Journal articles: 'Human renal epithelial cell'

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Demmers, M. W. H. J., S. S. Korevaar, M. Roemeling-van Rhijn, T. P. P. van den Bosch, M. J. Hoogduijn, M. G. H. Betjes, W. Weimar, C. C. Baan, and A. T. Rowshani. "Human renal tubular epithelial cells suppress alloreactive T cell proliferation." Clinical & Experimental Immunology 179, no. 3 (February 16, 2015): 509–19. http://dx.doi.org/10.1111/cei.12469.

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Elliott, Justine, Nadezhda N. Zheleznova, and Patricia D. Wilson. "c-Src inactivation reduces renal epithelial cell-matrix adhesion, proliferation, and cyst formation." American Journal of Physiology-Cell Physiology 301, no. 2 (August 2011): C522—C529. http://dx.doi.org/10.1152/ajpcell.00163.2010.

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c-Src is a non-receptor tyrosine kinase whose activity is induced by phosphorylation at Y418 and translocation from the cytoplasm to the cell membrane. Increased activity of c-Src has been associated with cell proliferation, matrix adhesion, motility, and apoptosis in tumors. Immunohistochemistry suggested that activated (pY418)-Src activity is increased in cyst-lining autosomal dominant polycystic kidney disease (ADPKD) epithelial cells in human and mouse ADPKD. Western blot analysis showed that SKI-606 (Wyeth) is a specific inhibitor of pY418-Src without demonstrable effects on epidermal growth factor receptor or ErbB2 activity in renal epithelia. In vitro studies on mouse inner medullary collecting duct (mIMCD) cells and human ADPKD cyst-lining epithelial cells showed that SKI-606 inhibited epithelial cell proliferation over a 24-h time frame. In addition, SKI-606 treatment caused a striking statistically significant decrease in adhesion of mIMCD and human ADPKD to extracellular collagen matrix. Retained viability of unattached cells was consistent with a primary effect on epithelial cell anchorage dependence mediated by the loss of extracellular matrix (ECM)-attachment due to α2β1-integrin function. SKI-606-mediated attenuation of the human ADPKD hyperproliferative and hyper-ECM-adhesive epithelial cell phenotype in vitro was paralleled by retardation of the renal cystic phenotype of Pkd1 orthologous ADPKD heterozygous mice in vivo. This suggests that SKI-606 has dual effects on cystic epithelial cell proliferation and ECM adhesion and may have therapeutic potential for ADPKD patients.

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Pathak, R. K., M. Yokode, R. E. Hammer, S. L. Hofmann, M. S. Brown, J. L. Goldstein, and R. G. Anderson. "Tissue-specific sorting of the human LDL receptor in polarized epithelia of transgenic mice." Journal of Cell Biology 111, no. 2 (August 1, 1990): 347–59. http://dx.doi.org/10.1083/jcb.111.2.347.

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The distribution of human low density lipoprotein (LDL) receptors was studied by immunofluorescence and immunoelectron microscopy in epithelial cells of transgenic mice that express high levels of receptors under control of the metallothionein-I promoter. In hepatocytes and intestinal epithelial cells, the receptors were confined to the basal and basolateral surfaces, respectively. Very few LDL receptors were present in coated pits or intracellular vesicles. In striking contrast, in the epithelium of the renal tubule the receptors were present on the apical (lumenal) surface where they appeared to be concentrated at the base of microvilli and were abundant in vesicles of the endocytic recycling pathway. Intravenously administered LDL colloidal gold conjugates bound to the receptors on hepatocyte microvilli and were slowly internalized, apparently through slow migration into coated pits. We conclude that (a) sorting of LDL receptors to the surface of different epithelial cells varies with each tissue; and (b) in addition to a signal for clustering in coated pits, the LDL receptor may contain a signal for retention in noncoated membrane that is manifest in hepatocytes and intestinal epithelial cells, but not in renal epithelial cells or cultured human fibroblasts.

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Balkovetz, Daniel F. "Claudins at the gate: determinants of renal epithelial tight junction paracellular permeability." American Journal of Physiology-Renal Physiology 290, no. 3 (March 2006): F572—F579. http://dx.doi.org/10.1152/ajprenal.00135.2005.

