Relevant bibliographies by topics / Tubular epithelial cell

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  2. Dissertations / Theses
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Academic literature on the topic 'Tubular epithelial cell'

Author: Grafiati
Published: 5 April 2025

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Journal articles on the topic "Tubular epithelial cell"

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Oberley, T. D., A. H. Yang, and J. Gould-Kostka. "Selection of kidney cell types in primary glomerular explant outgrowths by in vitro culture conditions." Journal of Cell Science 84, no. 1 (August 1, 1986): 69–92. http://dx.doi.org/10.1242/jcs.84.1.69.

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Adult guinea pig glomeruli were grown in vitro either in serum or in a chemically defined medium. Glomeruli were plated either directly into plastic flasks or into plastic flasks that had been coated with the extracellular matrix produced by the PF-HR-9 mouse teratocarcinoma endodermal cell line. Both the composition of the medium and the nature of the culture substrate affected whole glomerular attachment and the type of cells produced in culture. Quantitative studies demonstrated selection of cell types by different culture conditions. Three colony types, each composed of distinctive cell types, could be identified by morphological features. The cells constituting two of these colony types were epithelial in nature, but they were identified as different epithelial types by both histochemical and ultrastructural criteria. Previous studies suggested that one epithelial cell type was derived from the glomerular visceral epithelial cell. This study demonstrates that this cell type could be selectively grown in defined medium on plastic. A second cell type showed several features of renal tubular epithelial cells, including histochemical staining for catalase, cell surface microvilli and cilia, and formation of hemicysts and structures that resembled tubules after prolonged periods in culture. To demonstrate that the ‘glomerulus-derived’ tubular cells were indeed tubular epithelium, we isolated purified renal cortical tubules (greater than 99% pure) and cultured them on the HR-9 matrix in a serum-free chemically defined medium. The resultant outgrowths had morphological properties identical to those of the glomerulus-derived tubular cells. It seems likely that small tubular fragments attached to a minority of the glomeruli are the source of these glomerulus-derived tubular cells. Neither epithelial cell type could be subcultured on plastic, but both could be passaged on the HR-9 matrix. A third cell type, the spindle-shaped cell, was easily propagated on both plastic and the HR-9 matrix. The origin of this cell type is not clear. Our results demonstrate the important effect of culture conditions on the selection, growth and differentiation of kidney cell types in vitro.
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Liu, Lele, Yuanjun Deng, Yang Cai, Pingfan Lu, Yiyan Guo, Chunjiang Zhang, Qian Li, Tianjing Zhang, Min Han, and Gang Xu. "Ablation of Gsa impairs renal tubule proliferation after injury via CDK2/cyclin E." American Journal of Physiology-Renal Physiology 318, no. 3 (March 1, 2020): F793—F803. http://dx.doi.org/10.1152/ajprenal.00367.2019.

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Acute kidney injury has a high global morbidity associated with an increased risk of death and chronic kidney disease. Renal tubular epithelial cell regeneration following injury may be a decisive factor in renal repair or the progression of acute kidney injury to chronic kidney disease, but the underlying mechanism of abnormal renal tubular repair remains unclear. In the present study, we investigated the role of heterotrimeric G stimulatory protein α-subunit (Gsa) in renal tubular epithelial cell regeneration. We generated renal tubule epithelium-specific Gsa knockout (GsaKspKO) mice to show the essential role of Gsa in renal tubular epithelial cell regeneration in two AKI models: acute aristolochic acid nephropathy (AAN) and unilateral ischemia-reperfusion injury (UIRI). GsaKspKO mice developed more severe renal impairment after AAN and UIRI, higher serum creatinine levels, and more substantial tubular necrosis than wild-type mice. More importantly, Gsa inactivation impaired renal tubular epithelial cell proliferation by reducing bromodeoxyuridine+ cell numbers in the AAN model and inhibiting cyclin-dependent kinase 2/cyclin E1 expression in the UIRI model. This reduced proliferation was further supported in vitro with Gsa-targeting siRNA. Downregulation of Gsa inhibited tubular epithelial cell proliferation in HK-2 and mIMCD-3 cells. Furthermore, Gsa downregulation inhibited cyclin-dependent kinase 2/cyclin E1 expression, which was dependent on the Raf-MEK-ERK signaling pathway. In conclusion, Gsa is required for tubular epithelial cell regeneration during kidney repair after AKI. Loss of Gsa impairs renal tubular epithelial cell regeneration by blocking the Raf-MEK-ERK pathway.
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Breda, Philippe Christophe, Thorsten Wiech, Catherine Meyer-Schwesinger, Florian Grahammer, Tobias Huber, Ulf Panzer, Gisa Tiegs, and Katrin Neumann. "Renal proximal tubular epithelial cells exert immunomodulatory function by driving inflammatory CD4+ T cell responses." American Journal of Physiology-Renal Physiology 317, no. 1 (July 1, 2019): F77—F89. http://dx.doi.org/10.1152/ajprenal.00427.2018.

