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Glomerular endothelial cell

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https://www.readbyqxmd.com/read/28647211/tubuloreticular-inclusions-in-peritubular-capillaries-of-renal-allografts
#1
Jee Youn Lee, Seung Hwan Song, Yu Seun Kim, Beom Jin Lim, Soon Il Kim, Myoung Soo Kim, Hyeon Joo Jeong
BACKGROUND: Tubuloreticular inclusions (TRIs) are anastomosing networks of microtubules that are frequently found in autoimmune diseases and viral infections. In renal allografts, TRIs have been reported in glomerular endothelial cells in association with viral infections and donor specific antibodies (DSAs), but their presence in peritubular capillaries has not been explored. METHODS: We collected seven cases with TRIs out of 148 consecutive renal allograft biopsies taken from Dec...
June 6, 2017: Pathology, Research and Practice
https://www.readbyqxmd.com/read/28617168/renalase-assessment-with-regard-to-kidney-function-lipid-disturbances-and-endothelial-dysfunction-parameters-in-stable-renal-transplant-recipients
#2
Dijana Stojanovic, Tatjana Cvetkovic, Miodrag Stojanovic, Nikola Stefanovic, Radmila Velickovic-Radovanovic, Natasa Zivkovic
BACKGROUND: Renal transplant dysfunction has been shown to be independent predictor for premature cardiovascular disease and mortality. Renalase, a flavoprotein secreted by several tissues, including the kidney, has been found to regulate sympathetic tone and blood pressure. The purpose of this secondary analysis was to explore relationships among parameters of endothelial dysfunction, lipids, glomerular filtration rate, and renalase in 2 groups: renal transplant patients with controlled hypertension and healthy volunteers...
June 2017: Progress in Transplantation
https://www.readbyqxmd.com/read/28587670/high-mobility-group-box-1-contributes-to-anti-myeloperoxidase-antibody-induced-glomerular-endothelial-cell-injury-through-a-moesin-dependent-route
#3
Hui Deng, Chen Wang, Dong-Yuan Chang, Nan Hu, Min Chen, Ming-Hui Zhao
BACKGROUND: Our previous study found that circulating and urinary levels of high mobility group box-1 (HMGB1) were closely associated with disease activity in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Moreover, HMGB1 participates in ANCA-induced neutrophil activation. Cross-reactivity between moesin and anti-myeloperoxidase (MPO) antibody has been reported in both human and mouse. The current study investigated whether HMGB1 participated in MPO-ANCA-induced glomerular endothelial cell (GEnC) injury, which is one of the most important aspects in the pathogenesis of AAV...
June 6, 2017: Arthritis Research & Therapy
https://www.readbyqxmd.com/read/28584258/cathepsin-s-inhibition-combines-control-of-systemic-and-peripheral-pathomechanisms-of-autoimmune-tissue-injury
#4
Maia Tato, Santhosh V Kumar, Yajuan Liu, Shrikant R Mulay, Solange Moll, Bastian Popper, Jonathan N Eberhard, Dana Thomasova, Arne Christian Rufer, Sabine Gruner, Wolfgang Haap, Guido Hartmann, Hans-Joachim Anders
Cathepsin(Cat)-S processing of the invariant chain-MHC-II complex inside antigen presenting cells is a central pathomechanism of autoimmune-diseases. Additionally, Cat-S is released by activated-myeloid cells and was recently described to activate protease-activated-receptor-(PAR)-2 in extracellular compartments. We hypothesized that Cat-S blockade targets both mechanisms and elicits synergistic therapeutic effects on autoimmune tissue injury. MRL-(Fas)lpr mice with spontaneous autoimmune tissue injury were treated with different doses of Cat-S inhibitor RO5459072, mycophenolate mofetil or vehicle...
June 5, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28584011/regulatory-t-cell-augmentation-or-interleukin-17-inhibition-prevents-calcineurin-inhibitor-induced-hypertension-in-mice
#5
Valorie L Chiasson, Abhinandan R Pakanati, Marcos Hernandez, Kristina J Young, Kelsey R Bounds, Brett M Mitchell
The immunosuppressive calcineurin inhibitors cyclosporine A and tacrolimus alter T-cell subsets and can cause hypertension, vascular dysfunction, and renal toxicity. We and others have reported that cyclosporine A and tacrolimus decrease anti-inflammatory regulatory T cells and increase proinflammatory interleukin-17-producing T cells; therefore, we hypothesized that inhibition of these effects using noncellular therapies would prevent the hypertension, endothelial dysfunction, and renal glomerular injury induced by calcineurin inhibitor therapy...