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The epithelial tight junction (TJ) is responsible for the control of paracellular transport between epithelial cells (gate function) and the maintenance of apical/basolateral polarity by preventing the diffusion of membrane lipids and/or proteins from one surface domain to another (fence function). Renal tubule epithelia in the mammalian nephron have TJs that determine paracellular transport characteristics. Paracellular transport across renal tubular epithelial TJs (gate function) varies in different segments of the nephron. A large family of recently identified TJ-associated transmembrane proteins named claudins appear to determine the paracellular permeability properties of the TJ. A combination of inherited human diseases, renal epithelial cell culture models, and nephron expression patterns of claudins is providing important clues about how claudin molecules determine the TJ gate function of renal epithelia in different segments of the nephron.

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Nadasdy, T., Z. Laszik, G. Lajoie, K. E. Blick, D. E. Wheeler, and F. G. Silva. "Proliferative activity of cyst epithelium in human renal cystic diseases." Journal of the American Society of Nephrology 5, no. 7 (January 1995): 1462–68. http://dx.doi.org/10.1681/asn.v571462.

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Increased proliferative activity of the renal tubular epithelium is thought to be a prerequisite for renal cyst formation by many investigators. However, in humans, the exact in vivo proliferation rate of epithelial cells lining these cysts is not known. In this study, which used immunohistochemical methods with an antibody to proliferating cell nuclear antigen (PCNA), the proliferation index (PI) (percentage of PCNA positive cell nuclei among epithelial cells lining the renal cysts) was determined in 10 cases of autosomal dominant polycystic kidney disease (ADPKD), 8 cases of autosomal recessive polycystic kidney disease (ARPKD), and 8 cases of acquired cystic kidney disease (ACKD). Cysts with proximal and distal nephron phenotype and cysts with markedly thickened basement membranes, as well as cysts lined by atrophic (flattened), "regular" (cuboidal or cylindrical), and hyperplastic epithelium, were evaluated separately. The overall PI of cyst epithelium (excluding hyperplastic cysts) was 2.58 in ADPKD, was 10.5 in ARPKD, and was 3.61 in ACKD. Overall, there were only minor differences in the PI between the various types of cysts. Cysts with hyperplastic epithelium in ACKD (unlike in ADPKD) showed a high PI (9.1). For comparison, the PI of two renal cell carcinomas occurring in two ACKD cases was also determined (13.70 and 8.67%). The PI of tubular epithelium in normal kidneys was only 0.22 to 0.33%, depending on the tubule segment. In contrast, in polycystic kidneys, those noncystic segments of the nephron from which the cysts are thought to originate (distal nephron (specifically collecting duct)) in ARPKD, primarily distal in ADPKD, proximal and distal in ACKD, had PI values similar to those of the cyst epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

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Nadasdy, T., Z. Laszik, K. E. Blick, L. D. Johnson, and F. G. Silva. "Proliferative activity of intrinsic cell populations in the normal human kidney." Journal of the American Society of Nephrology 4, no. 12 (June 1994): 2032–39. http://dx.doi.org/10.1681/asn.v4122032.

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The proliferative activity of various normal human renal cell populations is unknown. Recently, antibodies to cell proliferation-associated nuclear proteins, such as proliferating cell nuclear antigen (PCNA) and KI-67, which are applicable to archival paraffin sections, became available. With antibodies to PCNA and Ki-67 after microwave pretreatment of the paraffin sections, the proliferation indexes (ratio of positive nuclei with PCNA and Ki-67 antibodies/all nuclei counted x 100, i.e. percentage of positive cells) of 12 different intrinsic renal cell populations in 20 normal human kidneys have been determined. The following proliferation indexes (percentages of positive cells) were found with the PCNA and the Ki-67 antibodies, respectively: proximal tubular epithelium, 0.22, 0.24; thin limb of Henle, 0.29, 0.30; thick ascending limb of Henle, 0.32, 0.29; distal tubular epithelium (distal convoluted tubules and cortical collecting ducts, 0.33, 0.44; medullary collecting ducts, 0.32, 0.3; glomerular mesangial cells, 0.07, 0.12; glomerular visceral epithelial cells, 0.04, 0.08; glomerular parietal epithelial cells, 0.07, 0.1; glomerular capillary endothelium, 0.42, 0.47; peritubular capillary endothelial cells, 0.38, 0.43; endothelium of large intrarenal vessels (arteries and veins), 0.09, 0.12. Thus, normally capillary endothelium (glomerular and peritubular) appears to have the highest proliferation index in the human kidney by these techniques. These results indicate major variation in the proliferative activity of normal human renal cell populations, along with a significant correlation between PCNA and Ki-67 staining. Furthermore, this study provides normal values for the proliferative activity of different human renal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)

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Tasnim, Farah, and Daniele Zink. "Cross talk between primary human renal tubular cells and endothelial cells in cocultures." American Journal of Physiology-Renal Physiology 302, no. 8 (April 15, 2012): F1055—F1062. http://dx.doi.org/10.1152/ajprenal.00621.2011.

