Bibliografie tematiche / Kidney epithelial cells

Letteratura scientifica selezionata sul tema "Kidney epithelial cells"

Autore: Grafiati

Pubblicato: 22 giugno 2024

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Articoli di riviste sul tema "Kidney epithelial cells":

Pastor-Soler, Núria M., Timothy A. Sutton, Henry E. Mang, Carol L. Kinlough, Sandra J. Gendler, Cathy S. Madsen, Sheldon I. Bastacky et al. "Muc1 is protective during kidney ischemia-reperfusion injury". American Journal of Physiology-Renal Physiology 308, n. 12 (15 giugno 2015): F1452—F1462. http://dx.doi.org/10.1152/ajprenal.00066.2015.

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Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced during IRI, and Muc1 transcripts and protein were also present in recovering proximal tubule cells. Kidney damage was worse and recovery was blocked during IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice had reduced levels of HIF-1α, reduced or aberrant induction of HIF-1 target genes involved in the shift of glucose metabolism to glycolysis, and prolonged activation of AMP-activated protein kinase, indicating metabolic stress. Muc1 clearly plays a significant role in enhancing the HIF protective pathway during ischemic insult and recovery in kidney epithelia, providing a new target for developing therapies to treat AKI. Moreover, our data support a role specifically for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present only in tubule epithelial cells.

Verghese, George M., Michael F. Gutknecht e George H. Caughey. "Prostasin regulates epithelial monolayer function: cell-specific Gpld1-mediated secretion and functional role for GPI anchor". American Journal of Physiology-Cell Physiology 291, n. 6 (dicembre 2006): C1258—C1270. http://dx.doi.org/10.1152/ajpcell.00637.2005.

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Prostasin, a trypsinlike serine peptidase, is highly expressed in prostate, kidney, and lung epithelia, where it is bound to the cell surface, secreted, or both. Prostasin activates the epithelial sodium channel (ENaC) and suppresses invasion of prostate and breast cancer cells. The studies reported here establish mechanisms of membrane anchoring and secretion in kidney and lung epithelial cells and demonstrate a critical role for prostasin in regulating epithelial monolayer function. We report that endogenous mouse prostasin is glycosylphosphatidylinositol (GPI) anchored to the cell surface and is constitutively secreted from the apical surface of kidney cortical collecting duct cells. Using site-directed mutagenesis, detergent phase separation, and RNA interference approaches, we show that prostasin secretion depends on GPI anchor cleavage by endogenous GPI-specific phospholipase D1 (Gpld1). Secretion of prostasin by kidney and lung epithelial cells, in contrast to prostate epithelium, does not depend on COOH-terminal processing at conserved Arg322. Using stably transfected M-1 cells expressing wild-type, catalytically inactive, or chimeric transmembrane (not GPI)-anchored prostasins we establish that prostasin regulates transepithelial resistance, current, and paracellular permeability by GPI anchor- and protease activity-dependent mechanisms. These studies demonstrate a novel role for prostasin in regulating epithelial monolayer resistance and permeability in kidney epithelial cells and, furthermore, show specifically that prostasin is a critical regulator of transepithelial ion transport in M-1 cells. These functions depend on the GPI anchor as well as the peptidase activity of prostasin. These studies suggest that cell-specific Gpld1- or peptidase-dependent pathways for prostasin secretion may control prostasin functions in a tissue-specific manner.

Kim, Bo Hye, Do Yeon Kim, Yejin Ahn, Eun Ji Lee, Hyunjoo Park, Meeyoung Park e Jong Hoon Park. "Semaphorin-3C Is Upregulated in Polycystic Kidney Epithelial Cells and Inhibits Angiogenesis of Glomerular Endothelial Cells". American Journal of Nephrology 51, n. 7 (2020): 556–64. http://dx.doi.org/10.1159/000508263.