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In immune-mediated glomerular diseases like crescentic glomerulonephritis (cGN), inflammatory CD4+ T cells accumulate within the tubulointerstitial compartment in close contact to proximal and distal tubular epithelial cells and drive renal inflammation and tissue damage. However, whether renal epithelial cell populations play a role in the pathogenesis of cGN by modulating CD4+ T cell responses is less clear. In the present study, we aimed to investigate the potential of renal epithelial cells to function as antigen-presenting cells, thereby stimulating CD4+ T cell responses. Using a FACS-based protocol that allowed comparative analysis of cortical epithelial cell populations, we showed that particularly proximal tubular epithelial cells (PTECs) express molecules linked with antigen-presenting cell function, including major histocompatibility complex class II (MHCII), CD74, CD80, and CD86 in homeostasis and nephrotoxic nephritis, a murine model of cGN. Protein expression was visualized at the PTEC single cell level by imaging flow cytometry. Interestingly, we found inflammation-dependent regulation of epithelium-expressed CD74, CD80, and CD86, whereas MHCII expression was not altered. Antigen-specific stimulation of CD4+ T cells by PTECs in vitro supported CD4+ T cell survival and induced CD4+ T cell activation, proliferation, and inflammatory cytokine production. In patients with antineutrophil cytoplasmic antibody-associated glomerulonephritis, MHCII and CD74 were expressed by both proximal and distal tubules, whereas CD86 was predominantly expressed by proximal tubules. Thus, particularly PTECs have the potential to induce an inflammatory phenotype in CD4+ T cells in vitro, which might also play a role in the pathology of immune-mediated kidney disease.
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TANG, Sydney, Kwok-Wah CHAN, Tak-Mao CHAN, and Kar-Neng LAI. "Sloughing renal tubular epithelial cell." Hong Kong Journal of Nephrology 4, no. 1 (April 2002): 61. http://dx.doi.org/10.1016/s1561-5413(09)60079-x.

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Carlisle, Rachel E., Alana Heffernan, Elise Brimble, Limin Liu, Danielle Jerome, Celeste A. Collins, Zahraa Mohammed-Ali, Peter J. Margetts, Richard C. Austin, and Jeffrey G. Dickhout. "TDAG51 mediates epithelial-to-mesenchymal transition in human proximal tubular epithelium." American Journal of Physiology-Renal Physiology 303, no. 3 (August 1, 2012): F467—F481. http://dx.doi.org/10.1152/ajprenal.00481.2011.

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Epithelial-to-mesenchymal transition (EMT) contributes to renal fibrosis in chronic kidney disease. Endoplasmic reticulum (ER) stress, a feature of many forms of kidney disease, results from the accumulation of misfolded proteins in the ER and leads to the unfolded protein response (UPR). We hypothesized that ER stress mediates EMT in human renal proximal tubules. ER stress is induced by a variety of stressors differing in their mechanism of action, including tunicamycin, thapsigargin, and the calcineurin inhibitor cyclosporine A. These ER stressors increased the UPR markers GRP78, GRP94, and phospho-eIF2α in human proximal tubular cells. Thapsigargin and cyclosporine A also increased cytosolic Ca2+ concentration and T cell death-associated gene 51 (TDAG51) expression, whereas tunicamycin did not. Thapsigargin was also shown to increase levels of active transforming growth factor (TGF)-β1 in the media of cultured human proximal tubular cells. Thapsigargin induced cytoskeletal rearrangement, β-catenin nuclear translocation, and α-smooth muscle actin and vinculin expression in proximal tubular cells, indicating an EMT response. Subconfluent primary human proximal tubular cells were induced to undergo EMT by TGF-β1 treatment. In contrast, tunicamycin treatment did not produce an EMT response. Plasmid-mediated overexpression of TDAG51 resulted in cell shape change and β-catenin nuclear translocation. These results allowed us to develop a two-hit model of ER stress-induced EMT, where Ca2+ dysregulation-mediated TDAG51 upregulation primes the cell for mesenchymal transformation via Wnt signaling and then TGF-β1 activation leads to a complete EMT response. Thus the release of Ca2+ from ER stores mediates EMT in human proximal tubular epithelium via the induction of TDAG51.
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Monteiro, Maria B., Susanne Ramm, Vidya Chandrasekaran, Sarah A. Boswell, Elijah J. Weber, Kevin A. Lidberg, Edward J. Kelly, and Vishal S. Vaidya. "A High-Throughput Screen Identifies DYRK1A Inhibitor ID-8 that Stimulates Human Kidney Tubular Epithelial Cell Proliferation." Journal of the American Society of Nephrology 29, no. 12 (October 25, 2018): 2820–33. http://dx.doi.org/10.1681/asn.2018040392.

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BackgroundThe death of epithelial cells in the proximal tubules is thought to be the primary cause of AKI, but epithelial cells that survive kidney injury have a remarkable ability to proliferate. Because proximal tubular epithelial cells play a predominant role in kidney regeneration after damage, a potential approach to treat AKI is to discover regenerative therapeutics capable of stimulating proliferation of these cells.MethodsWe conducted a high-throughput phenotypic screen using 1902 biologically active compounds to identify new molecules that promote proliferation of primary human proximal tubular epithelial cells in vitro.ResultsThe primary screen identified 129 compounds that stimulated tubular epithelial cell proliferation. A secondary screen against these compounds over a range of four doses confirmed that eight resulted in a significant increase in cell number and incorporation of the modified thymidine analog EdU (indicating actively proliferating cells), compared with control conditions. These eight compounds also stimulated tubular cell proliferation in vitro after damage induced by hypoxia, cadmium chloride, cyclosporin A, or polymyxin B. ID-8, an inhibitor of dual-specificity tyrosine-phosphorylation-regulated kinase 1A (DYRK1A), was the top candidate identified as having a robust proproliferative effect in two-dimensional culture models as well as a microphysiologic, three-dimensional cell culture system. Target engagement and genetic knockdown studies and RNA sequencing confirmed binding of ID-8 to DYRK1A and upregulation of cyclins and other cell cycle regulators, leading to epithelial cell proliferation.ConclusionsWe have identified a potential first-in-class compound that stimulates human kidney tubular epithelial cell proliferation after acute damage in vitro.
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Liukang, Chengyin, Jing Zhao, Jiaxin Tian, Min Huang, Rong Liang, Ye Zhao, and Guozhong Zhang. "Deciphering infected cell types, hub gene networks and cell-cell communication in infectious bronchitis virus via single-cell RNA sequencing." PLOS Pathogens 20, no. 5 (May 14, 2024): e1012232. http://dx.doi.org/10.1371/journal.ppat.1012232.