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Interactions between renal tubular epithelial cells and adjacent endothelial cells are essential for normal renal functions but also play important roles in renal disease and repair. Here, we investigated cocultures of human primary renal proximal tubular cells (HPTC) and human primary endothelial cells to address the cross talk between these cell types. HPTC showed improved proliferation, marker gene expression, and enzyme activity in cocultures. Also, the long-term maintenance of epithelia formed by HPTC was improved, which was due to the secretion of transforming growth factor-β1 and its antagonist α2-macroglobulin. HPTC induced endothelial cells to secrete increased amounts of these factors, which balanced each other functionally and only displayed in combination the observed positive effects. In addition, in the presence of HPTC endothelial cells expressed increased amounts of hepatocyte growth factor and vascular endothelial growth factor, which have well-characterized effects on renal tubular epithelial cells as well as on endothelial cells. Together, the results showed that HPTC stimulated endothelial cells to express a functionally balanced combination of various factors, which in turn improved the performance of HPTC. The results give new insights into the cross talk between renal epithelial and endothelial cells and suggest that cocultures could be also useful models for the analysis of cellular communication in renal disease and repair. Furthermore, the characterization of defined microenvironments, which positively affect HPTC, will be helpful for improving the performance of this cell type in in vitro applications including in vitro toxicology and kidney tissue engineering.

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Demmers, Martijn W. H. J., Carla C. Baan, Els van Beelen, Jan N. M. IJzermans, Willem Weimar, and Ajda T. Rowshani. "Differential Effects of Activated Human Renal Epithelial Cells on T-Cell Migration." PLoS ONE 8, no. 5 (May 22, 2013): e64916. http://dx.doi.org/10.1371/journal.pone.0064916.

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McAteer, James A., Stephen A. Kempson, and Andrew P. Evan. "Culture of human renal cortex epithelial cells." Journal of Tissue Culture Methods 13, no. 3 (September 1991): 143–47. http://dx.doi.org/10.1007/bf02388118.

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Kadomoto, Suguru, Kouji Izumi, Kaoru Hiratsuka, Taito Nakano, Renato Naito, Tomoyuki Makino, Hiroaki Iwamoto, et al. "Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis." Cancers 12, no. 1 (December 30, 2019): 89. http://dx.doi.org/10.3390/cancers12010089.

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This study investigated tumor-associated macrophages activity in the microenvironment of renal cell carcinoma. Via a co-culture with macrophage-like cells differentiated from human monocyte cell line THP-1 and U937 cells, the migration ability of ACHN and Caki-1 cells, which are human renal cell carcinoma cell line cells, was significantly increased, as was the epithelial–mesenchymal transition change. A chemokine array identified the CCL20-CCR6 axis as a concentration-dependent signal in ACHN and Caki-1 cell migration. Akt in the ACHN and Caki-1 cells was activated by macrophage-like cells, and the CCL20 neutralizing antibody suppressed migration ability, epithelial–mesenchymal transition, and Akt phosphorylation in the ACHN and Caki-1 cells. Akt inhibitor AZD5363 also decreased the epithelial–mesenchymal transition change and migration ability in the ACHN and Caki-1 cells. In 42 renal cell carcinoma tissues, patients with CCR6 and macrophage infiltration indicated poor prognoses. In the tumor microenvironment of renal cell carcinoma, cancer cells are activated by CCL20 secreted by tumor-associated macrophages through Akt activation, followed by epithelial–mesenchymal transition and an acquired migration ability. Thus, inhibition of the CCL20-CCR6 axis may be a potential therapeutic strategy for renal cell carcinoma.

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Kato, Takashi, Man Hagiyama, Yasutoshi Takashima, Azusa Yoneshige, and Akihiko Ito. "Cell adhesion molecule-1 shedding induces apoptosis of renal epithelial cells and exacerbates human nephropathies." American Journal of Physiology-Renal Physiology 314, no. 3 (March 1, 2018): F388—F398. http://dx.doi.org/10.1152/ajprenal.00385.2017.

