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https://www.readbyqxmd.com/read/27914709/podocyte-specific-chemokine-c-c-motif-receptor-2%C3%A2-overexpression-mediates-diabetic-renal-injury-in%C3%A2-mice
#1
Hanning You, Ting Gao, Wesley M Raup-Konsavage, Timothy K Cooper, Sarah K Bronson, W Brian Reeves, Alaa S Awad
Inflammation is a central pathophysiologic mechanism that contributes to diabetes mellitus and diabetic nephropathy. Recently, we showed that macrophages directly contribute to diabetic renal injury and that pharmacological blockade or genetic deficiency of chemokine (C-C motif) receptor 2 (CCR2) confers kidney protection in diabetic nephropathy. However, the direct role of CCR2 in kidney-derived cells such as podocytes in diabetic nephropathy remains unclear. To study this, we developed a transgenic mouse model expressing CCR2 specifically in podocytes (Tg[NPHS2-Ccr2]) on a nephropathy-prone (DBA/2J) and CCR2-deficient (Ccr2(-/-)) background with heterozygous Ccr2(+/-) littermate controls...
November 30, 2016: Kidney International
https://www.readbyqxmd.com/read/27914703/evidence-from-the-oxford-classification-cohort-supports-the-clinical-value-of-subclassification-of%C3%A2-focal-segmental-glomerulosclerosis-in-iga%C3%A2-nephropathy
#2
Shubha S Bellur, Fanny Lepeytre, Olga Vorobyeva, Stéphan Troyanov, H Terence Cook, Ian S D Roberts
Focal segmental glomerulosclerosis (FSGS) is a common finding in IgA nephropathy (IgAN). Here we assessed FSGS lesions in the Oxford Classification patient cohort and correlated histology with clinical presentation and outcome to determine whether subclassification of the S score in IgAN is reproducible and of clinical value. Our subclassification of lesions in 137 individuals with segmental glomerulosclerosis or adhesion (S1) identified 38% with podocyte hypertrophy, 10% with hyalinosis, 9% with resorption droplets within podocytes, 7% with tip lesions, 3% with perihilar sclerosis, and 2% with endocapillary foam cells...
November 30, 2016: Kidney International
https://www.readbyqxmd.com/read/27914528/food-advanced-glycation-end-products-aggravate-the-diabetic-vascular-complications-via-modulating-the-ages-rage-pathway
#3
Xing Lv, Gao-Hong Lv, Guo-Ying Dai, Hong-Mei Sun, Hui-Qin Xu
The aim of this study was to investigate the effects of high-advanced glycation end products (AGEs) diet on diabetic vascular complications. The Streptozocin (STZ)-induced diabetic mice were fed with high-AGEs diet. Diabetic characteristics, indicators of renal and cardiovascular functions, and pathohistology of pancreas, heart and renal were evaluated. AGEs/RAGE/ROS pathway parameters were determined. During the experiments, the diabetic mice exhibited typical characteristics including weight loss, polydipsia, polyphagia, polyuria, high-blood glucose, and low-serum insulin levels...
November 2016: Chinese Journal of Natural Medicines
https://www.readbyqxmd.com/read/27913625/absence-of-mir-146a-in-podocytes-increases-risk-of-diabetic-glomerulopathy-via-upregulation-of-erbb4-and-notch-1
#4
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
#5
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
#6
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
#7
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
#8
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/27887947/berberine-enhances-the-ampk-activation-and-autophagy-and-mitigates-high-glucose-induced-apoptosis-of-mouse-podocytes
#9
Yingli Jin, Shuping Liu, Qingshan Ma, Dong Xiao, Li Chen
High glucose concentration can induce injury of podocytes and berberine has a potent activity against diabetic nephropathy. However, whether and how berberine can inhibit high glucose-mediated injury of podocytes have not been clarified. This study tested the effect of berberine on high glucose-mediated apoptosis and the AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) activation and autophagy in podocytes. The results indicated that berberine significantly mitigated high glucose-decreased cell viability, and nephrin and podocin expression as well as apoptosis in mouse podocytes...
November 22, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27885584/wt1-and-nphs2-gene-mutation-analysis-and-clinical-management-of-steroid-resistant-nephrotic-syndrome
#10
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
#11
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
#12
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/27882943/metadherin-facilitates-podocyte-apoptosis-in-diabetic-nephropathy
#13
Wen-Ting Liu, Fen-Fen Peng, Hong-Yu Li, Xiao-Wen Chen, Wang-Qiu Gong, Wen-Jing Chen, Yi-Hua Chen, Pei-Lin Li, Shu-Ting Li, Zhao-Zhong Xu, Hai-Bo Long
Apoptosis, one of the major causes of podocyte loss, has been reported to have a vital role in diabetic nephropathy (DN) pathogenesis, and understanding the mechanisms underlying the regulation of podocyte apoptosis is crucial. Metadherin (MTDH) is an important oncogene, which is overexpressed in most cancers and responsible for apoptosis, metastasis, and poor patient survival. Here we show that the expression levels of Mtdh and phosphorylated p38 mitogen-activated protein kinase (MAPK) are significantly increased, whereas those of the microRNA-30 family members (miR-30s) are considerably reduced in the glomeruli of DN rat model and in high glucose (HG)-induced conditionally immortalized mouse podocytes (MPC5)...
November 24, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27882344/slit2-robo2-signaling-pathway-inhibits-nonmuscle-myosin-iia-activity-and-destabilizes-kidney-podocyte-adhesion
#14
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/27881606/mitochondria-protection-after-acute-ischemia-prevents-prolonged-upregulation-of-il-1%C3%AE-and-il-18-and-arrests-ckd
#15
Hazel H Szeto, Shaoyi Liu, Yi Soong, Surya V Seshan, Leona Cohen-Gould, Viacheslav Manichev, Leonard C Feldman, Torgny Gustafsson
The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1β It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month...
November 23, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27878608/claudins-in-barrier-and-transport-function-the-kidney
#16
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
#17
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/27871084/olmesartan-prevents-microalbuminuria-in-db-db-diabetic-mice-through-inhibition-of-angiotensin-ii-p38-sirt1-induced-podocyte-apoptosis
#18
Junhui Gu, Ming Yang, Na Qi, Shuqin Mei, Jiejian Chen, Shuwei Song, Ying Jing, Meihan Chen, Liangliang He, Lijun Sun, Huimin Hu, Lin Li, Rudolf P Wüthrich, Ming Wu, Changlin Mei
BACKGROUND/AIMS: Blockage of the renin-angiotensin II system (RAS) prevents or delays albuminuria in diabetic patients. The aim of this study was to investigate the inhibitory mechanism of the angiotensin receptor blocker olmesartan on albuminuria in a murine model of diabetic nephropathy. METHODS: Male db/db diabetic mice were fed with placebo or 20 mg/kg olmesartan by daily gavage for 12 weeks. Conditionally immortalized mouse podocytes were treated with glucose, angiotensin II, olmesartan or p38 inhibitor s8307 in different experimental conditions after differentiation...
November 21, 2016: Kidney & Blood Pressure Research
https://www.readbyqxmd.com/read/27864431/apol1-mediated-cell-injury-involves-disruption-of-conserved-trafficking-processes
#19
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
#20
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
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