June 5, 2017: Hypertension
https://www.readbyqxmd.com/read/28579836/update-on-the-renal-toxicity-of-iodinated-contrast-drugs-used-in-clinical-medicine
#6
REVIEW
Michele Andreucci, Teresa Faga, Raffaele Serra, Giovambattista De Sarro, Ashour Michael
An important side effect of diagnostic contrast drugs is contrast-induced acute kidney injury (CI-AKI; a sudden decrease in renal function) occurring 48-72 hours after injection of a contrast drug that cannot be attributed to other causes. Its existence has recently been challenged, because of some retrospective studies in which the incidence of AKI was not different between subjects who received a contrast drug and those who did not, even using propensity score matching to prevent selection bias. For some authors, only patients with estimated glomerular filtration rate <30 mL/min/1...
2017: Drug, Healthcare and Patient Safety
https://www.readbyqxmd.com/read/28574576/vegf-a165-b-protects-against-proteinuria-in-a-mouse-model-with-progressive-depletion-of-all-endogenous-vegf-a-splice-isoforms-from-the-kidney
#7
Megan Stevens, Christopher R Neal, Andrew Hj Salmon, David O Bates, Steven J Harper, Sebastian Oltean
Chronic kidney disease (CKD) is strongly associated with a decrease in the expression of VEGF-A. However, little is known about the contribution of VEGF-A splice isoforms to kidney physiology and pathology. Previous studies suggest that the splice isoform VEGF-A165 b (resulting from alternative usage of a 3' splice site in the terminal exon) is protective for kidney function. We show here, in a quad-transgenic model, that over-expression of VEGF-A165 b alone is sufficient to rescue the increase in proteinuria as well as glomerular water permeability in the context of progressive depletion of all VEGF-A isoforms from the podocytes...
June 2, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28573487/low-vascularization-of-the-nephrogenic-zone-of-the-fetal-kidney-suggests-a-major-role-for-hypoxia-in-human-nephrogenesis
#8
C Gerosa, D Fanni, A Faa, P Van Eyken, A Ravarino, V Fanos, G Faa
CD31 reactivity is generally utilized as a marker of endothelial cells. CD31 immunoreactivity in the developing human kidney revealed that fetal glomerular capillary endothelial cells change their immunohistochemical phenotype during maturation. The aim of this study was to analyze CD31 reactivity in the fetal human kidney in the different stages of intrauterine development: We observed different distribution of CD31-reactive vascular progenitors in the different areas of the developing kidney. In particular, the nephrogenic zone and the renal capsule were characterized by a scarcity of CD31-reactive cells at all gestational ages...
June 1, 2017: International Urology and Nephrology
https://www.readbyqxmd.com/read/28542220/expression-of-receptor-type-protein-tyrosine-phosphatase-in-developing-and-adult-renal-vasculature
#9
Keiko Takahashi, Rachel Kim, Colette Lauhan, Yuna Park, Nghiep G Nguyen, Dietmar Vestweber, Melissa G Dominguez, David M Valenzuela, Andrew J Murphy, George D Yancopoulos, Nicholas W Gale, Takamune Takahashi
Renal vascular development is a coordinated process that requires ordered endothelial cell proliferation, migration, intercellular adhesion, and morphogenesis. In recent decades, studies have defined the pivotal role of endothelial receptor tyrosine kinases (RPTKs) in the development and maintenance of renal vasculature. However, the expression and the role of receptor tyrosine phosphatases (RPTPs) in renal endothelium are poorly understood, though coupled and counterbalancing roles of RPTKs and RPTPs are well defined in other systems...
2017: PloS One
https://www.readbyqxmd.com/read/28536464/the-protective-effect-of-human-renal-sinus-fat-on-glomerular-cells-is-reversed-by-the-hepatokine-fetuin-a
#10
R Wagner, J Machann, M Guthoff, P P Nawroth, S Nadalin, M A Saleem, N Heyne, A Königsrainer, F Fend, F Schick, A Fritsche, N Stefan, H-U Häring, E Schleicher, D I Siegel-Axel
Renal sinus fat (RSF) is a perivascular fat compartment located around renal arteries. In this in vitro and in vivo study we hypothesized that the hepatokine fetuin-A may impair renal function in non alcoholic fatty liver disease (NAFLD) by altering inflammatory signalling in RSF. To study effects of the crosstalk between fetuin-A, RSF and kidney, human renal sinus fat cells (RSFC) were isolated and cocultured with human endothelial cells (EC) or podocytes (PO). RSFC caused downregulation of proinflammatory and upregulation of regenerative factors in cocultured EC and PO, indicating a protective influence of RFSC...