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Infectious bronchitis virus (IBV) is a coronavirus that infects chickens, which exhibits a broad tropism for epithelial cells, infecting the tracheal mucosal epithelium, intestinal mucosal epithelium, and renal tubular epithelial cells. Utilizing single-cell RNA sequencing (scRNA-seq), we systematically examined cells in renal, bursal, and tracheal tissues following IBV infection and identified tissue-specific molecular markers expressed in distinct cell types. We evaluated the expression of viral RNA in diverse cellular populations and subsequently ascertained that distal tubules and collecting ducts within the kidney, bursal mucosal epithelial cells, and follicle-associated epithelial cells exhibit susceptibility to IBV infection through immunofluorescence. Furthermore, our findings revealed an upregulation in the transcription of proinflammatory cytokines IL18 and IL1B in renal macrophages as well as increased expression of apoptosis-related gene STAT in distal tubules and collecting duct cells upon IBV infection leading to renal damage. Cell-to-cell communication unveiled potential interactions between diverse cell types, as well as upregulated signaling pathways and key sender-receiver cell populations after IBV infection. Integrating single-cell data from all tissues, we applied weighted gene co-expression network analysis (WGCNA) to identify gene modules that are specifically expressed in different cell populations. Based on the WGCNA results, we identified seven immune-related gene modules and determined the differential expression pattern of module genes, as well as the hub genes within these modules. Our comprehensive data provides valuable insights into the pathogenesis of IBV as well as avian antiviral immunology.
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Djudjaj, Sonja, Panagiotis Kavvadas, Niki Prakoura, Roman D. Bülow, Tiffany Migeon, Sandrine Placier, Christos E. Chadjichristos, Peter Boor, and Christos Chatziantoniou. "Activation of Notch3 in Renal Tubular Cells Leads to Progressive Cystic Kidney Disease." International Journal of Molecular Sciences 23, no. 2 (January 14, 2022): 884. http://dx.doi.org/10.3390/ijms23020884.

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Background: Polycystic kidney disease (PKD) is a genetic disorder affecting millions of people worldwide that is characterized by fluid-filled cysts and leads to end-stage renal disease (ESRD). The hallmarks of PKD are proliferation and dedifferentiation of tubular epithelial cells, cellular processes known to be regulated by Notch signaling. Methods: We found increased Notch3 expression in human PKD and renal cell carcinoma biopsies. To obtain insight into the underlying mechanisms and the functional consequences of this abnormal expression, we developed a transgenic mouse model with conditional overexpression of the intracellular Notch3 (ICN3) domain specifically in renal tubules. We evaluated the alterations in renal function (creatininemia, BUN) and structure (cysts, fibrosis, inflammation) and measured the expression of several genes involved in Notch signaling and the mechanisms of inflammation, proliferation, dedifferentiation, fibrosis, injury, apoptosis and regeneration. Results: After one month of ICN3 overexpression, kidneys were larger with tubules grossly enlarged in diameter, with cell hypertrophy and hyperplasia, exclusively in the outer stripe of the outer medulla. After three months, mice developed numerous cysts in proximal and distal tubules. The cysts had variable sizes and were lined with a single- or multilayered, flattened, cuboid or columnar epithelium. This resulted in epithelial hyperplasia, which was observed as protrusions into the cystic lumen in some of the renal cysts. The pre-cystic and cystic epithelium showed increased expression of cytoskeletal filaments and markers of epithelial injury and dedifferentiation. Additionally, the epithelium showed increased proliferation with an aberrant orientation of the mitotic spindle. These phenotypic tubular alterations led to progressive interstitial inflammation and fibrosis. Conclusions: In summary, Notch3 signaling promoted tubular cell proliferation, the alignment of cell division, dedifferentiation and hyperplasia, leading to cystic kidney diseases and pre-neoplastic lesions.
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Kazeminia, Sara, and Alfonso Eirin. "Role of mitochondria in endogenous renal repair." Clinical Science 138, no. 15 (July 30, 2024): 963–73. http://dx.doi.org/10.1042/cs20231331.