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Background: Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner. Methods: To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD epithelial cells were used for further analysis, and GECs were exposed to recombinant SEMA3C (rSEMA3C). Also, co-culture and treatment of conditioned media were employed to confirm whether PKD epithelial cells could influence on GECs via SEMA3C secretion. Results: SEMA3C knockdown reduced proliferation of PKD epithelial cells. In case of GECs, exposure to rSEMA3C decreased angiogenesis, which resulted from suppressed migratory ability not cell proliferation. Conclusions: This study indicates that SEMA3C is the aggravating factor in PKD. Thus, it is proposed that targeting SEMA3C can be effective to mitigate PKD.

TUFRO, ALDA, VICTORIA F. NORWOOD, ROBERT M. CAREY e R. ARIEL GOMEZ. "Vascular Endothelial Growth Factor Induces Nephrogenesis and Vasculogenesis". Journal of the American Society of Nephrology 10, n. 10 (ottobre 1999): 2125–34. http://dx.doi.org/10.1681/asn.v10102125.

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Abstract. The expression of vascular endothelial growth factor (VEGF) and its receptors Flt-1 and Flk-1 in the rat kidney was examined during ontogeny using Northern blot analysis and immunocytochemistry. In prevascular embryonic kidneys (embryonic day 14 [E14]), immunoreactive Flt-1 and Flk-1 were observed in isolated angioblasts, whereas VEGF was not detected. Angioblasts aligned forming cords before morphologically differentiating into endothelial cells. In late fetal kidneys (E19), immunoreactive VEGF was detected in glomerular epithelial and tubular cells, whereas Flt-1 and Flk-1 were expressed in contiguous endothelial cells. To determine whether VEGF induces endothelial cell differentiation and vascular development in the kidney, the effect of recombinant human VEGF (5 ng/ml) was examined on rat metanephric organ culture, a model known to recapitulate nephrogenesis in the absence of vessels. After 6 d in culture in serum-free, defined media, metanephric kidney growth and morphology were assessed. DNA content was higher in VEGF-treated explants (1.9 ± 0.17 μg/kidney, n = 9) than in paired control explants (1.4 ± 0.10 μg/kidney, n = 9) (P < 0.05). VEGF induced proliferation of tubular epithelial cells, as indicated by an increased number of tubules and tubular proliferating cell nuclear antigen-containing cells. VEGF induced upregulation of Flk-1 and Flt-1 expression, as assessed by Western blot analysis. Developing endothelial cells were identified and localized using immunocytochemistry and electron microscopy. Flt-1, Flk-1, and angiotensin-converting enzyme-containing cells were detected in VEGF-treated explants, whereas control explants were negative. These studies confirmed previous reports indicating that the expression of VEGF and its receptors is temporally and spatially associated with kidney vascularization and identified angioblasts expressing Flt-1 and Flk-1 in prevascular embryonic kidneys. The data indicate that VEGF expression is downregulated in standard culture conditions and that VEGF stimulates growth of embryonic kidney explants by expanding both endothelium and epithelium, resulting in vasculogenesis and enhanced tubulogenesis. These data suggest that VEGF plays a critical role in renal development by promoting endothelial cell differentiation, capillary formation, and proliferation of tubular epithelia.

Cramer, E. B., L. C. Milks, M. J. Brontoli, G. K. Ojakian, S. D. Wright e H. J. Showell. "Effect of human serum and some of its components on neutrophil adherence and migration across an epithelium." Journal of Cell Biology 102, n. 5 (1 maggio 1986): 1868–77. http://dx.doi.org/10.1083/jcb.102.5.1868.

