS...
November 25, 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27884511/effects-of-previous-physical-training-on-adriamycin-nephropathy-and-its-relationship-with-endothelial-lesions-and-angiogenesis-in-the-renal-cortex
#9
Camila M Faleiros, Heloisa Francescato, Marcelo Papoti, Lucas Chaves, Cleonice Silva, Roberto Costa, Terezila Machado Coimbra
AIMS: Adriamycin (ADR)-induced nephropathy is one of the most experimental models used in progressive kidney disease. A single dose of this drug induces a progressive and irreversible proteinuria that progresses to focal segmental glomerulosclerosis and tubulointerstitial lesions. Regular physical activity has been considered as a therapeutic intervention in several diseases. This study evaluated the influence of previous physical training in renal damage induced by ADR and the role of endothelial lesions and angiogenesis in this process...
November 21, 2016: Life Sciences
https://www.readbyqxmd.com/read/27884308/talking-back-the-podocytes-and-endothelial-cells-duke-it%C3%A2-out
#10
Agnes B Fogo
Thrombotic microangiopathy has numerous causes and may result in chronic kidney disease with secondary glomerulosclerosis. Detailed analyses of this interplay of lesions have been lacking. Buob et al. report on their adult, mostly Caucasian patients, showing frequent sclerosis, most often of collapsing type, with worse prognosis than in those without segmental scars. The complex interplay of glomerular cells and possible ways in which the endothelial cells may talk back to the podocytes, and vice versa, are discussed...
December 2016: Kidney International
https://www.readbyqxmd.com/read/27882344/slit2-robo2-signaling-pathway-inhibits-nonmuscle-myosin-iia-activity-and-destabilizes-kidney-podocyte-adhesion
#11
Xueping Fan, Hongying Yang, Sudhir Kumar, Kathleen E Tumelty, Anna Pisarek-Horowitz, Hila Milo Rasouly, Richa Sharma, Stefanie Chan, Edyta Tyminski, Michael Shamashkin, Mostafa Belghasem, Joel M Henderson, Anthony J Coyle, David J Salant, Stephen P Berasi, Weining Lu
The repulsive guidance cue SLIT2 and its receptor ROBO2 are required for kidney development and podocyte foot process structure, but the SLIT2/ROBO2 signaling mechanism regulating podocyte function is not known. Here we report that a potentially novel signaling pathway consisting of SLIT/ROBO Rho GTPase activating protein 1 (SRGAP1) and nonmuscle myosin IIA (NMIIA) regulates podocyte adhesion downstream of ROBO2. We found that the myosin II regulatory light chain (MRLC), a subunit of NMIIA, interacts directly with SRGAP1 and forms a complex with ROBO2/SRGAP1/NMIIA in the presence of SLIT2...
November 17, 2016: JCI Insight
https://www.readbyqxmd.com/read/27878608/claudins-in-barrier-and-transport-function-the-kidney
#12
REVIEW
Yongfeng Gong, Jianghui Hou
Claudins are discovered to be key players in renal epithelial physiology. They are involved in developmental, physiological, and pathophysiological differentiation. In the glomerular podocytes, claudin-1 is an important determinant of cell junction fate. In the proximal tubule, claudin-2 plays important roles in paracellular salt reabsorption. In the thick ascending limb, claudin-14, -16, and -19 regulate the paracellular reabsorption of calcium and magnesium. Recessive mutations in claudin-16 or -19 cause an inherited calcium and magnesium losing disease...
November 23, 2016: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/27872232/therapeutic-potential-of-progranulin-in-hyperhomocysteinemia-induced-cardiorenal-dysfunction
#13
Yi Fu, Yu Sun, Meng Zhou, Xiaojie Wang, Ziying Wang, Xinbing Wei, Yan Zhang, Zeyu Su, Kaili Liang, Wei Tang, Fan Yi
Hyperhomocysteinemia (hHcys) is an important independent risk factor for the development of cardiovascular disease and end-stage renal disease. Although multiple approaches lowering the levels of homocysteine have been used in experimental studies and clinical trials, there is no effective therapy available to fully prevent homocysteine-induced injury. Therefore, identifying key molecules in the pathogenic pathways may provide clues to develop new therapeutic strategies for the treatment of hHcys-associated injury beyond lowering the plasma homocysteine levels...
November 21, 2016: Hypertension
https://www.readbyqxmd.com/read/27864431/apol1-mediated-cell-injury-involves-disruption-of-conserved-trafficking-processes
#14
Etty Kruzel-Davila, Revital Shemer, Ayala Ofir, Ira Bavli-Kertselli, Ilona Darlyuk-Saadon, Pazit Oren-Giladi, Walter G Wasser, Daniella Magen, Eid Zaknoun, Maya Schuldiner, Adi Salzberg, Daniel Kornitzer, Zvonimir Marelja, Matias Simons, Karl Skorecki
APOL1 harbors C-terminal sequence variants (G1 and G2), which account for much of the increased risk for kidney disease in sub-Saharan African ancestry populations. Expression of the risk variants has also been shown to cause injury to podocytes and other cell types, but the underlying mechanisms are not understood. We used Drosophila melanogaster and Saccharomyces cerevisiae to help clarify these mechanisms. Ubiquitous expression of the human APOL1 G1 and G2 disease risk alleles caused near-complete lethality in D...