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Abstract Renal tubules have potential to regenerate and repair after mild-to-moderate injury. Proliferation of tubular epithelial cells represents the initial step of this reparative process. Although for many years, it was believed that proliferating cells originated from a pre-existing intra-tubular stem cell population, there is now consensus that surviving tubular epithelial cells acquire progenitor properties to regenerate the damaged kidney. Scattered tubular-like cells (STCs) are dedifferentiated adult renal tubular epithelial cells that arise upon injury and contribute to renal self-healing and recovery by replacing lost neighboring tubular epithelial cells. These cells are characterized by the co-expression of the stem cell surface markers CD133 and CD24, as well as mesenchymal and kidney injury markers. Previous studies have shown that exogenous delivery of STCs ameliorates renal injury and dysfunction in murine models of acute kidney injury, underscoring the regenerative potential of this endogenous repair system. Although STCs contain fewer mitochondria than their surrounding terminally differentiated tubular epithelial cells, these organelles modulate several important cellular functions, and their integrity and function are critical to preserve the reparative capacity of STCs. Recent data suggest that the microenviroment induced by cardiovascular risk factors, such as obesity, hypertension, and renal ischemia may compromise STC mitochondrial integrity and function, limiting the capacity of these cells to repair injured renal tubules. This review summarizes current knowledge of the contribution of STCs to kidney repair and discusses recent insight into the key role of mitochondria in modulating STC function and their vulnerability in the setting of cardiovascular disease.
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White, Lindsay R., Jason B. Blanchette, Li Ren, Ali Awn, Kiril Trpkov, and Daniel A. Muruve. "The characterization of α5-integrin expression on tubular epithelium during renal injury." American Journal of Physiology-Renal Physiology 292, no. 2 (February 2007): F567—F576. http://dx.doi.org/10.1152/ajprenal.00212.2006.

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The hallmark of progressive chronic kidney disease is the deposition of extracellular matrix proteins and tubulointerstitial fibrosis. Integrins mediate cell-extracellular matrix interaction and may play a role tubular epithelial injury. Murine primary tubular epithelial cells (TECs) express α5-integrin, a fibroblast marker and the natural receptor for fibronectin. Microscopy localized α5-integrin on E-cadherin-positive cells, confirming epithelial expression. The expression of α5-integrin increased in TECs grown on fibronectin and occurred in parallel with an upregulation of α-smooth muscle actin (αSMA), a marker of epithelial-mesenchymal transition (EMT). Exposure of TECs to transforming growth factor (TGF)-β also increased TEC α5-integrin expression in association with αSMA and EMT. Knock-down of α5-integrin expression with short interfering RNA attenuated the TGF-β induction of αSMA but did not alter morphologic EMT. Rather, α5-integrin was necessary for epithelial cell migration on fibronectin but not type IV collagen during cell spreading and epithelial wound healing in vitro. Immunohistochemistry revealed basolateral tubular epithelial α5-integrin expression in mouse kidneys after unilateral ureteric obstruction but not in contralateral control kidneys. In patient biopsies of nondiabetic kidney disease, α5-integrin expression was increased significantly in the renal interstitium. Focal basolateral staining was also detected in injured, but not in normal, tubular epithelium. In summary, these data show that TECs are induced to express α5-integrin during EMT and tubular epithelial injury in vitro and in vivo. These results increase our understanding of the biology of integrins during EMT and tubular injury in chronic kidney disease.
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Dissertations / Theses on the topic "Tubular epithelial cell"

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Neumann, Marc. "Epithelial cell rearrangements during tubular organ formation /." [S.l.] : [s.n.], 2005. http://edoc.unibas.ch/diss/DissB_7371.

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Kipari, Tiina Marika Johanna. "Inflammatory macrophages and renal tubular epithelial cell apoptosis." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29197.

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Macrophages play a key role in renal inflammation and may be cytotoxic to resident cells within tissues. I begin this thesis by examining the effect of macrophages upon the level of apoptosis and proliferation in tubular epithelial cells in vitro. I then went on to examine the role of NO in vivo in the murine model of unilateral ureteric obstruction (UUO) characterised by tubular cell apoptosis and interstitial fibrosis. The specific iNOS inhibitor L-NIL (control D-NIL) was administered between days 5 to 7 following UUO. Mice were sacrificed at day 7 and the obstructed kidney removed for histological analysis. L-NIL treatment did not affect macrophage infiltration but did reduce both tubular and interstitial cell apoptosis. Proliferation of tubular cells and interstitial cells was unaffected. Interstitial fibrosis was significantly increased by L-NIL treatment. I also investigated the effect of conditional macrophage ablation in the UUO model. The conditional macrophage ablation mice used in these studies are transgenic for the human diphtheria toxin receptor (DTR) under the CD11b promoter (CD11b-DTR mice). Intraperitoneal (IP) administration of diphtheria toxin (DT) to DTR mice results in the rapid and specific depletion of monocytes and macrophages. DTR mice underwent UUO at day 0 and either DT or PBS was administered IP on days 5, 6 and 7. Mice were sacrificed at day 7 and the obstructed kidney removed for histological analysis. Administration of DT resulted in a 3-fold reduction in interstitial macrophage accumulation in obstructed kidneys. However, macrophage depletion had no effect upon proximal or distal tubular cell proliferation or apoptosis. Interestingly, macrophage depletion had no effect upon the accumulation of myofibroblasts but attenuated interstitial fibrosis.
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Tang, Chi-wai Sydney, and 鄧智偉. "The many facets of the renal proximal tubular epithelial cell inhuman." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31992468.

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Tang, Chi-wai Sydney. "The many facets of the renal proximal tubular epithelial cell in human." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31992468.

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Meimaridou, Eirini. "Calcium oxalate modulation of tubular epithelial cell mitochondria : oxidative vulnerability due to restricted glutathione homeostasis." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444828/.

