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American Journal of Physiology. Renal Physiology

Vineet Gupta, Jochen Reiser
October 19, 2016: American Journal of Physiology. Renal Physiology
Olga Ruiz-Andres, Maria Dolores Sanchez-Niño, Juan Antonio Moreno, Marta Ruiz-Ortega, Adrian Mario Ramos, Ana Belén Sanz, Alberto Ortiz
Chronic kidney disease (CKD) is associated to an increased risk of death, CKD progression and acute kidney injury (AKI) even from early stages, when glomerular filtration rate (GFR) is preserved. The link between early CKD and these risks is unclear, since there is no accumulation of uremic toxins. However, pathological albuminuria and kidney inflammation are frequent features of early CKD and the production of kidney protective factors may be decreased. Indeed, Klotho expression is already decreased in CKD category G1 (normal GFR)...
October 19, 2016: American Journal of Physiology. Renal Physiology
Hyun Jun Jung, Tae-Hwan Kwon
Kidney collecting duct is an important renal tubular segment for regulation of body water homeostasis and urine concentration. Water reabsorption in the collecting duct principal cells is controlled by vasopressin, a peptide hormone which induces the osmotic water transport across the collecting duct epithelia through regulation of water channel proteins aquaporin-2 (AQP2) and aquaporin-3 (AQP3). In particular, vasopressin induces both intracellular translocation of AQP2-bearing vesicles to the apical plasma membrane and transcription of Aqp2 gene to increase AQP2 protein abundance...
October 19, 2016: American Journal of Physiology. Renal Physiology
Birong Li, Babitha Haridas, Ashley R Jackson, Hanna Cortado, Nicholas Mayne, Rebecca Kohnken, Brad Bolon, Kirk M McHugh, Andrew L Schwaderer, John D Spencer, Christina B Ching, David S Hains, Sheryl S Justice, Santiago Partida-Sanchez, Brian Becknell
Acquired renal scarring occurs in a subset of patients following febrile urinary tract infections and is associated with hypertension, proteinuria, and chronic kidney disease. Limited knowledge of histopathology, immune cell recruitment and gene expression changes during pyelonephritis restricts the development of therapies to limit renal scarring. Here, we address this knowledge gap using immunocompetent mice with vesicoureteral reflux. Transurethral inoculation of uropathogenic Escherichia coli in C3H/HeOuJ mice leads to renal mucosal injury, tubulointerstitial nephritis, and cortical fibrosis...
October 19, 2016: American Journal of Physiology. Renal Physiology
Eugen Widmeier, Weizhen Tan, Merlin Airik, Friedhelm Hildebrandt
INTRODUCTION: Steroid-resistant nephrotic syndrome (SRNS) inevitably progresses to end-stage kidney disease, requiring dialysis or transplantation for survival. However, treatment modalities and drug discovery remain limited. Mutations in over 30 genes have been discovered as monogenic causes of SRNS. Most of these genes are predominantly expressed in the glomerular epithelial cell, the podocyte, placing it at the center of the pathogenesis of SRNS. Podocyte migration rate (PMR) represents a relevant intermediate phenotype of disease in monogenic causes of SRNS...
October 19, 2016: American Journal of Physiology. Renal Physiology
Fahmy A Mamuya, Jose Luis Cano-Peñalver, Wei U Li, Diego Rodriguez-Puyol, Manuel Rodríguez-Puyol, Dennis Brown, Sergio de Frutos, Hua Jenny Lu
Within the past decade tremendous efforts have been made to understand the mechanism behind aquaporin-2 (AQP2) water channel trafficking and recycling, in order to open a path towards effective diabetes insipidus therapeutics. A recent study has shown that Integrin-Linked Kinase (ILK) conditional-knockdown mice developed polyuria along with decreased expression of AQP2. To understand whether ILK also regulates AQP2 trafficking in kidney tubular cells, we performed in vitro analysis using LLCPK1 cells stably expressing rat AQP2 (LLC-AQP2 cells)...
October 19, 2016: American Journal of Physiology. Renal Physiology
Futoshi Matsui, Stephen Babitz, Audrey Rhee, Karen L Hile, Hongji Zhang, Kirstan Kathleen Meldrum
STAT3 is a transcription factor implicated in renal fibrotic injury, but the role of STAT3 in mesenchymal stem cell (MSC)-induced renoprotection during renal fibrosis remains unknown. We hypothesized that MSCs protect against obstruction-induced renal fibrosis by downregulating STAT3 activation and STAT3-induced matrix metalloproteinase 9 (MMP-9) expression. Male Sprague-Dawley rats underwent renal arterial injection of vehicle or MSCs (1 x 106 per rat) immediately prior to sham operation or induction of unilateral ureteral obstruction (UUO)...