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The effect of human serum and some of its components on the process of transepithelial migration of human neutrophils was investigated in an in vitro system. 10% autologous serum caused an increase in neutrophil adherence to and migration across canine kidney epithelial cells. This increase in neutrophil binding also occurred if the epithelium but not the neutrophils had been preincubated with serum. The binding was lost if the serum was either preabsorbed over the kidney epithelium before use or heat inactivated. Indirect immunofluorescence studies indicated that IgG, IgM, and a component of C3 bound to the epithelial surface, whereas IgA, IgE, or C5a were not detectable. The majority of epithelial cells were immunofluorescent, however epithelial cells with varying degrees of reactivity were also apparent and approximately 5% of the epithelial cells did not bind IgG, IgM, and C3. When epithelia were simultaneously tested for the presence of either IgG, IgM, or C3, and bound neutrophils the few epithelial cells which did not bind IgG or IgM also did not bind C3 or neutrophils. Studies with monoclonal antibodies against Fc and C3 receptors indicate that neutrophil adherence to the epithelial surface was mediated predominately by the receptors for C3b and C3bi. In response to a chemotactic gradient, bound neutrophils were able to detach and migrate across the epithelium. A separate heat-stable factor(s) in serum was able to increase neutrophil migration across the epithelial monolayer. This factor acted independently of the factors which caused the increase in neutrophil binding as the increase in neutrophil migration also occurred under conditions (preabsorption over the kidney epithelium or heat inactivation) that prevented the increase in neutrophil binding. The increase in neutrophil migration may be caused by the permeability-increasing properties of this factor as both serum and heat-inactivated serum lowered the transepithelial electrical resistance an average of 38 and 35%, respectively, in 40 min. Upon removal of serum or heat-inactivated serum, the resistance returned 100 and 81%, respectively, in 5 h.

Kuberka, M., G. Rau e B. Glasmacher. "CRYOPRESERVATION OF EPITHELIAL KIDNEY CELLS". Biomedizinische Technik/Biomedical Engineering 48, s1 (2003): 322–23. http://dx.doi.org/10.1515/bmte.2003.48.s1.322.

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Dahl, Ulf, Anders Sjödin, Lionel Larue, Glenn L. Radice, Stefan Cajander, Masatoshi Takeichi, Rolf Kemler e Henrik Semb. "Genetic Dissection of Cadherin Function during Nephrogenesis". Molecular and Cellular Biology 22, n. 5 (1 marzo 2002): 1474–87. http://dx.doi.org/10.1128/mcb.22.5.1474-1487.2002.

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ABSTRACT The distinct expression of R-cadherin in the induced aggregating metanephric mesenchyme suggests that it may regulate the mesenchymal-epithelial transition during kidney development. To address whether R-cadherin is required for kidney ontogeny, R-cadherin-deficient mice were generated. These mice appeared to be healthy and were fertile, demonstrating that R-cadherin is not essential for embryogenesis. The only kidney phenotype of adult mutant animals was the appearance of dilated proximal tubules, which was associated with an accumulation of large intracellular vacuoles. Morphological analysis of nephrogenesis in R-cadherin −/− mice in vivo and in vitro revealed defects in the development of both ureteric bud-derived cells and metanephric mesenchyme-derived cells. First, the morphology and organization of the proximal parts of the ureteric bud epithelium were altered. Interestingly, these morphological changes correlated with an increased rate of apoptosis and were further supported by perturbed branching and patterning of the ureteric bud epithelium during in vitro differentiation. Second, during in vitro studies of mesenchymal-epithelial conversion, significantly fewer epithelial structures developed from R-cadherin −/− kidneys than from wild-type kidneys. These data suggest that R-cadherin is functionally involved in the differentiation of both mesenchymal and epithelial components during metanephric kidney development. Finally, to investigate whether the redundant expression of other classic cadherins expressed in the kidney could explain the rather mild kidney defects in R-cadherin-deficient mice, we intercrossed R-cadherin −/− mice with cadherin-6−/− , P-cadherin −/−, and N-cadherin +/− mice. Surprisingly, however, in none of the compound knockout strains was kidney development affected to a greater extent than within the individual cadherin knockout strains.

Pat, Betty, David W. Johnson e Glenda C. Gobe. "Role of JAK3 in the Pathogenesis of Oxidative Stress-Induced Kidney Fibrosis". Journal of Renal and Hepatic Disorders 2, n. 1 (14 maggio 2018): 18–26. http://dx.doi.org/10.15586/jrenhep.2018.30.

