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American Journal of Physiology. Renal Physiology

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https://www.readbyqxmd.com/read/30207172/aging-phenotype-s-in-kidneys-of-diabetic-mice-are-p66shca-dependent
#1
Himanshu Vashistha, L Marrero, Krzysztof Reiss, Ari Cohen, Ashwani Malhotra, Tariq Javed, Allyson E Bradley, Frank Abbruscato, Sixto Giusti, Antonio Jimenez, Smriti Mehra, Deepak Kaushal, Marco Giorgio, Pier Giuseppe Pelicci, Masao Kakoki, Pravin C Singhal, Bruce Bunnell, Leonard G Meggs
The p66ShcA protein controls cellular responses to oxidative stress, senescence and apoptosis. Here, we test the hypothesis that aging phenotype(s) commonly associated with broad category of chronic kidney disease are accelerated in diabetic kidneys and linked to the p66ShcA locus. At the organ level, tissue stem cells antagonize senescent phenotypes, by replacing old dysfunctional cells. Using established methods, we isolated a highly purified population of stem cell antigen-1 positive mesenchymal stem cells (Sca-1+ MSCs) from kidneys of Wild Type (WT) and p66 Knock Out (KO) mice...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207171/podocytes-contribute-and-respond-to-the-inflammatory-environment-in-lupus-nephritis
#2
Rachael Deborah Wright, Michael W Beresford
Lupus nephritis (LN) affects up to 80% of juvenile-onset systemic lupus erythematosus patients, leading to end-stage renal failure requiring dialysis or transplantation in 10-15%. Podocytes are specialised epithelial cells of the glomerulus known to be a key site of damage in glomerular diseases. However, their roles in LN have yet to be fully identified. This project aims to identify the structural and functional roles of podocytes in an in vitro model of LN. Conditionally immortalised podocytes were treated with pro-inflammatory cytokines (IL-1β, TNF-α, IFN-α, IFN-γ) alone and in combination, in an in vitro model of LN and were assessed for their structural and functional characteristics...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207170/adiponection-a-novel-player-to-save-the-kidneys
#3
Shan Chen, Hui Cai
No abstract text is available yet for this article.
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207169/the-chemokine-receptor-cx3cr1-reduces-renal-injury-in-mice-with-angiotensin-ii-induced-hypertension
#4
Erfan Ahadzadeh, Alva Rosendahl, Daniel Czesla, Paula Steffens, Lennard Prüßner, Catherine Meyer-Schwesinger, Nicola Wanner, Hans Joachim Paust, Tobias B Huber, Rolf Ak Stahl, Thorsten Wiech, Christian Kurts, Anika Seniuk, Heimo Ehmke, Ulrich O Wenzel
The role of CX3 CR1, also known as fractalkine receptor, in hypertension is unknown. The present study determined the role of the fractalkine receptor CX3 CR1 in hypertensive renal and cardiac injury. Expression of CX3 CR1 was determined using CX3 CR1GFP/+ mice that express a GFP reporter in CX3 CR1+ cells. FACS analysis of leukocytes isolated from the kidney showed that 34% of CD45+ cells expressed CX3 CR1. Dendritic cells were the majority of positive cells (67%) followed by macrophages (10%), NK cells (6%) and T cells (10%)...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207168/enhanced-renal-ischemia-reperfusion-injury-in-aging-and-diabetes
#5
Yoshikazu Muroya, Xiaochen He, Letao Fan, Shaoxun Wang, Rui Xu, Fan Fan, Richard J Roman
The incidence and severity of acute kidney injury is increased in diabetic patients and with aging. However, the mechanisms involved have not been clearly established. The present study examined the effects of aging and diabetes on the severity of renal ischemia reperfusion (IR) injury in Sprague Dawley (SD) and type-2 diabetic (T2DN) rats. T2DN rats develop diabetes at 3 months of age and progressive proteinuria and diabetic nephropathy as they age from 6 to 18 months. Plasma creatinine levels after bilateral IR were significantly higher (3...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207167/caveolae-facilitate-trpv4-mediated-ca2-signaling-and-the-hierachical-activation-of-ca2-activated-k-channels-in-k-secreting-renal-collecting-duct-cell