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Chronic kidney disease (CKD) is an important problem throughout the world, associated with the increase of blood urea nitrogen (BUN) and serum creatinine (sCre) and with renal tubular injuries. It is crucial to elucidate the molecular mechanisms of renal injuries to identify the new therapeutics and early diagnostic methods. We focused on cell adhesion molecule-1 (CADM1) protein. CADM1, its isoform SP4, is expressed in the epithelial cells of various tissues, including renal distal tubules, localized on the lateral cell membrane, mediates cell-cell adhesion via trans-homophilic binding, and interacts with various proteins. We previously reported that its expression was downregulated by post-proteolytic cleavage (α- and β-shedding) in pulmonary diseases. To investigate whether CADM1 α-shedding occurs in human nephropathies, we performed Western blotting and immunohistochemical analysis of specimens with arterionephrosclerosis (AS) and diabetic nephropathy (DN) from autopsied kidneys. CADM1 α-shedding was induced in AS and DN kidneys and derived from the decrease in full-length CADM1 (FL-CADM1) and increase of the COOH-terminal fragment (α-CTF). In particular, the reduced FL-CADM1 level was correlated with tubular and tubulointerstitial injuries and the increases in BUN and sCre levels. Apoptosis of renal tubular epithelial cells (TECs) was promoted in both nephropathies, and it was significantly correlated with the decrease in the FL-CADM1. Furthermore, FL-CADM1 knockdown by small interfering RNA downregulated anti-apoptotic Bcl-2 protein and promoted apoptosis of cultured renal TECs. The present study suggests that the reduction of FL-CADM1 leads to renal TEC apoptosis and could exacerbate renal tubular and tubulointerstitial injuries, which contribute to the development of CKD.

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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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Wilson, P. D. "Epithelial cell polarity and disease." American Journal of Physiology-Renal Physiology 272, no. 4 (April 1, 1997): F434—F442. http://dx.doi.org/10.1152/ajprenal.1997.272.4.f434.

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The establishment and maintenance of epithelial polarity is essential for the integrity and function of epithelial organs and is particularly critical in the kidney, where vectorial reabsorption and secretion are effected in different segments of the nephron by the differential polarized insertion of channels, transporters, and related proteins into apical membranes lining the tubule lumen or basolateral membranes adjacent to the interstitium and blood space. Faulty intracellular delivery and polarization of membrane proteins can lead to serious diseases such as cystic fibrosis, I cell disease, and renal cystic diseases. The best understood disease of epithelial polarity is autosomal dominant polycystic kidney disease (ADPKD) caused by mutations in a >462-kDa, developmentally regulated membrane protein, “polycystin.” ADPKD cysts are characteristically lined by a single layer of structurally polarized epithelial cells with normal functional intercellular tight junctions but with aberrant polarization of some important membrane proteins. Abnormal apical membrane polarity of biochemically active, ouabain-sensitive Na-K-adenosinetriphosphatase (Na-K-ATPase) in ADPKD cyst epithelia leads to abnormal sodium ion secretion and provides a mechanism for aberrant fluid secretion. In addition, apically mislocated, functional epidermal growth factor (EGF) receptors on cyst epithelia, together with EGF synthesis and secretion into cyst lumens, provide a mechanism for autocrine regulation of increased epithelial cell proliferation in ADPKD. Underlying mechanisms for these abnormalities in polarized distribution of membrane proteins include the aberrant expression of fetal gene products, such as the beta2-subunit of Na-K-ATPase, in ADPKD kidneys. Overexpression of polycystin protein in ADPKD cyst epithelia, low levels restricted to medullary collecting tubules in normal adult kidneys, and high levels in ureteric bud-derived structures in human fetal kidneys further suggest a failure of downregulation of fetal genes as a mechanism for the polarity abnormalities that characterize ADPKD.

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Pelletier, Glenn J., Steven L. Brody, Helen Liapis, Robert A. White, and Brian P. Hackett. "A human forkhead/winged-helix transcription factor expressed in developing pulmonary and renal epithelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 3 (March 1, 1998): L351—L359. http://dx.doi.org/10.1152/ajplung.1998.274.3.l351.

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Members of the forkhead/winged-helix transcription factor family play crucial roles during vertebrate development. A human hepatocyte nuclear factor/forkhead homolog (HFH)-4 cDNA encoding a 421-amino acid protein was isolated from a human fetal lung cDNA library. By Southern blot analysis of human-rodent somatic cell hybrid genomic DNA, the human HFH-4 gene localizes to chromosome 17q23-qter. This is the locus of another forkhead/winged-helix gene, the interleukin enhancer binding factor gene. RNA blot analysis revealed a 2.5-kilobase human HFH-4 transcript in fetal lung, kidney, and brain as well as in adult reproductive tissues, lung, and brain. By in situ hybridization, HFH-4 expression is associated with differentiation of the proximal pulmonary epithelium, starting during the pseudoglandular stage of human lung development. During human renal morphogenesis, HFH-4 is expressed in the developing epithelial cells of the ureteric duct, glomerulus, and epithelial vesicles. The unique pattern of HFH-4 expression during human fetal development suggests a role for this forkhead/winged-helix factor during pulmonary and renal epithelial development.

