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American Journal of Physiology. Renal Physiology

Abdel A Alli, Ling Yu, Meaghan Rayann Holzworth, Jacob Richards, Kit-Yan Cheng, I Jeanette Lynch, Charles S Wingo, Michelle L Gumz
Circadian rhythms govern physiological functions and are important for overall health. The molecular circadian clock is comprised of several transcription factors that mediate circadian control of physiological function in part by regulating gene expression in a tissue-specific manner. These connections are well established but the underlying mechanisms are incompletely understood. The overall goal of this study was to examine the connection between the circadian clock protein Per1, ENaC, and BP using a multi-pronged approach...
February 13, 2019: American Journal of Physiology. Renal Physiology
Michael J Ryan, Jennifer C Sullivan
No abstract text is available yet for this article.
February 13, 2019: American Journal of Physiology. Renal Physiology
In O Sun, Lilach O Lerman
MicroRNAs (miRNAs) are small, noncoding single-stranded RNA oligonucleotides that modulate physiological and pathological processes by modulating target gene expression. Many miRNAs display tissue-specific expression patterns, the dysregulation of which has been associated with various disease states, including kidney disease. Mounting evidence implicates miRNAs in various biological processes, such as cell proliferation, differentiation, and cancer. Because miRNAs are relatively stable in tissue and biological fluids, particularly when carried by extracellular vesicles, changes in their levels may reflect development of human disease...
February 13, 2019: American Journal of Physiology. Renal Physiology
Matthew J Clarkson, Paul N Bennett, Steve F Fraser, Stuart Anthony Warmington
BACKGROUND: Patients with end stage kidney disease on dialysis have increased mortality and reduced physical activity contributing to impaired physical function. While exercise programmes have demonstrated a positive effect on physiological outcomes such as cardiovascular function and strength, there is a reduced focus on physical function. The aim of this review was to determine whether exercise programmes improve objective measures of physical function indicative of activities of daily living for end stage kidney disease patients on dialysis...
February 13, 2019: American Journal of Physiology. Renal Physiology
Marika Manolopoulou, Brittany K Matlock, Stellor Nlandu Khodo, Alan J Simmons, Ken S Lau, Melanie Phillips-Mignemi, Alla Ivanova, Catherine E Alford, David K Flaherty, Leslie S Gewin
Flow cytometry studies on injured kidney tubules are complicated by a low yield of nucleated single cells. Furthermore, cell-specific responses such as cell cycle dynamics in vivo has conventionally relied on indirect immunohistochemistry and proximal tubule markers that may be downregulated in injury. We report a new tissue dissociation protocol for kidney with an early fixation step that greatly enhances the yield of single cells. Genetic labeling of the proximal tubule with either the mT/mG "tomato" or the R26Fucci2aR (Fucci) cell cycle reporter mice allows us to follow proximal tubule-specific changes in cell cycle after renal injury...
February 13, 2019: American Journal of Physiology. Renal Physiology
Donald J Marsh, Dmitry D Postnov, Olga V Sosnovtseva, Niels-Henrik Holstein-Rathlou
Tubuloglomerular feedback and the myogenic mechanism form an ensemble in renal afferent arterioles that regulates single nephron blood flow and glomerular filtration. Each mechanism generates a self-sustained oscillation, the mechanisms interact, and the oscillations synchronize. The synchronization generates a bimodal electrical signal in the arteriolar wall that propagates retrograde to a vascular node where it meets similar electrical signals from other nephrons. Each signal carries information about the time dependent behavior of the regulatory ensemble...
February 13, 2019: American Journal of Physiology. Renal Physiology
Steven D Funk, Raymond H Bayer, Jeffrey H Miner
The glomerular basement membrane (GBM) is a critical component of the kidney's blood filtration barrier. Alport syndrome, a hereditary disease leading to kidney failure, is caused by the loss or dysfunction of the GBM's major type IV collagen (COL4) isoform, α3α4α5. The constituent COL4 achains assemble into heterotrimers in the endoplasmic reticulum prior to secretion into the extracellular space. If any one of the α3, α4, or α5 chains is lost due to mutation of one of the genes, then the entire heterotrimer is lost...
February 6, 2019: American Journal of Physiology. Renal Physiology
Ann-Christin Gnirck, Malte Wunderlich, Martina Becker, Tingting Xiong, Ella Weinert, Catherine Meyer-Schwesinger, Laure Dumoutier, Jean-Christophe Renauld, Samuel Huber, Ulf Panzer, Jan-Eric Turner
In recent years, the cytokine IL-22 attracted considerable attention due to its important immunoregulatory function in barrier tissues, such as the gut, lung and skin. While a regenerative role of IL-22 in renal tubular damage has been demonstrated, the role of IL-22 in the immunopathogenesis of glomerular injury is still unknown. Here, we demonstrate that the IL-22 receptor is expressed in the glomerular compartment of the kidney and that IL-22 expression increases in the renal cortex after induction of glomerular injury in a mouse model for crescentic glomerulonephritis (cGN, nephrotoxic nephritis)...