#6
Yue Li, Hongxiang Hu, Roger G O'Neil
TRPV4-mediated Ca2+ signaling induces early activation of small/intermediate Ca2+-activated K+ channels, SK3 (KCNN3) and IK1 (KCNN4), that leads to membrane hyperpolarization and enhanced Ca2+ influx that is critical for subsequent activation of the large conductance Ca2+-activated K+ channel BK (KCNMA1) and K+ secretion in kidney cortical collecting duct (CCD) cells. The focus of the present study was to determine if such coordinated hierarchical /sequential activation of these channels in CCD was orchestrated within caveolae, a known microcompartment underlying selective Ca2+-signaling events in other cells...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207166/nix-mediated-mitophagy-protects-against-proteinuria-induced-tubular-cell-apoptosis-and-renal-injury
#7
Dan Xu, Panpan Chen, Bao Wang, Yanzhe Wang, Naijun Miao, Fan Yin, Qian Cheng, Zhuanli Zhou, Hongyan Xie, Li Zhou, Jun Liu, Xiaoxia Wang, Roy Zent, Limin Lu, Wei Zhang
Proteinuria, the most common symptom of renal injury, is an independent factor for renal tubular injury. However, the underlying mechanism remains to be fully elucidated. Mitochondrion is an important target for proteinuria-induced renal tubular cell injury. Insufficient mitophagy exacerbates cell injury by initiating mitochondrial dysfunction-related cell apoptosis. In the experiment, the role of NIX-mediated mitophagy was investigated in proteinuria-induced renal injury. In this study we demonstrated NIX expression was reduced in renal tubules and correlated with decline of eGFR and increase of the proteinuria in patients...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30207165/impact-of-mpo-anca-mediated-oxidative-imbalance-on-renal-vasculitis
#8
Marc Hilhorst, Alexandre Tj Maria, Niloufar Kavian, Frederic Batteux, Didier Borderie, Alain Le Quellec, Pieter van Paassen, Philippe Guilpain
Glomerulonephritis is a severe complication of microscopic polyangiitis (MPA), a small-vessel vasculitis associated with anti-myeloperoxidase antibodies (MPO-ANCA). We previously showed the pathogenic effects of MPO-ANCA that activate MPO to trigger an oxidative burst mainly through HOCl production, contributing to endothelial injury and lung fibrosis. The aim of this study was to investigate the relationship between MPO-induced oxidative stress, anti-oxidant defenses and renal histological lesions in MPA patients...
September 12, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30156116/the-void-spot-assay-recommendations-on-the-use-of-a-simple-micturition-assay-for-mice
#9
Warren G Hill, Mark L Zeidel, Dale E Bjorling, Chad M Vezina
Investigators have for decades used mouse voiding patterns as endpoints for studying behavioral biology. It is only recently that mouse voiding patterns were adopted for study of lower urinary tract physiology. The spontaneous void spot assay (VSA), a popular micturition assessment tool, involves placing a mouse in an enclosure lined by filter paper and quantifying the resulting urine spot pattern. The VSA has advantages of being inexpensive and non-invasive, but some investigators challenge its ability to distinguish lower urinary tract function from behavioral voiding...
August 29, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30156115/nephron-specific-knockout-of-tmem16a-leads-to-reduced-number-of-glomeruli-and-albuminuria
#10
Laura Katharina Schenk, Bjoern Buchholz, Sebastian Franz Henke, Ulf Michgehl, Christoph Daniel, Kerstin Amann, Karl Kunzelmann, Hermann J Pavenstädt
TMEM16A is a transmembrane protein from a conserved family of calcium activated proteins, which is highly expressed in the kidney. TMEM16A confers calcium-activated chloride channel activity which is of importance for various cellular functions in secretory epithelia and involved in secretion-dependent renal cyst growth. However, its specific function in renal physiology has remained elusive so far. Therefore we generated conditional nephron specific TMEM16A knockout mice and found that these animals suffered from albuminuria...