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The Janus kinase (JAK) tyrosine kinase family and JAK/STAT signal transduction pathway may act in kidney fibrogenesis. JAK3 expression was investigated in in vitro and in vivo models of kidney fibrosis involving oxidative stress. There was a marked down-regulation of JAK3 mRNA in rat kidney tubular epithelial cells (NRK52E) and fibroblasts (NRK49F) exposed to 1.0 mM H2O2 for 18–20 h compared with controls, which correlated with increased apoptosis and decreased mitosis in both cell lines. However, JAK3 protein levels were not significantly different in control and H2O2-treated epithelial and fibroblast cultures. JAK3 activation (phospho-tyrosine) increased in NRK52E cells and decreased in NRK49F cells with oxidative stress. STAT3 phosphorylation decreased in both cell lines with oxidative stress compared with controls. JAK3 protein expression and localisation were investigated in kidneys using the unilateral ureteral obstruction (UUO) model (0–7 days, rats) of kidney fibrosis that involves oxidative stress. JAK3 protein expression did not differ between UUO and controls; however, JAK3 localisation increased temporally with UUO, with strong epithelial expression in mitotic cells compared with controls. Apoptotic tubular epithelium showed minimal JAK3. In summary, in vitro, decreased kidney JAK3 mRNA after oxidative stress was not seen translationally. Differences in the activation of the JAK3/STAT3 pathway may have different consequences for renal fibrosis. In vivo, changes in JAK3 protein localisation, and especially its co-localisation with mitotic cells, indicate that JAK3 protein may contribute to renal tubular epithelial cell proliferation after oxidative stress.

White, Lindsay R., Jason B. Blanchette, Li Ren, Ali Awn, Kiril Trpkov e Daniel A. Muruve. "The characterization of α5-integrin expression on tubular epithelium during renal injury". American Journal of Physiology-Renal Physiology 292, n. 2 (febbraio 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.

Sorokin, L., A. Sonnenberg, M. Aumailley, R. Timpl e P. Ekblom. "Recognition of the laminin E8 cell-binding site by an integrin possessing the alpha 6 subunit is essential for epithelial polarization in developing kidney tubules." Journal of Cell Biology 111, n. 3 (1 settembre 1990): 1265–73. http://dx.doi.org/10.1083/jcb.111.3.1265.

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It has been previously shown that A-chain and domain(E8)-specific antibodies to laminin that inhibit cell adhesion also interfere with the establishment of epithelial cell polarity during kidney tubule development (Klein, G., M. Langegger, R. Timpl, and P. Ekblom. 1988. Cell. 55:331-341). A monoclonal antibody specific for the integrin alpha 6 subunit, which selectively blocks cell binding to E8, was used to study the receptors involved. Immunofluorescence staining of embryonic kidneys and of organ cultures of metanephric mesenchyme demonstrated coappearance of the integrin alpha 6 subunit and the laminin A-chain in regions where nonpolarized mesenchymal cells convert into polarized epithelial cells. Both epitopes showed marked colocalization in basal areas of tubules, while an exclusive immunostaining for alpha 6 was observed in lateral and apical cell surfaces of the tubular epithelial cells. Organ culture studies demonstrated a consistent inhibition of kidney epithelium development by antibodies against the alpha 6 subunit. The data suggest that the recognition of E8 cell-binding site of laminin by a specific integrin is crucial for the formation of kidney tubule epithelium from undifferentiated mesenchymal stem cells. In some other cell types (endothelium, some ureter cells) an exclusive expression of alpha 6 with no apparent colocalization of laminin A-chain in the corresponding basement membrane was seen. Thus, in these cells, integrins possessing the alpha 6 subunit may bind to laminin isoforms that differ from those synthesized by developing tubules.

Più fonti

Tesi sul tema "Kidney epithelial cells":

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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Tang, Chi-wai Sydney, e 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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Measures, H. R. "A study of desmosome formation in kidney epithelial cells". Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234435.

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Xie, Jianxun. "Involvement of transcription factors in cadmium-induced apoptosis and cell cycle arrest in rat kidney cells /". View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3206258.