November 18, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27864430/apol1-g1-in-nephrocytes-induces-hypertrophy-and-accelerates-cell-death
#15
Yulong Fu, Jun-Yi Zhu, Adam Richman, Yi Zhang, Xuefang Xie, Jharna R Das, Jinliang Li, Patricio E Ray, Zhe Han
People of African ancestry carrying certain APOL1 mutant alleles are at elevated risk of developing renal diseases. However, the mechanisms underlying APOL1-associated renal diseases are unknown. Because the APOL1 gene is unique to humans and some primates, new animal models are needed to understand the function of APOL1 in vivo We generated transgenic Drosophila fly lines expressing the human APOL1 wild type allele (G0) or the predominant APOL1 risk allele (G1) in different tissues. Ubiquitous expression of APOL1 G0 or G1 in Drosophila induced lethal phenotypes, and G1 was more toxic than was G0...
November 18, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27862669/association-between-nephrinuria-podocyturia-and-proteinuria-in-women-with-pre-eclampsia
#16
Itsuko Furuta, Tianyue Zhai, Satoshi Ishikawa, Takeshi Umazume, Kinuko Nakagawa, Takahiro Yamada, Mamoru Morikawa, Hisanori Minakami
AIM: Podocyte depletion in the kidney is associated with end-stage kidney disease (ESKD). Pre-eclampsia (PE) increases the risk of ESKD in later life. This study was performed to determine whether nephrinuria (soluble nephrin in the urine) is correlated with proteinuria and/or podocyturia (podocytes in the urine) in PE women. METHODS: Eighty-three urine samples, consisting of 45 and 38 samples from 27 normotensive and nine PE women, respectively, underwent simultaneous determination of nephrin, protein, and creatinine concentrations in the urine supernatant and quantitative analysis of podocyte-specific protein mRNA expression...
November 12, 2016: Journal of Obstetrics and Gynaecology Research
https://www.readbyqxmd.com/read/27858997/a-novel-assay-to-assess-the-effect-of-pharmaceutical-compounds-on-the-differentiation-of-podocytes
#17
Frances Kindt, Elke Hammer, Stefan Kemnitz, Antje Blumenthal, Paul Klemm, Rabea Schlüter, Susan E Quaggin, Jens van den Brandt, Georg Fuellen, Uwe Völker, Karlhans Endlich, Nicole Endlich
BACKGROUND AND PURPOSE: Therapeutic options to treat glomerulopathies, the main cause of chronic kidney disease, are limited. Podocyte dedifferentiation is a major event in the pathogenesis of glomerulopathies. The goal of the present study was therefore to develop an assay to monitor podocyte differentiation suited for compound screening. EXPERIMENTAL APPROACH: We isolated and cultured glomeruli from transgenic mice, expressing cyan fluorescent protein (CFP) under control of the promoter of nephrin, a marker of podocyte differentiation...
November 14, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27849017/elmo1-protects-renal-structure-and-ultrafiltration-in-kidney-development-and-under-diabetic-conditions
#18
Krishna Rakesh Sharma, Karl Heckler, Sandra J Stoll, Jan-Luuk Hillebrands, Katharina Kynast, Esther Herpel, Stefan Porubsky, Marlies Elger, Boris Hadaschik, Karen Bieback, Hans-Peter Hammes, Peter P Nawroth, Jens Kroll
Engulfment and cell motility 1 (ELMO1) functions as a guanine exchange factor for Rac1 and was recently found to protect endothelial cells from apoptosis. Genome wide association studies suggest that polymorphisms within human elmo1 act as a potential contributing factor for the development of diabetic nephropathy. Yet, the function of ELMO1 with respect to the glomerulus and how this protein contributes to renal pathology was unknown. Thus, this study aimed to identify the role played by ELMO1 in renal development in zebrafish, under hyperglycaemic conditions, and in diabetic nephropathy patients...
November 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27816946/advanced-glycation-end-products-mediated-cellular-and-molecular-events-in-the-pathology-of-diabetic-nephropathy
#19
Anil Kumar Pasupulati, P Swathi Chitra, G Bhanuprakash Reddy
Diabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients and a leading cause of end-stage renal disease (ESRD). Degenerative changes such as glomerular hypertrophy, hyperfiltration, widening of basement membranes, tubulointerstitial fibrosis, glomerulosclerosis and podocytopathy manifest in various degrees of proteinuria in DN. One of the key mechanisms implicated in the pathogenesis of DN is non-enzymatic glycation (NEG). NEG is the irreversible attachment of reducing sugars onto free amino groups of proteins by a series of events, which include the formation of Schiff's base and an Amadori product to yield advanced glycation end products (AGEs)...
December 1, 2016: Biomolecular Concepts
https://www.readbyqxmd.com/read/27815317/macrophage-cyclooxygenase-2-protects-against-development-of-diabetic-nephropathy
#20
Xin Wang, Bing Yao, Yinqiu Wang, Xiaofeng Fan, Suwan Wang, Aolei Niu, Haichun Yang, Agnes Fogo, Ming-Zhi Zhang, Raymond C Harris
Diabetic nephropathy (DN) is characterized by increased macrophage infiltration, and proinflammatory "M1" macrophages contribute to development of DN. Previous studies by us and others have reported that macrophage cyclooxygenase-2 (COX-2) plays a role in polarization and maintenance of a macrophage tissue reparative "M2" phenotype. We examined the effects of macrophage COX-2 on development of DN in type I diabetes. Cultured macrophages with COX-2 deletion exhibited an "M1" phenotype, as demonstrated by higher iNOS and NF-κB levels but lower IL-4Rα levels...
November 4, 2016: Diabetes
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