August 29, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30156114/immune-cells-and-inflammation-in-aki-to-ckd-progression
#11
Yuki Sato, Motoko Yanagita
Acute kidney injury (AKI) is a common clinical state resulting from pathogenic conditions such as ischemic and toxic insults. The pathophysiology of AKI shares common pathogenic denominators including cell death/injury, inflammation, and fibrosis, regardless of the initiating insults. Recent clinical studies have shown that a single episode of AKI can lead to subsequent chronic kidney disease (CKD). Although the involvement of multiple types of cells in the pathophysiology of AKI is becoming increasingly clear, the precise mechanisms for this "AKI to CKD progression" are still unknown, and no drug has been shown to halt this progression...
August 29, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132348/multiphoton-imaging-reveals-axial-differences-in-metabolic-auto-fluorescence-signals-along-the-kidney-proximal-tubule
#12
Milica Bugarski, Joana Martins, Dominik Haenni, Andrew M Hall
Kidney proximal tubules (PTs) are densely packed with mitochondria, and defects in mitochondrial function are implicated in many kidney diseases. However, little is known about intrinsic mitochondrial function within PT cells. Here, using intravital multiphoton microscopy and live slices of mouse kidney cortex, we show that auto-fluorescence signals provide important functional readouts of redox state and substrate metabolism, and that there are striking axial differences in signals along the PT. Mitochondrial NAD(P)H intensity was similar in both S1 and S2 PT segments, and was sensitive to changes in respiratory chain (RC) redox state, while cytosolic NAD(P)H intensity was significantly higher in S2...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132347/electrically-stimulated-acupuncture-increases-renal-blood-flow-through-exosomes-carried-mir-181
#13
Zhen Su, Yanggang Yuan, Manshu Yu, Yan Liu, Janet D Klein, Xiaonan H Wang
Acupuncture with low frequency electrical stimulation (Acu/LFES) can prevent muscle atrophy by increasing muscle protein anabolism in mouse models of chronic kidney disease. During the treatment of muscle wasting, we found that Acu/LFES on the gastrocnemius muscle of the leg enhances renal blood flow. We also found that Acu/LFES increases exosome abundance and alters exosome-associated microRNA expression in the circulation. When exosome secretion was blocked using GW4869 the Acu/LFES-induced increase in renal blood flow was limited...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132346/deletion-of-the-formin-diaph1-protects-from-structural-and-functional-abnormalities-in-the-murine-diabetic-kidney
#14
Michaele B Manigrasso, Richard A Friedman, Ravichandran Ramasamy, Vivette D D'Agati, Ann Marie Schmidt
Diaphanous 1 (DIAPH1), a member of the formin family, binds to the cytoplasmic domain of the receptor for advanced glycation end products (RAGE) and is required for RAGE signal transduction. Experiments employing genetic over-expression or deletion of Ager (the gene encoding RAGE) or its pharmacological antagonism, implicate RAGE in the pathogenesis of diabetes-associated nephropathy. We hypothesized that DIAPH1 contributes to pathological and functional derangements in the kidneys of diabetic mice. Here, we show that DIAPH1 is expressed in the human and murine diabetic kidney, at least in part in the tubulointerstitium and glomerular epithelial cells, or podocytes...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132345/electrical-stimulation-of-the-pudendal-nerve-promotes-neuroregeneration-and-functional-recovery-from-stress-urinary-incontinence-in-a-rat-model
#15
Hai-Hong Jiang, Qi-Xiang Song, Bradley C Gill, Brian M Balog, Raul Juarez, Yolanda Cruz, Margot S Damaser