May 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28535204/colocalization-of-receptors-for-shiga-toxins-with-lipid-rafts-in-primary-human-renal-glomerular-endothelial-cells-and-influence-of-d-pdmp-on-synthesis-and-distribution-of-glycosphingolipid-receptors
#11
Nadine Legros, Gottfried Pohlentz, Jana Runde, Stefanie Dusny, Hans-Ulrich Humpf, Helge Karch, Johannes Müthing
Damage of human renal glomerular endothelial cells (HRGECs) of the kidney represents the linchpin in the pathogenesis of the hemolytic uremic syndrome (HUS) caused by Shiga toxins (Stxs) of enterohemorrhagic Escherichia coli (EHEC). We performed a comprehensive structural analysis of the Stx receptor glycosphingolipids (GSLs) globotriaosylceramide (Gb3Cer, Galα4alβ4Glcβ1Cer) and globotetraosylceramide (Gb4Cer, GalNAcβ3Galα4Galβ4Glcβ1Cer) and their distribution in lipid raft analogue detergent-resistant membranes (DRMs) and nonDRMs prepared from primary HRGECs...
May 23, 2017: Glycobiology
https://www.readbyqxmd.com/read/28509120/complex-glomerular-pathology-of-thrombotic-microangiopathy-and-focal-segmental-glomerulosclerosis-forms-tumor-like-mass-in-a-renal-transplant-donor-with-severe-renovascular-hypertension
#12
Michio Nagata, Yutaka Yamaguchi, Daisuke Toki, Izumi Yamamoto, Hiroaki Shinmura, Hiroshi Kawaguchi
The pathogenesis of glomerular hypertension-mediated FSGS and its histological variations in humans remains unknown. A 47-year-old man developed nephrotic syndrome, renal dysfunction, and malignant hypertension 2 years after donating a kidney to his son. The donor's remnant kidney developed renal mass at an upper pole which was fed by an aberrant artery that branched from the root of the renal artery. Furthermore, the main non-aberrant renal artery demonstrated severe stenosis that caused renovascular hypertension, resulting in malignant hypertension...
May 2017: CEN Case Reports
https://www.readbyqxmd.com/read/28508970/glomerulopathy-with-distinctive-fibrillar-deposits-but-lacking-glomerular-deposition-of-type-iii-collagen
#13
Tatsuo Yamamoto, Akashi Togawa, Masanobu Eguchi, Naro Ohashi, Hideo Yasuda, Yutaka Harita, Motoshi Hattori, Yutaka Yamaguchi, Kunio Ohyama
A 62-year-old woman with nephrotic syndrome underwent a renal biopsy. Under light microscopy, the biopsy findings included lobulation and enlargement of glomeruli, occasional thickening of glomerular capillary walls, and narrowing of the capillary lumen by swollen endothelial cells. Congo red staining was negative for amyloid. No significant intraglomerular fibrin deposition was found by phosphotungstic acid hematoxylin staining. Immunofluorescence microscopy showed no deposition of immunoglobulin G, A, or M; no κ or λ light chains; and no C3 or C1q...
November 2016: CEN Case Reports
https://www.readbyqxmd.com/read/28495931/neutrophil-extracellular-traps-drive-endothelial-to-mesenchymal-transition
#14
Elmar Pieterse, Nils Rother, Marjolein Garsen, Julia Hofstra, Simon Satchell, Markus Hoffmann, Markus Loeven, Hanneke Knaapen, Olivier van der Heijden, Jo Berden, Luuk Hilbrands, Johan van der Vlag
OBJECTIVE: An excessive release and impaired degradation of neutrophil extracellular traps (NETs) leads to the continuous exposure of NETs to the endothelium in a variety of hematologic and autoimmune disorders, including lupus nephritis. This study aims to unravel the mechanisms through which NETs jeopardize vascular integrity. APPROACH AND RESULTS: Microvascular and macrovascular endothelial cells were exposed to NETs, and subsequent effects on endothelial integrity and function were determined in vitro and in vivo...
May 11, 2017: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28476555/the-third-path-of-tubulointerstitial-fibrosis-aberrant-endothelial-secretome
#15
REVIEW
Mark Lipphardt, Jong W Song, Kei Matsumoto, Sina Dadafarin, Hassan Dihazi, Gerhard Müller, Michael S Goligorsky
The secretome, defined as a portion of proteins secreted by specific cells to the extracellular space, secures a proper microenvironmental niche not only for the donor cells, but also for the neighboring cells, thus maintaining tissue homeostasis. Communication via secretory products exists between endothelial cells and fibroblasts, and this local mechanism maintains the viability and density of each compartment. Endothelial dysfunction, apart from obvious cell-autonomous defects, leads to the aberrant secretome, which predisposes fibroblasts to acquire a myofibroblastic fibrogenic phenotype...