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Calcium oxalate (COM) crystals are the commonest component of kidney stones. These arise mainly in the distal tubules and collecting ducts. To gain further insight for the cellular damage in terms of oxidative stress caused by COM deposition, in vitro and in vivo model studies were performed. In vitro In renal distal tubule cells, COM and free oxalate treatment caused a 3- and 2-fold increase respectively in superoxide (O2*") formation, originating from mitochondria. This was measured by lucigenin chemiluminescence in digitonin permeabilised cells. However, hydroxyapatite produced a much lower but significant enhancement of 02*", whilst other micro-particles, uric acid crystals, brushite, zymosan, and latex beads had no effect. When EDTA was omitted during O2*" monitoring, COM induced mitochondrial 02*" was ablated indicating a requirement for the release of free oxalate. Mitochondrial oxalate uptake was studied by employing different oxalate transport inhibitors. Omitting phosphate from the media or using mersalyl both of which block dicarboxylate transport, caused a significant decrease in the 02*" formation evoked by COM treatments. Using the membrane potential sensitive-probe tetramethylrhodamine methyl ester (TMRM) together with confocal microscopy, evidence is presented that in cells where COM binding had occurred a marked change in the mitochondrial membrane potential (Aij/m) occurred. COM also modulated intracellular Ca2+ signalling as demonstrated using the Ca2- sensitive dye Fura-2 AM, and this was via a non-mitochondrial mechanism. In Vivo Using a rat model of crystalluria and renal stones initiated by treatment with ethylene glycol (EG) and 1, 25-dihydroxycholecalciferol (DHC), nephrolithiasis arose in kidneys and this was linked to oxidative stress. In the EG + DHC treated animals where crystalluria was evident, this oxidative insult was manifest by a decrease in total and mitochondrial glutathione concentration, as well as an increased activity of glucose-6-phosphate dehydrogenase. Severe kidney damage at the mitochondria level was a further observation, indicated by the diminished O2 consumption resulting in a lowered O2 production. In addition, histopathological analysis revealed increased renal tubular pathology characterised by obstruction, distension and interstitial inflammation. The above findings were not observed in hyperoxaluria (EG) or calciuria (DHC) and are therefore a direct effect of crystal formation in kidney distal tubules that have implications in kidney stone disease which are discussed.
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Machiguchi, Toshihiko. "Cellular interactions via conditioned media induce in vivo nephron generation from tubular epithelial cells or mesenchymal stem cells." Kyoto University, 2014. http://hdl.handle.net/2433/189325.

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Ashman, Neil. "L-Arginine Transport and Metabolism in an In Vivo Model of Proteinuric Proximal Tubular Epithelial Cell Injury." Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498591.

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Li, Moying [Verfasser], and Hans-Joachim [Akademischer Betreuer] Anders. "Mdm2 prevents spontaneous tubular epithelial cell death and acute kidney injury / Moying Li ; Betreuer: Hans-Joachim Anders." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1186629444/34.

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Gallagher, Hugh. "Megalin, cubilin and the proximal tubular epithelial cell : extracellular and intracellular interactions and their relevance to the progression of chronic renal disease." Thesis, St George's, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416020.

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Breda, Philippe Christophe [Verfasser]. "Renal proximal tubular epithelial cells exert immunomodulatory function by driving inflammatory CD4+ T cell responses : Renale proximale Tubulusepithelzellen üben durch Auslösen von inflammatorischen T-Zell-Antworten eine immunmodulatorische Funktion aus / Philippe Christophe Breda." Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2020. http://d-nb.info/1221276344/34.

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Books on the topic "Tubular epithelial cell"

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Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.
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Srisawat, Nattachai, and John A. Kellum. Promoting renal recovery in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0379.

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Better understanding the process of renal recovery following acute kidney injury (AKI) is one of the key steps in improving AKI outcome. We are still lacking the standard definition of renal recovery. Recent progress on the pathophysiology of renal injury and recovery is encouraging. Repopulation of surviving renal tubular epithelial cells with the assistance of certain renal epithelial cell and specific growth factors, play a major role in the recovery process. Moreover, accurate prediction would help physicians distinguish patients with poor renal prognosis in whom further therapy is likely to be futile from those who are likely to have good renal prognosis. Unfortunately, current general clinical severity scores (APACHE, SOFA, etc.) and AKI-specific severity scores are not good predictors of renal recovery. This review describes the current definition, pathobiology of renal recovery, epidemiology of renal recovery, the role of clinical severity scores, and novel biomarkers in predicting renal recovery, and strategies for facilitating renal recovery.
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Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Chapman, Hannah, and Christine Elwell. Renal and bladder cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0167.

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This chapter addresses the diagnosis and management of bladder and renal cancers. In the UK, bladder cancer is the fourth most common cancer in men, and the eighth most common cancer in women. Bladder cancer arises from the bladder urothelium, and is typically a papillary transitional cell carcinoma. Chronic infection with the parasite Schistosoma haematobium is associated with squamous cell carcinoma of the bladder, and is most prevalent in Egypt and sub-Saharan Africa. Renal cancer accounts for 3% of cancers in adults in the UK and, in most cases, is a renal cell carcinoma arising from proximal renal tubule epithelium. A further 5%–10% of renal cancers are transitional cell (urothelial) carcinomas of the renal pelvis. Benign kidney tumours, such as cysts, are also common.
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Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.

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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
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Winyard, Paul. Human kidney development. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0343.