The pudendal nerve can be injured during vaginal delivery of children and slowed pudendal nerve regeneration has been correlated with development of stress urinary incontinence (SUI). Simultaneous injury to the pudendal nerve and its target muscle, the external urethral sphincter (EUS), during delivery likely leads to slowed neuroregeneration. The goal of this study was to determine if repeat electrical stimulation of the pudendal nerve improves SUI recovery and promotes neuroregeneration in a dual muscle and nerve injury rat model of SUI...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132344/down-regulation-of-microrna-429-contributes-to-angiotensin-ii-induced-profibrotic-effect-in-rat-kidney
#16
Zhengchao Wang, Qing Zhu, Weili Wang, Junping Hu, Pin-Lan Li, Fan Yi, Ningjun Li
MicroRNA (miR) 429 has been shown to inhibit epithelial-to-mesenchymal transition (EMT) in cancer cells. However, the role of miR429 in EMT in non-cancer cells has not been defined, especially in the kidneys. The present study determined whether miR429 participated in angiotensin (ANG) II-induced EMT and fibrogenesis in renal cells. In NRK-52E cells, a rat proximal tubular cell line, incubation of ANG II (10-9 M) for 24 h significantly reduced the level of miR429 by 60%, and meanwhile increased the protein levels of mesenchymal markers α-smooth muscle actin and fibroblast-specific protein-1 by 3 fold and decreased epithelial marker E-cadherin by 60%, which was blocked by Losartan, a AT1 receptor antagonist...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30132343/urine-inositol-pentakisphosphate-2-kinase-and-changes-in-kidney-structure-in-early-diabetic-kidney-disease-in-type-1-diabetes
#17
Helen C Looker, Michael L Merchant, Madhavi J Rane, Robert G Nelson, Paul L Kimmel, Brad H Rovin, Jon B Klein, Michael Mauer, Ckd Biomarkers Consortium
We examined the association of urine inositol pentakisphosphate 2-kinase (IPP2K) with the presence and progression of diabetic kidney disease (DKD) lesions. Urine IPP2K was measured at baseline by quantitative liquid chromatography mass spectrometry in 215 participants from the Renin-Angiotensin System Study who had type 1 diabetes and were normoalbuminuric and normotensive with normal or increased glomerular filtration rate (GFR). Urine IPP2K was detectable in 166 participants. Participants with IPP2K below the limit of quantification (LOQ) were assigned concentrations of LOQ/√2...
August 22, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30110573/why-until-just-now-undiscovered-uniqueness-of-the-human-glomerulus
#18
L Gabriel Navar, Owen Richfield
No abstract text is available yet for this article.
August 15, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30110572/superoxide-via-sp3-mechanism-increases-renal-renin-activity-renal-at1-receptor-function-and-blood-pressure-in-rats
#19
Mohammad Saleem, Xitao Wang, Indira Pokkunuri, Mohammad Asghar
We tested a hypothesis that superoxide, by inducing Sp3, increases renal renin activity, renal AT1 receptor (AT1R) function and blood pressure (BP) in rats. Group 1 rats were treated with vehicle, saline. Group 2 rats were treated with superoxide dismutase (SOD) inhibitor diethylthiocarbamate (DETC). Group 3 rats were treated with DETC and an SOD mimetic, tempol. Group 4 rats were treated with tempol only. All 4 groups of rats were treated for 2 weeks, anesthetized and BP recorded. Thereafter, diuresis and natriuresis in response to AT1R blocker candesartan were determined...
August 15, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/30110571/potassium-conservation-is-impaired-in-mice-with-reduced-renal-expression-of-kir4-1
#20
Sundeep Malik, Emily Lambert, Junhui Zhang, Tong Wang, Heather Clark, Michael Cypress, Bruce Goldman, George A Porter, Salvador Pena, Wilson Nino, Daniel Gray
To better understand the role of the inward-rectifying K channel, Kir4.1 (KCNJ10), in the distal nephron, we initially studied a global Kir4.1 knock out mouse (gKO) which demonstrated the hypokalemia and hypomagnesemia seen in SeSAME/EAST syndrome and was associated with reduced Na/Cl cotransporter (NCC) expression. Lethality by ~3 wks, however, limits the usefulness of this model, so we developed a kidney specific Kir4.1 "knock down" mouse (ksKD) using a cadherin 16 promoter and Cre-loxP methodology...
August 15, 2018: American Journal of Physiology. Renal Physiology
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