October 19, 2016: American Journal of Physiology. Renal Physiology
Steven J Kleene, Nancy K Kleene
Autosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening monogenic renal disease. ADPKD results from mutations in either of two proteins: polycystin-1 (also known as PC1 or PKD1) or transient receptor potential cation channel, subfamily P, member 2 (TRPP2, also known as polycystin-2, PC2, or PKD2). Each of these proteins is expressed in the primary cilium that extends from many renal epithelial cells. Existing evidence suggests that the cilium can promote renal cystogenesis, while PC1 and TRPP2 counter this cystogenic effect...
October 19, 2016: American Journal of Physiology. Renal Physiology
Grazyna Nowak, Diana Takacsova Bakajsova, Judit Megyesi
Previously, we documented that activation of protein kinase C-ε (PKC-ε) mediates mitochondrial dysfunction in cultured renal proximal tubule cells (RPTC). This study tested whether deletion of the PKC-ε decreases dysfunction of renal cortical mitochondria and improves kidney function after renal ischemia. PKC-ε levels in mitochondria of ischemic kidneys increased 24h after ischemia. Complex I- and complex II-coupled state 3 respirations were reduced 44% and 27%, respectively, in wild-type (WT) but unchanged and increased in PKC-ε-deficient (KO) mice after ischemia...
October 19, 2016: American Journal of Physiology. Renal Physiology
Oleg Palygin, Daria V Ilatovskaya, Alexander Staruschenko
Protease-activated receptors (PARs) are a well-known family of transmembrane G-protein-coupled receptors (GPCRs). To date, four PARs have been identified and PAR1 and PAR2 are the most abundant receptors, which were shown to be expressed in the kidney vascular and tubular cells. PAR signaling is mediated by an N-terminus tethered ligands that can be unmasked by serine protease cleavage. PARs are activated by endogenous serine proteases, such as thrombin (acts on PARs 1, 3 and 4) and trypsin (PAR2). PARs can be involved in glomerular, microvascular and inflammatory regulation of renal function in both normal and pathological conditions...
October 12, 2016: American Journal of Physiology. Renal Physiology
Kevin D Burns, Yuliya Lytvyn, Farid H Mahmud, Denis Daneman, Livia Deda, David B Dunger, John E Deanfield, R Neil Dalton, Yesmino Elia, Ronnie Har, Julie A D Van, Timothy J Bradley, Cameron Slorach, Wei Hui, Fengxia Xiao, Joseph Zimpelmann, Luc Mertens, Rahim Moineddin, Heather N Reich, Etienne B Sochett, James W Scholey, David Z I Cherney
AIMS: The relationship between the renal renin-angiotensin aldosterone system (RAAS) and cardiorenal pathophysiology is unclear. Our aims were to assess (1) levels of urinary RAAS components and (2) the association between RAAS components and HbA1c, urine albumin/creatinine ratio (ACR), estimated glomerular filtration rate (eGFR) and blood pressure in otherwise healthy adolescents with type 1 diabetes mellitus (TID) vs. healthy controls (HC). METHODS: Urinary angiotensinogen and ACE2 levels, activity of ACE and ACE2, blood pressure (BP), HbA1c, ACR and eGFR were measured in 65 HC and 194 T1D from the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial (AdDIT)...
October 12, 2016: American Journal of Physiology. Renal Physiology
Søren Brandt Poulsen, Birgitte M Christensen
Renal Na+-Cl- cotransporter (NCC) is expressed in early distal convoluted tubule (DCT) 1 and late DCT (DCT2). NCC activity can be stimulated by aldosterone, and the mechanism is assumed to depend on the enzyme, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which inactivates glucocorticoids that would otherwise occupy aldosterone receptors. Because 11β-HSD2 in rat may only be abundantly expressed in DCT2 cells and not in DCT1 cells, it has been speculated that aldosterone specifically stimulates NCC activity in DCT2 cells...
October 12, 2016: American Journal of Physiology. Renal Physiology
Mi Suk Lee, Hyo-Jung Choi, Eui-Jung Park, Hye-Jeong Park, Tae-Hwan Kwon
Carboxyl-terminus of AQP2 (AQP2c) undergoes post-translational modifications, including phosphorylation and ubiquitination, for the regulation of aquaporin-2 (AQP2) translocation and protein abundance. We aimed to identify novel proteins interacting with AQP2c. Recombinant AQP2c protein was made in E. coli BL21 (DE3) by exploiting the pET32 TrxA fusion system. Lysates of rat kidney inner medullary collecting duct (IMCD) tubule suspensions interacted with rat AQP2c bound to Ni(2+)-resin were subjected to LC-MS/MS proteomic analysis...