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The kidneys perform diverse functions including excretion of nitrogenous waste products, homeostasis of water, electrolytes and acid–base balance, and hormone secretion. The simplest functional unit within the kidneys is the nephron, which consists of specialized segments from glomerulus, through proximal tubule, loop of Henle, and distal tubule. Human nephrogenesis starts with two stages of transient kidneys, termed the pronephros and mesonephros, and ends with development of a permanent organ from the metanephros on each side. The latter consists of just a few hundred cells when it is formed in the fifth week of pregnancy but progresses to a nephron endowment of between 0.6 to 1.3 million by the time nephrogenesis is completed at 32–36 weeks of gestation. Key events during this process include outgrowth of the epithelial ureteric bud from the mesonephric duct, interactions between the bud and the metanephric blastema (a specific region of mesenchyme) that cause the bud to branch and mesenchyme to condense, epithelialization of the mesenchyme to form proximal parts of the nephron, and differentiation of segment specific cells. Molecular control of these events is being unpicked with data from human genetic syndromes and animal models, and this chapter highlights several of the most important factors/systems involved. Increased understanding of development is not just relevant to congenital kidney malformations, but may also be important in designing rational therapies for diseases of the mature kidney where recapitulation of developmental pathways is common.
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Servais, Aude, and Bertrand Knebelmann. Cystinuria. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0024.

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Cystinuria (OMIM #220100) is an autosomal recessive disorder of a dibasic amino acid transport in the apical membrane of epithelial cells of the renal proximal tubule and small intestine. It leads to increased urinary cystine excretion and recurrent urolithiasis. The cystine transporter is an heterodimeric transporter which is composed of a heavy subunit, rBAT, linked to a light subunit, b0,+AT. Two genes, SLC3A1 (solute carrier family 3 member 1) and SLC7A9, coding for rBAT and b0,+AT, account for the genetic basis of cystinuria. Cystinuria may lead to obstruction, infections, and ultimately to renal insufficiency. The diagnosis of cystinuria mainly relies on stone analysis, urinary cystine measurement, or urinary cystine crystal identification. Medical treatment is based upon a stepwise strategy using hydration and alkalinization as basic measures, with the addition of thiol derivatives in refractory cases. Urological interventions are often indicated for the management of cystine stones >5 mm in diameter.
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Daudon, Michel, and Paul Jungers. Cystine stones. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0203_update_001.

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Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine stones represent 1–2% of all stones in adults and 5–8% in paediatric patients, with an equal distribution between males and females.Cystinuria is caused by inactivating mutations in the gene SLC3A1 or SLC7A9, both encoding proteins contributing to the function of the heterodimeric transport system of cystine.Cystine nephrolithiasis may present in infants, most frequently in adolescents or young adults, sometimes later. Cystine calculi are weakly radio-opaque. Stone analysis using infrared spectroscopy (or X-ray diffraction) allows immediate and accurate diagnosis. Urinary amino acid chromatography quantifies urinary cystine excretion, needed to define the therapeutic strategy.Urological treatment of cystine stones currently uses extracorporeal stone wave lithotripsy or flexible ureterorenoscopy with Holmium laser, that is, minimally invasive techniques. However, as cystine stones are highly recurrent, preventive therapy is essential.Medical treatment combines reduced methionine and sodium intake, to lower cystine excretion; hyperdiuresis (> 3 L/day) to reduce cystine concentration; and active alkalinization preferably using potassium citrate (40–80 mEq/day) to increase cystine solubility by rising urine pH up to 7.5–8. If these measures are insufficient to prevent recurrent stone formation, a thiol derivative (D-penicillamine or tiopronin), which converts cystine into a more soluble disulphide, should be added. Close monitoring and adherence of the patient to the therapeutic programme are needed to ensure life-long compliance, the key for successful prevention in the long term.
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Book chapters on the topic "Tubular epithelial cell"

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Liu, Bi-Cheng, Tao-Tao Tang, and Lin-Li Lv. "How Tubular Epithelial Cell Injury Contributes to Renal Fibrosis." In Advances in Experimental Medicine and Biology, 233–52. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_11.

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Condorelli, L., I. Cattaneo, C. Arrigoni, L. Antiga, N. Perico, and A. Remuzzi. "Effect of fluid shear stress on tubular kidney epithelial cell structure." In IFMBE Proceedings, 50–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03900-3_15.

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Zink, Sabrina, and Ralf Jacob. "Tubulin Detyrosination in Epithelial Cells." In The Cytoskeleton in Health and Disease, 187–94. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2904-7_8.

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Sepúlveda, Francisco V., and Jeremy D. Pearson. "Amino Acid Transport in Cultured Kidney Tubule Cells." In Tissue Culture of Epithelial Cells, 87–104. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_6.

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Larsen, Erik Hviid, and Jens Nørkær Sørensen. "Stationary and Nonstationary Ion and Water Flux Interactions in Kidney Proximal Tubule: Mathematical Analysis of Isosmotic Transport by a Minimalistic Model." In Reviews of Physiology, Biochemistry and Pharmacology, 101–47. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/112_2019_16.

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AbstractOur mathematical model of epithelial transport (Larsen et al. Acta Physiol. 195:171–186, 2009) is extended by equations for currents and conductance of apical SGLT2. With independent variables of the physiological parameter space, the model reproduces intracellular solute concentrations, ion and water fluxes, and electrophysiology of proximal convoluted tubule. The following were shown: Water flux is given by active Na+ flux into lateral spaces, while osmolarity of absorbed fluid depends on osmotic permeability of apical membranes. Following aquaporin “knock-out,” water uptake is not reduced but redirected to the paracellular pathway. Reported decrease in epithelial water uptake in aquaporin-1 knock-out mouse is caused by downregulation of active Na+ absorption. Luminal glucose stimulates Na+ uptake by instantaneous depolarization-induced pump activity (“cross-talk”) and delayed stimulation because of slow rise in intracellular [Na+]. Rate of fluid absorption and flux of active K+ absorption would have to be attuned at epithelial cell level for the [K+] of the absorbate being in the physiological range of interstitial [K+]. Following unilateral osmotic perturbation, time course of water fluxes between intraepithelial compartments provides physical explanation for the transepithelial osmotic permeability being orders of magnitude smaller than cell membranes’ osmotic permeability. Fluid absorption is always hyperosmotic to bath. Deviation from isosmotic absorption is increased in presence of glucose contrasting experimental studies showing isosmotic transport being independent of glucose uptake. For achieving isosmotic transport, the cost of Na+ recirculation is predicted to be but a few percent of the energy consumption of Na+/K+ pumps.
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Trump, Benjamin F., and Irene K. Berezesky. "Ion Deregulation in Injured Proximal Tubule Epithelial Cells." In Nephrotoxicity, 731–41. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2040-2_113.