February 6, 2019: American Journal of Physiology. Renal Physiology
Kyle A Bauckman, Rina Matsuda, Cassandra B Higgins, Brian J DeBosch, Caihong Wang, Indira U Mysorekar
Iron is a critical nutrient required by hosts and pathogens. Uropathogenic Escherichia coli (UPEC), the principal causative agent of urinary tract infections (UTIs), chelate iron for their survival and persistence. Here, we demonstrate that dietary modulation of iron availability limits UPEC burden in a mouse model of UTI. Mice on a low iron diet exhibit reduced systemic and bladder mucosal iron availability, harbor significantly lower bacterial burden, concomitant with dampened inflammation. Hepcidin is a master regulator of iron that controls iron-dependent UPEC intracellular growth...
February 6, 2019: American Journal of Physiology. Renal Physiology
Elena Mironova, Faroug Suliman, James D Stockand
Stimulation of Gq-coupled metabotropic P2Y2 receptors decrease the activity of ENaC in renal principal cells of the distal nephron. The physiological consequences of disrupting P2Y2 receptor signaling in the P2Y2 receptor knockout mouse are decreased sodium excretion and increased arterial blood pressure. However, because of the global nature of this knockout model, the quantitative contribution of ENaC and the distal nephron versus that of upstream renal vascular and tubular elements to changes in urinary excretion and arterial blood pressure are obscure...
February 6, 2019: American Journal of Physiology. Renal Physiology
Rakel Nyrén, Elena Makoveichuk, Sandhya Malla, Sander Kersten, Stefan K Nilsson, Madelene Ericsson, Gunilla Olivecrona
Activity of lipoprotein lipase (LPL) is high in mouse kidney, but the reason is poorly understood. The aim was to characterize localization, regulation and function of LPL in kidney of C57BL/6J mice. We found LPL mainly in proximal tubules, localized inside the tubular epithelial cells, under all conditions studied. In fed mice some LPL colocalized with the endothelial markers CD31 and GPIHBP1, and could be removed by perfusion with heparin, indicating a vascular location. The role of angiopoietin-like protein 4 (ANGPTL4) for nutritional modulation of LPL activity was studied in wild-type and Angptl4-/- mice...
January 30, 2019: American Journal of Physiology. Renal Physiology
Wei Gong, Jiayu Song, Xi Chen, Shuzhen Li, Jing Yu, Weiwei Xia, Guixia Ding, Yue Zhang, Zhanjun Jia, Aihua Zhang, Songming Huang
Glomerular diseases are the leading causes of chronic kidney disease and mesangial cells (MCs) were demonstrated to be involved in the pathogenesis. Puromycin aminonucleoside (PAN) is a nephrotoxic drug that induced glomerular injury with elusive mechanisms. The present study is undertaken to investigate the role of PAN in MC apoptosis, as well as the underlying mechanism. Here we found that PAN induced MC apoptosis accompanied by the declined cell viability and enhanced inflammatory response. The apoptosis was further evidenced by the increments of BAX and Caspase-3 expression...
January 30, 2019: American Journal of Physiology. Renal Physiology
Richard A Zager, Ali Cm Johnson
P21, a cyclin kinase inhibitor, is acutely up-regulated during AKI and exerts cytoprotective effects. A proposed mechanism is oxidant stress- induced activation of p53, the dominant p21 transcription factor. Glycerol-induced rhabdomyolysis induces profound renal oxidant stress. Hence, we studied this AKI model to determine whether p53 activation corresponds with p21 gene induction, and/or whether alternative mechanism(s) might be involved. CD-1 mice were subjected to glycerol-induced AKI. Either 4 or 18 hrs later, plasma, urinary, and renal cortical p21 protein and mRNA levels were assessed...
January 30, 2019: American Journal of Physiology. Renal Physiology
Giuseppe Stefano Netti, Fabio Sangregorio, Federica Spadaccino, Francesco Staffieri, Antonio Crovace, Barbara Infante, Annamaria Maiorano, Giulia Godeas, Giuseppe Castellano, Anna Maria Di Palma, Clelia Prattichizzo, Antonella Cotoia, Lucia Mirabella, Loreto Gesualdo, Gilda Cinnella, Giovanni Stallone, Elena Ranieri, Giuseppe Grandaliano
LPS-induced sepsis is a leading cause of acute kidney injury (AKI) in critically ill patients. LPS may induce CD80 expression in podocytes with subsequent onset of proteinuria, a risk factor for progressive chronic kidney disease (CKD) frequently observed after AKI. This study aimed to investigate the therapeutic efficacy of LPS removal in decreasing albuminuria through the reduction of podocyte CD80 expression. Between January 2015 and December 2017, 70 consecutive patients with Gram-negative sepsis-induced AKI were randomised to either have Coupled Plasma Filtration and Adsorption (CPFA) added to the standard care (n=35) or not (n=35)...