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Lim, Ai Ing, e 林艾盈. "Shedding of kidney injury molecule-1 by kidney proximal tubular epithelial cells: the role of matrixmetalloproteinase-3". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49799745.

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Regardless of the original cause and etiology, the progression of kidney disease follows a final common pathway associated with tubulointerstitial injury, in which proximal tubular epithelial cells (PTEC) are instrumental. Kidney injury molecule-1 (KIM-1) is an emerging biomarker of kidney tubular damage. It is markedly expressed and released into urine in various animal models and human kidney diseases. This study aimed to explore the underlying mechanism regulating the release of KIM-1 by PTEC. First, expression and release of KIM-1 by primary cultured human PTEC were examined. In quiescent PTEC, KIM-1 was detected at the plasma membrane and in the cytoplasm. A transwell system, in which PTEC were grown as monolayer on permeable membrane, was used to examine the polarized release of KIM-1. PTEC constitutively released KIM-1 from their apical surface, and the release was independent of gene expression or protein synthesis. The KIM-1 release process by PTEC was enhanced dose- and time-dependently by two important kidney injury mediators, human serum albumin (HSA) and tumor necrosis factor (TNF)-α, and was inhibited by the presence of broad-spectrum inhibitors of matrix metalloproteinases (MMP). Second, the potential sheddases responsible for KIM-1 shedding were identified by quantitative polymerase chain reaction (PCR) array system, in which the gene expression of a panel of MMP members was screened. The gene expression of MMP-3, MMP-7 and MMP-9 was up-regulated by PTEC under HSA or TNF-α activation. Blockade experiments with synthetic MMP inhibitors or MMP gene knockdown by small interfering RNA transfection, revealed that the constitutive or accelerated KIM-1 shedding was mediated by MMP-3, but not MMP-7 or MMP-9. The role of MMP-3 in KIM-1 shedding was further defined by additional data showing the enhanced MMP-3 synthesis by HSA- or TNF-α-stimulated PTEC, and the up-regulated KIM-1 shedding by PTEC following exogenous MMP-3 treatment. Third, the regulatory mechanism of MMP-3-mediated KIM-1 shedding was investigated. Treatment of PTEC with HSA or TNF-α up-regulated the reactive oxygen species (ROS) generation, and its kinetics ran parallel to the increase of KIM-1 shedding and MMP-3 synthesis. In addition, exogenous hydrogen peroxide dose-dependently induced KIM-1 shedding and MMP-3 synthesis, which were abolished by the presence of an oxidation inhibitor. These evidence suggest that ROS play an essential role in regulating the MMP-3-mediated KIM-1 shedding by PTEC. Finally, a mouse model of acute kidney injury induced by renal ischemia and reperfusion (I/R) was established to translate the in vitro findings. Reduced kidney function and increased urinary KIM-1 level were observed in mice after renal I/R treatment. Strikingly, the expression of MMP-3 and KIM-1 in the I/R treated mice was most profound in the S3 segments of the proximal tubules, where is the most susceptible area to oxidative stress. Taken together, these in vivo data have further strengthened the distinct roles of ROS and MMP-3 in KIM-1 shedding during PTEC injury. In conclusion, ROS generated by the injured PTEC activate MMP-3, which release the soluble KIM-1 through the ectodomain shedding process.
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Medicine
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Master of Philosophy

Zhou, Li. "The molecular mechanisms of aristolochic acid nephropathy". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43224349.

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Laestadius, Åsa. "Cellular mechanisms of interaction between uropathogenic Escherichia coli and renal epithelial cells /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-187-X.

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Sampangi, Sandeep. "Autologous human kidney proximal tubule epithelial cells (PTEC) modulate dendritic cell (DC), T cell and B cell responses". Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82033/1/Sandeep_Sampangi_Thesis.pdf.