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Bowman, B. B., and D. B. McCormick. "Pyriloxine Uptake by Proximal Tubular Epithelial Cells Isolated from Rat Kidney." In Biochemistry of Vitamin B6, 403–6. Basel: Birkhäuser Basel, 1987. http://dx.doi.org/10.1007/978-3-0348-9308-4_72.

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Bertelli, R., F. Ginevri, P. Altieri, A. Garberi, G. M. Ghiggeri, and R. Gusmano. "Morphological and Biochemical Characteristics of Human Tubular Epithelial Cells “In Culture” Deriving from Nephronophthisis." In Tubulo-Interstitial Nephropathies, 311–15. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3892-9_36.

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Feng, Ying, Shumei Lin, Xiaoyan Zhao, Qunhui Yang, Gaofeng Wu, Qiufeng Lv, Jiancheng Yang, and Jianmin Hu. "Taurine Inhibited Uric Acid Uptake in HK-2 Renal Tubular Epithelial Cells." In Advances in Experimental Medicine and Biology, 147–54. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8023-5_13.

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Du, Caigan, Ximo Wang, and Huifang Chen. "Oxidative Stress to Renal Tubular Epithelial Cells – A Common Pathway in Renal Pathologies." In Systems Biology of Free Radicals and Antioxidants, 2605–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_187.

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Conference papers on the topic "Tubular epithelial cell"

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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, Giovanna A. Giannico, Roy Zent, Raymond Clement Harris, Peter Clark, Punita Dhawan, and Amar B. Singh. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1767.

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Kumar, Balawant, Rizwan Ahmad, Pinelopi Kapitsino, Giovanna A. Giannico, Roy Zent, Raymond Clement Harris, Peter Clark, Punita Dhawan, and Amar B. Singh. "Abstract 1767: Rho-GTPase inhibits claudin-2 expression to promote proximal tubular epithelial cell plasticity and renal cell carcinoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1767.

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Soni, Abhishek, Nupur Bansal, A. K. Dhull, Vivek Kaushal, Rajeev Atri, and Monica Verma. "Diagnostic dilemma of mesonephric adenocarcinoma cervix." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685283.

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Introduction: Mesonephric carcinoma is a rare type of epithelial tumor of the uterine cervix which derive from the remnants of the paired mesonephric (Wolff’s) ducts. The incidence of such neoplasms is difficult to determine due to rarity, previous misclassification of clear cell carcinomas and yolk sac tumours as mesonephric carcinomas and potential underreporting due to misclassification of mesonephric carcinoma as Mullerian tumours or mesonephric hyperplasia. The evidence regarding the clinical course, prognosis and optimal treatment is limited. Materials and Methods: Searches were performed on MEDLINE, EMBASE and Google Scholarly articles. All the relevant articles were included in the study. Only approximate 40 cases have been reported till now. Discussion: Mesonephric adenocarcinoma cervix has different morphologies like ductal, tubular, solid, retiform, sex-cord like pattern, clear cell and serous papillary structures. IHC assessment is helpful in differentiating it from Mullerian counterpart, as it is negative for CEA, CK20, p16, PAX2, ER/PR and vimentin and positive for CD10, calretinin, CK7, CAM5.2 and EMA. It has no relation with HPV infection. Unlike squamous epithelial carcinoma, it is rarely presenting with the abnormal cervical smear result, has more advanced age at presentation and its incidence does not appear to decline with age. The diagnosis has been supported by endometrial curettings, directed/cone cervical biopsies and hysterectomy specimens. The majority of patients are diagnosed at stage IB with mean DFS of 48.6 months. Recurrence rate is 23%, with a mean interval of 40 months. Hysterectomy is the primary treatment. Advanced stage disease of adenocarcinoma seemed to respond to radiotherapy, but for the MMMTs the combination of chemotherapy with radiotherapy appears to be preferable. Conclusion: Rarity of the neoplasm, varied morphology, mix presentation and very low number of cases leads to difficulty in correct diagnosis in a small biopsy specimen. IHC helpful in differentiating it from other lesions.
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Liu, Haijun, Xiaoyan Cai, Lie Dai, MA Jianda, Yingqian Mo, and Minyan Xie. "FRI0226 LOW EXPRESSION OF ESTROGEN RECEPTOR BETA IN RENAL TUBULAR EPITHELIAL CELL MAY CONTRIBUTE TO HYPERURICEMIA IN PREMENOPAUNITED STATES OF AMERICAL FEMALE SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3586.

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Wang, Jianbin, Jinseok Heo, and Susan Z. Hua. "Development of Microfluidic Chips to Study the Effects of Shear Stress on Cell Functions." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13132.