October 12, 2016: American Journal of Physiology. Renal Physiology
Mark R Hanudel, Kristine Chua, Maxime Rappaport, Victoria Gabayan, Erika Valore, David Goltzman, Tomas Ganz, Elizabeta Nemeth, Isidro B Salusky
In the setting of normal kidney function, iron deficiency is associated with increased FGF23 production and cleavage, altering circulating FGF23 levels. Our objective was to determine how chronic kidney disease (CKD) and dietary iron intake affect FGF23 production and metabolism in wild type (WT) and hepcidin knockout (HKO) mice. For eight weeks, the mice were fed diets that contained adenine (to induce CKD) or no adenine (control group), with either low iron (4 ppm) or standard iron (335 ppm) concentrations...
October 12, 2016: American Journal of Physiology. Renal Physiology
Yang Gao, Deborah Stuart, Jennifer S Pollock, Takamune Takahashi, Donald E Kohan
Nitric oxide (NO) inhibits collecting duct (CD) Na+ and water reabsorption. Mice with CD-specific knockout (KO) of NO synthase 1 (NOS1) have salt-sensitive hypertension. In contrast, the role of NOS3 in CD salt and water reabsorption is unknown. Mice with CD NOS3 KO were generated with loxP-flanked exons 9-12 (encodes the calmodulin binding site) of the NOS3 gene and the aquaporin-2 promoter-Cre transgene. There were no differences between control and CD NOS3 KO mice, irrespective of sex, in food intake, water intake, urine volume, urinary Na+ or K+ excretion, plasma renin concentration, blood pressure or pulse during 7 days of normal (0...
October 5, 2016: American Journal of Physiology. Renal Physiology
Belinda Spoto, Anna Pisano, Carmine Zoccali
Insulin resistance (IR) is an early metabolic alteration in CKD patients, being apparent when the glomerular filtration rate is still within the normal range and becoming almost universal in those who reach the ESKF. The skeletal muscle represents the primary site of IR in CKD and post-receptor alterations are recognized as the main defect underlying IR in this condition. Estimates of IR based on fasting insulin concentration are easier but may not be adequate in CKD patients because renal insufficiency reduces insulin catabolism...
October 5, 2016: American Journal of Physiology. Renal Physiology
Anita T Layton, Kamel Laghmani, Volker Vallon, Aurélie Edwards
Sodium and its associated anions are the major determinant of extracellular fluid volume, and renal Na+ reabsorption plays a crucial role in long-term blood pressure control. The goal of this study was to investigate the extent to which inhibitors of transepithelial Na$^+$ transport (T$_{\rm Na}$) along the nephron alter urinary solute excretion and T$_{\rm Na}$ efficiency, and how those effects may vary along different nephron segments. We used the multi-nephron model developed in the companion study [28], which represents detailed transcellular and paracellular transport processes along the nephrons of a rat kidney...
October 5, 2016: American Journal of Physiology. Renal Physiology
Anita T Layton, Volker Vallon, Aurélie Edwards
The goal of this study was to investigate water and solute transport, with a focus on sodium transport (T$_{\rm Na}$) and metabolism along individual nephron segments under differing physiological and pathophysiological conditions. To accomplish this goal, we developed a computational model of solute transport and oxygen consumption (Q$_{\rm O2}$) along different nephron populations of a rat kidney. The model represents detailed epithelial and paracellular transport processes along both the superficial and juxtamedullary nephrons, with the loop of Henle of each model nephron extending to differing depths of the inner medulla...
October 5, 2016: American Journal of Physiology. Renal Physiology
Robyn F R Letts, Xiao-Yue Zhai, Charita Bhikha, Birgitte L Grann, Nicklas B Blom, Jesper Skovhus Thomsen, David M Rubin, Erik Christensen, Arne Andreasen
The aim was to quantify the glomerular capillary surface area, the segmental tubular radius, length, and area of single nephrons in mouse and rat kidneys. Multiple 2.5-µm-thick serial Epon sections were obtained from three mouse and three rat kidneys for three-dimensional reconstruction of the nephron tubules. Micrographs were aligned for each kidney, and 359 nephrons were traced and their segments localized. 30 mouse and 30 rat nephrons were selected for further investigation. The luminal radius of each segment was determined by two methods...
October 5, 2016: American Journal of Physiology. Renal Physiology
Crystal A West, Jennifer M Sasser, Chris Baylis
Pregnancy is characterized by avid renal sodium retention and plasma volume expansion in the presence of decreased blood pressure. Decreased maternal blood pressure is a consequence of reduced systemic vascular tone which results from an increased production of vasodilators (nitric oxide (NO), prostaglandins, and relaxin) and decreased vascular responsiveness to the potent vasoconstrictor (angiotensin II (Ang II)). The kidneys participate in this vasodilatory response resulting in marked increases in renal plasma flow and glomerular filtration rate (GFR) during pregnancy...
October 5, 2016: American Journal of Physiology. Renal Physiology
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