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This is a comprehensive study of human kidney proximal tubular epithelial cells (PTEC) which are known to respond to and mediate the pathological process of a range of kidney diseases. It identifies various molecules expressed by PTEC and how these molecules participate in down-regulating the inflammatory process, thereby highlighting the clinical potential of these molecules to treat various kidney diseases. In the disease state, PTEC gain the ability to regulate the immune cell responses present within the interstitium. This down-regulation is a complex interaction of contact dependent/independent mechanisms involving various immuno-regulatory molecules including PD-L1, sHLA-G and IDO. The overall outcome of this down-regulation is suppressed DC maturation, decreased number of antibody producing B cells and low T cell responses. These manifestations within a clinical setting are expected to dampen the ongoing inflammation, preventing the damage caused to the kidney tissue.

Broadbelt, Nalini V. "Regulation of iNOS expression : in response to pressure in proximal tubule epithelial cells /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1619205731&sid=2&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Miskovic, Dragana. "A characterization of BiP gene expression in Xenopus laevis embryos and A6 kidney epithelial cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ38257.pdf.

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Libri sul tema "Kidney epithelial cells":

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi e Brian B. Ratliff. Pathophysiology of acute kidney injury. A cura di 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.

Tsai, Ching-Wei, Sanjeev Noel e 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.

Winyard, Paul. Human kidney development. A cura di 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.

Kühn, Wolfgang, e Gerd Walz. The molecular basis of ciliopathies and cyst formation. A cura di 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.

Srisawat, Nattachai, e 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.

Sebastio, Gianfranco, Manuel Schiff e Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progressively appear. Lung involvement (specifically pulmonary alveolar proteinosis), chronic renal disease that may lead to end stage renal disease, and hemophagocytic lymphohistiocytosis with macrophage activation all represent complications of LPI that may appear at any time from childhood to adulthood. The great variability of the clinical presentation frequently causes misdiagnosis or delayed diagnosis. The basic therapy of LPI consist of a low-protein diet, low-dose citrulline supplementation, nitrogen-scavenging compounds to prevent hyperammonemia, lysine, and carnitine supplements.

Chapman, Hannah, e Christine Elwell. Renal and bladder cancer. A cura di Patrick Davey e 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.

Lameire, Norbert, Raymond Vanholder e Wim Van Biesen. Clinical approach to the patient with acute kidney injury. A cura di 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.

Capitoli di libri sul tema "Kidney epithelial cells":

Sorokin, Lydia, Gerd Klein, Gabriele Mugrauer, Lothar Fecker, Marja Ekblom e Peter Ekblom. "Development of kidney epithelial cells". In Epithelial Organization and Development, 163–90. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2354-9_6.

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Liehr, Joachim G., e David A. Sirbasku. "Estrogen-Dependent Kidney Tumors". In Tissue Culture of Epithelial Cells, 205–34. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_11.

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Guggino, Sandra. "Channels in Kidney Epithelial Cells". In Ionic Channels in Cells and Model Systems, 207–20. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5077-4_13.

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Sepúlveda, Francisco V., e 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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Kuure, Satu. "Analysis of Migration in Primary Ureteric Bud Epithelial Cells". In Kidney Development, 147–55. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-851-1_13.

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Saier, Milton H. "Application of the Microbiological Approach to the Study of Passive Monovalent Salt Transport in a Kidney Epithelial Cell Line, MDCK". In Tissue Culture of Epithelial Cells, 51–67. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_4.

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Leonard, Jack L. "Thyroid Hormone Metabolism in Kidney Epithelial Cells in Continuous Culture". In Frontiers in Thyroidology, 437–41. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5260-0_77.

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Bowman, B. B., e 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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Toback, F. Gary, Sreedharan Kartha e Margaret M. Walsh-Reitz. "Determinants of Autocrine and Paracrine Growth Factor Release by Kidney Epithelial Cells". In Nephrology, 1322–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-35158-1_135.

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Brown, Dennis, e Ivan Sabolić. "Acidic and non-acidic endosomes in kidney epithelial cells: their role in cell-specific membrane recycling processes". In Molecular and Cellular Mechanisms of H+ Transport, 127–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79301-1_15.