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Fluid shear stress has profound effect on many cell functions, including proliferation, migration, transport, and gene expression. Cellular systems such as endothelial cells in heart artery and epithelial cells in kidney tubule are constantly subject to fluid flow. We have developed a series of microfluidic chips that generate a wide range and modes of shear stresses within a perfusion chamber, enabling us to culture cells on chip and examine the effects of shear stress on cell growth and cell functions.
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Kaewpaiboon, Sunisa, Titpawan Nakpheng, and Teerapol Srichana. "Biocompatibility of Polymyxin B Sulfate Based on Sodium Deoxycholate Sulfate Formulations with Kidney Cell Lines, Macrophage Cells, and Red Blood Cells." In 5th International Conference and Exhibition on Pharmaceutical Sciences and Technology 2022. Switzerland: Trans Tech Publications Ltd, 2022. http://dx.doi.org/10.4028/p-7490x3.

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Antibiotic-resistant has emerged without new drug challenges. Polymyxin B (PMB) was the last resort therapy for multiple-drug resistant Gram-negative bacteria. However, the toxicity of PMB including nephrotoxicity (61%) and neurotoxicity (7%) was dose-limitation. PMB-based sodium deoxycholate sulfate (SDCS) formulations were prepared in the 2-different mole ratios of SDCS to PMB (5:1 and 10:1). Particle size, zeta-potential, and drug content were evaluated. The biocompatibility of PMB formulations was investigated with normal human primary renal proximal tubule epithelial cells (PCS-400-010), human kidney epithelial cell lines (HEK 293T/17), human kidney cell lines (WT 9-12), macrophage-like cells (RAW 264.7) and red blood cells (RBC). PMB formulations had smaller particle sizes and lower zeta-potential when compared to PMB. PMB content presented from 97-100% after lyophilization. PMB-SDCS formulations revealed lower toxicity to cell lines than PMB, especially SDCS: PMB (5:1) and low lysis of RBC. PMB-SDCS mixture had better biocompatibility than those PMB and SDCS alone.
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Al Meselmani, M. A., and N. A. Glinskaya. "ANALYSIS OF MORPHOLOGICAL CHANGES OF TESTES AFTER γ- IRRADIA-TION." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.183-184.

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We studied the effects of radiation in small doses (0.5 Gy) on the spermatogenic epithelium of white rats, counted the number of transversely cut convoluted seminiferous tubules, and de-termined the types of tubules. A decrease in the number of seminiferous tubules was noted, with damage to the cells of the spermatogenic epithelium.
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Lee, Gi-Ja, Ji-Hye Kim, Hun-Kuk Park, Kyung-Hwan Jeong, Hyun-Jung Kang, and Tae Won Lee. "Observation of angiotensin II-induced changes in tubular epithelial cells utilizing AFM: Angiotensin II-induced changes in tubular cells." In 2010 IEEE 4th International Conference on Nano/Molecular Medicine and Engineering (NANOMED). IEEE, 2010. http://dx.doi.org/10.1109/nanomed.2010.5749834.

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GUO, Da, Jian-min WANG, and Jian-ming OUYANG. "Injured Human Kidney Proximal Tubular Epithelial Cells Modulate Nucleation and Growth of Calcium Oxalate Crystals." In 2nd International Conference on Biomedical and Biological Engineering 2017 (BBE 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/bbe-17.2017.27.

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Lagies, Simon, Soeren Lienkamp, Bernd Kammerer, Roman Pichler, Michael Kaminski, Manuel Schlimpert, and Gerd Walz. "Directly reprogrammed renal tubular epithelial cells are sensitive to typical metabolic alterations occurring in hyperglycemia." In The 2nd International Electronic Conference on Metabolomics. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/iecm-2-04991.

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Reports on the topic "Tubular epithelial cell"

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Pines, Mark, Arieh Bar, David A. Carrino, Arnold I. Caplan, and James A. Dennis. Extracellular Matrix Molecules of the Eggshell as Related to Eggshell Quality. United States Department of Agriculture, 1997. http://dx.doi.org/10.32747/1997.7575270.bard.

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The extracellular matrix of the mineralizing eggshell contains molecules hypothesized to be regulators biomineralization. To study eggshell matrix molecules, a bank of monoclonal antibodies was generated that bound demineralized eggshell matrix or localized to oviduct epithelium. Immunofluorescence staining revealed several staining patterns for antibodies that recognized secretory cells: staining for a majority of columnar lining cells, staining for a minor sub-set of columnar lining cells, intensified staining within epithelial crypts, and staining of the entire tubular gland. Western blotting with the antibody Epi2 on eggshell matrix showed binding to molecules with the apparent molecular weight of eggshell matrix dermatan sulfate proteoglycan (eggshell DSPG) (Carrino, et al., 1997). Immunoblots of cyanogen bromide-cleaved eggshell DSPG revealed broad band of reactivity that shifted to 25 kDa after chondroitinase digestion; indicating that the Epi2 binding site is located on a fragment which contains dermatan sulfate side chains. Immunogold labeling showed that Epi2 binds to secretory vesicles within the non-ciliated cells of the columnar epithelium, while the antibodies Tg1 and Tg2 bind to secretory vesicles of tubular gland cells. Immunogold labeling of demineralized shell matrix showed binding of Epi2, Tg1, and Tg2 to the matrix of the palisades layer, and showed little reactivity to other regions of the shell matrix. Quantification of the immunogold particles within the eggshell matrix revealed that antibodies Epi2 and Tg1 bind all calcified regions equally while antibody Tg2 has a greater affinity for the baseplate region of the calcium reserve assembly.
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