May 2, 2017: Kidney International
https://www.readbyqxmd.com/read/28435991/polycythemia-capillary-rarefaction-and-focal-glomerulosclerosis-in-two-adolescents-born-extremely-low-birth-weight-and-premature
#16
Nariaki Asada, Takanori Tsukahara, Megumi Furuhata, Daisuke Matsuoka, Shunsuke Noda, Kuniaki Naganuma, Akinori Hashiguchi, Midori Awazu
BACKGROUND: Low birthweight infants have a reduced number of nephrons and are at high risk of chronic kidney disease. Preterm birth and/or intrauterine growth restriction (IUGR) may also affect peritubular capillary development, as has been shown in other organs. CASE-DIAGNOSIS/TREATMENT: We report two patients with a history of preterm birth and extremely low birthweight who showed polycythemia and renal capillary rarefaction. Patient 1 and 2, born at 25 weeks of gestation with a birthweight of 728 and 466 g, showed mild proteinuria at age 8 and 6 years, respectively...
April 24, 2017: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
https://www.readbyqxmd.com/read/28432469/renal-findings-in-patients-with-mulibrey-nanism
#17
Johanna Sivunen, Susann Karlberg, Jouko Lohi, Niklas Karlberg, Marita Lipsanen-Nyman, Hannu Jalanko
BACKGROUND: Mulibrey nanism (MUL) is a rare inherited disease caused by genetic defects affecting peroxisomal TRIM37 protein. MUL affects multiple organs, leading to growth retardation and early onset type 2 diabetes. We aimed to characterize the structure and function of kidneys and the urinary tract in a large cohort of Finnish MUL patients. METHODS: Ultrasound, magnetic resonance imaging (MRI), and autopsy findings of the kidneys and urinary tract from 101 MUL patients were retrospectively analyzed...
April 22, 2017: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
https://www.readbyqxmd.com/read/28418422/a-disease-model-of-diabetic-nephropathy-in-a-glomerulus-on-a-chip-microdevice
#18
Li Wang, Tingting Tao, Wentao Su, Hao Yu, Yue Yu, Jianhua Qin
Diabetic nephropathy is a major chronic renal complication of diabetes mellitus, and is the leading cause of end-stage kidney diseases. Establishing a disease model of diabetic nephropathy in vitro can accelerate the understanding of its mechanisms and pharmaceutical development. We provide the proof-of-principle for using a glomerulus-on-a-chip microdevice that reconstitutes organ-level kidney functions to create a human disease model of early stage diabetic nephropathy on chip. The microfluidic device, which recapitulates the glomerular microenvironment, consists of parallel channels lined by isolated primary glomerular microtissues that experience fluid flow to mimic the glomerular filtration barrier (GFB), including glomerular endothelial cells, 3D basement membrane and podocytes...
April 18, 2017: Lab on a Chip
https://www.readbyqxmd.com/read/28414198/ly333531-a-pkc%C3%AE-inhibitor-attenuates-glomerular-endothelial-cell-apoptosis-in-the-early-stage-of-mouse-diabetic-nephropathy-via-down-regulating-swiprosin-1
#19
Zhi-Bin Wang, Su Zhang, Ya Li, Rong-Mei Wang, Ling-Chang Tong, Yue Wang, Wei-Ye Liu, Ding-Feng Su, Ye Tu, Li-Chao Zhang, Ling Li
Glomerular endothelial cell (GEC) injury plays an important role in the early stage of diabetic nephropathy (DN). Previous studies show that a PKCβ inhibitor is effective for treating DN. In the current study we further explored the effects and molecular mechanisms of PKCβ inhibitors on GEC apoptosis in DN in streptozotocin-induced diabetic mice in vivo and high glucose- or PMA-treated human renal glomerular endothelial cells (HRGECs) in vitro. In the diabetic mice, hyperglycemia caused aggravated nephropathy and GEC apoptosis accompanied by significantly increased expression of swiprosin-1, a potentally pro-apoptotic protein...
April 17, 2017: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/28404593/physiopathological-implications-of-p2x1-and-p2x7-receptors-in-regulation-of-glomerular-hemodynamics-in-angiotensin-ii-induced-hypertension
#20
Martha Franco, Rocio Bautista-Pérez, Agustina Cano-Martínez, Ursino Pacheco, José Santamaría, Leonardo Del Valle-Mondragón, Oscar Pérez-Méndez, L Gabriel Navar
Deleterious effects of purinergic P2X1 and P2X7 receptors (P2XR) in angiotensin II (AngII)-dependent hypertension include increased renal vascular resistance, and impaired autoregulation and pressure natriuresis. However, their specific effects on the determinants of glomerular hemodynamics remain incompletely delineated. To investigate the P2XR contributions to altered glomerular hemodynamics in hypertension, the effects of acute blockade of P2X1R, P2X7R and P2X4R with NF449, A438079 and PSB12054 respectively, were evaluated in AngII-infused rats (435 ng/kg/min)...
April 12, 2017: American Journal of Physiology. Renal Physiology
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