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Atti di convegni sul tema "Kidney epithelial cells":

Kaewpaiboon, Sunisa, Titpawan Nakpheng e 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.

Vitol, Elina A., Timothy P. Kurzweg e Bahram Nabet. "Light scattering properties of kidney epithelial cells and nuclei". In Biomedical Optics 2006, a cura di Robert R. Alfano e Alvin Katz. SPIE, 2006. http://dx.doi.org/10.1117/12.644863.

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Wang, Jianbin, Jinseok Heo e 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.

Azeloglu, Evren U., Mark Stothers, Thomas J. Deerinck, Cibele Falkenberg, Yibang Chen, John Cijiang He, James C. Hone, Leslie M. Loew, Mark H. Ellisman e Ravi Iyengar. "3-D Quantitative Microanatomy of Rat Kidney Podocytes as Determined by Serial Block-Face Scanning Electron Microscopy". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80650.

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The shape of a cell is critical for proper signaling and resultant biological function [1]. Podocytes, kidney visceral epithelial cells, have a distinctive morphology with interdigitating foot processes that wrap around the capillaries of the glomeruli and, together with endothelial cells and the basement membrane, form the glomerular filtration barrier. In addition to forming the filtration barrier, slit diaphragms that connect the alternating foot processes from two podocytes are thought to be signaling hubs that regulate cell morphology and function.

Loh, Jeremy, Karl Schumacher, Annegret Schumacher, Shyi-Herng Kan e Jackie Y. Ying. "Engineering Homogeneous Micromagnetic Fields for Cell Patterning". In ASME 2006 International Manufacturing Science and Engineering Conference. ASMEDC, 2006. http://dx.doi.org/10.1115/msec2006-21041.

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Micropatterning of cells was achieved by the application of micromagnetic fields using ferromagnetic field modulators. These modulators were made of low carbon steel, and micromachined using the wire-cut method. They were engineered to disrupt the regular pathways of magnetic flux lines, and create localized regions of micromagnetic fields. Uniform micromagnetic fields were achieved via design evaluation using Maxwell®2D magnetostatic simulations. Application of the micromagnetic field modulators on Madin-Darby canine kidney (MDCK) epithelial cells demonstrated good cell adhesion and uniform cell columns of 200 μm-wide, spaced 200 μm apart. This approach would be useful towards cell micropatterning for tissue engineering, artificial organ and implant applications.

Chang, Yu-Wei, e Kamaleshwar Singh. "Abstract 3080: Chronic exposure to arsenic induces malignant transformation in human kidney epithelial cells". In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3080.

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GUO, Da, Jian-min WANG e 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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Di´az, Rube´n, e Boris Rubinsky. "A Single Cell Study on the Temperature Effects of Electroporation". In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61151.

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In electroporation, the charging of the cell membrane due to an applied electric field is followed by a localized structural rearrangement of the membrane, which consequently creates pores or aqueous pathways that perforate the membrane. A tremendous increase in ionic and molecular transport through the membrane occurs because of the presence of these aqueous pores. As part of a comprehensive study on the effects of temperature on electroporation of cells, we have designed a micro device capable of integrating single cells into an electronic circuit while controlling the temperature. In the present work, we have studied the effect of temperature on the electroporation of Madin-Darby canine kidney epithelial cells (MDCK) with a micro-electroporation device. It was found that the critical voltage for electropermeabilization was strongly dependent on temperature, increasing by a factor of 2 with decreasing temperature from 37 to 5 °C. Data shows there is a correlation among the viscoelastic properties of the cell membrane and the temperature.

Nguyen, Thi-Ngoc, e Tien Hsu. "Abstract B92: VHL inactivated kidney epithelial cells reprogram macrophage behavior through IL-6 and CXCL-1 secretion". In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-b92.

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Chang, Yuwei, e Kamaleshwar Singh. "Abstract 879: Nicotine-induced oxidative stress causes epigenetic alterations during malignant transformation of human kidney epithelial cells". 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.sabcs18-879.

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