January 23, 2019: American Journal of Physiology. Renal Physiology
Mari Watanabe, Yuji Oe, Emiko Sato, Akiyo Sekimoto, Hiroshi Sato, Sadayoshi Ito, Nobuyuki Takahashi
Acute kidney injury (AKI) is associated with hypercoagulability. Tissue factor/factor VIIa complex and factor Xa in the coagulation cascade activate protease-activated receptor 2 (PAR2). Previously, we have shown that PAR2-mediated inflammation aggravates kidney injury in models of diabetic kidney disease and adenine-induced renal fibrosis. However, the role of PAR2 in AKI remains unclear. In order to clarify the role of PAR2, we administered cisplatin, one of the most common causal factors of AKI, to wild-type and PAR2-deficient mice...
January 23, 2019: American Journal of Physiology. Renal Physiology
Yan Zhang, Shun Li, Todd Yecies, Tara Morgan, Haotian Cai, Natalie Pace, Bing Shen, Jicheng Wang, James R Roppolo, William C de Groat, Changfeng Tai
This study in α-chloralose anesthetized cats revealed a role of hypogastric nerve afferent axons in nociceptive bladder activity induced by bladder irritation using 0.25% acetic acid (AA). In cats with intact hypogastric and pelvic nerves, AA irritation significantly (p<0.05) reduced bladder capacity to 45.0±5.7% of the control capacity measured during a saline cystometrogram (CMG). In cats with the hypogastric nerves transected bilaterally, AA irritation also significantly (p<0.05) reduced bladder capacity but the change was significantly smaller (capacity reduced to 71...
January 23, 2019: American Journal of Physiology. Renal Physiology
Clintoria R Williams, Monisha Mistry, Aswathy Miriam Cheriyan, Jasmine M Williams, Meagan K Naraine, Carla L Ellis, Rickta Mallick, Abinash C Mistry, Jennifer L Gooch, Benjamin Ko, Hui Cai, Robert S Hoover
Zn2+ deficiency (ZnD) is a common comorbidity of many chronic diseases. In these settings, ZnD exacerbates hypertension. Whether ZnD alone is sufficient to alter blood pressure (BP) is unknown. To explore the role of Zn2+ in BP regulation, adult mice were fed a Zn2+ adequate (ZnA) or Zn2+ deficient (ZnD) diet. A subset of ZnD mice were either returned to a ZnA diet or administered hydrochlorothiazide (HCTZ), a sodium chloride cotransporter (NCC) inhibitor. To reduce intracellular Zn2+ in vitro, mouse distal convoluted tubule cells were cultured in TPEN (Zn2+ chelator)- or vehicle (DMSO)-containing medium...
January 16, 2019: American Journal of Physiology. Renal Physiology
John R Montford, Colin Bauer, Evgenia Dobrinskikh, Katharina Hopp, Moshe Levi, Mary Cm Weiser-Evans, Raphael A Nemenoff, Seth B Furgeson
In inflammatory diseases, the 5-lipoxygenase (5-LO) pathway contributes to epithelial damage and fibrosis by catalyzing the production of leukotrienes. Antagonists of the 5-LO pathway are currently approved for use in patients and are well tolerated. We found that expression of 5-LO is strongly induced in three models of chronic kidney disease, unilateral ureteral obstruction (UUO), folate nephropathy, and an orthologous mouse model of polycystic kidney disease. Immunohistochemistry showed that macrophages are the dominant source of 5-LO...
January 16, 2019: American Journal of Physiology. Renal Physiology
Min Tao, Yingfeng Shi, Lunxian Tang, Yi Wang, Lu Fang, Wei Jiang, Tao Lin, Andong Qiu, Shougang Zhuang, Na Liu
Extracellular signal-regulated kinases 1 and 2 (ERK1/2) are serine/threonine kinases and function as regulators of cellular proliferation and differentiation. Recently, we demonstrated that inhibition of ERK1/2 alleviates the development and progression of hyperuricemia nephropathy (HN). However, its potential roles in uric acid-induced tubular epithelial-mesenchymal transition (EMT) and tubular epithelial cell injury are unknown. In this study, we showed that hyperuricemic injury induced EMT as characterized by down-regulation of E-cadherin and up-regulation of Vimentin and Snail1 in a rat model of HN...
January 16, 2019: American Journal of Physiology. Renal Physiology
Stefanie Klinge, Karsten Yan, Daniel Reimers, Karen-Maria Brede, Joanna Schmid, Hans-Joachim Paust, Christian F Krebs, Ulf Panzer, Helmut Hopfer, Hans-Willi Mittrücker
Anti-glomerular basement membrane (anti-GBM) disease is characterized by antibodies and T cells directed against the Goodpasture antigen α3(IV)NC1 of the GBM. Consequences are the deposition of autoantibodies along the GBM and the development of crescentic glomerulonephritis (GN) with rapid loss of renal function. Foxp3+ regulatory T cells (Treg cells) are crucial for the maintenance of peripheral tolerance to self-antigens and the prevention of immunopathology. Here we use the mouse model of experimental autoimmune glomerulonephritis (EAG) to characterize the role of Treg cells in anti-GBM disease...
January 16, 2019: American Journal of Physiology. Renal Physiology
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