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Browne, James Alexander, Alexander L. Pearson, Riad Abou Zahr, Ioana Niculescu-Duvaz, Deborah L. Baines, and Mark E. C. Dockrell. "TGF-β activates ERK5 in human renal epithelial cells." Biochemical and Biophysical Research Communications 373, no. 3 (August 2008): 440–44. http://dx.doi.org/10.1016/j.bbrc.2008.06.058.

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Liapis, Helen, M. Nag, and Deepak M. Kaji. "K-Cl cotransporter expression in the human kidney." American Journal of Physiology-Cell Physiology 275, no. 6 (December 1, 1998): C1432—C1437. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1432.

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The K-Cl cotransporter protein KCC1 is a membrane transport protein that mediates the coupled, electroneutral transport of K and Cl across plasma membranes. The precise cell type(s) in the kidney that express the K-Cl cotransporter have remained unknown. The aim of the present investigation was to define the distribution of KCC1 mRNA in the human kidney. We used in situ hybridization with a nonradioactive digoxigenin-labeled riboprobe. We identified abundant KCC1 mRNA expression in the epithelial cells throughout the distal and proximal renal tubular epithelium. The transporter was also expressed in glomerular mesangial cells and endothelial cells of the renal vessels. These findings suggest that the K-Cl cotransporter may have an important role in transepithelial K and Cl reabsorption.

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Bignon, Yohan, Virginie Poindessous, Luca Rampoldi, Violette Haldys, and Nicolas Pallet. "Chemically based transmissible ER stress protocols are unsuitable to study cell-to-cell UPR transmission." Biochemical Journal 477, no. 20 (October 29, 2020): 4037–51. http://dx.doi.org/10.1042/bcj20200699.

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Renal epithelial cells regulate the destructive activity of macrophages and participate in the progression of kidney diseases. Critically, the Unfolded Protein Response (UPR), which is activated in renal epithelial cells in the course of kidney injury, is required for the optimal differentiation and activation of macrophages. Given that macrophages are key regulators of renal inflammation and fibrosis, we suppose that the identification of mediators that are released by renal epithelial cells under Endoplasmic Reticulum (ER) stress and transmitted to macrophages is a critical issue to address. Signals leading to a paracrine transmission of ER stress (TERS) from a donor cell to a recipient cells could be of paramount importance to understand how ER-stressed cells shape the immune microenvironment. Critically, the vast majority of studies that have examined TERS used thaspigargin as an inducer of ER stress in donor cells in cellular models. By using multiple sources of ER stress, we evaluated if human renal epithelial cells undergoing ER stress can transmit the UPR to human monocyte-derived macrophages and if such TERS can modulate the inflammatory profiles of these cells. Our results indicate that carry-over of thapsigargin is a confounding factor in chemically based TERS protocols classically used to induce ER Stress in donor cells. Hence, such protocols are not suitable to study the TERS phenomenon and to identify its mediators. In addition, the absence of TERS transmission in more physiological models of ER stress indicates that cell-to-cell UPR transmission is not a universal feature in cultured cells.

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Kagami, Shoji, Yuji Morimoto, Kaname Okada, Koji Yasutomo, Takashi Kuhara, and Yasuhiro Kuroda. "A Monoclonal Antibody (1F3) to Human Glomerular Epithelial Cells: A New Marker for Renal Epithelial Cell Injury." Nephron 75, no. 1 (1997): 65–71. http://dx.doi.org/10.1159/000189501.

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Morimoto, Yuji, Shoji Kagami, Kaname Okada, Kouji Yasutomo, Takashi Kuhara, and Yasuhiro Kuroda. "A monoclonal antibody (1F3) to human glomerular epithelial cells: A new marker for renal epithelial cell injury." Nihon Shoni Jinzobyo Gakkai Zasshi 9, no. 2 (1996): 222–28. http://dx.doi.org/10.3165/jjpn.9.222.

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Wong, Victoria Y., Paul M. Keller, Mark E. Nuttall, Kristine Kikly, Walter E. DeWolf, Dennis Lee, Shujath M. Ali, et al. "Role of caspases in human renal proximal tubular epithelial cell apoptosis." European Journal of Pharmacology 433, no. 2-3 (December 2001): 135–40. http://dx.doi.org/10.1016/s0014-2999(01)01517-5.

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Dong, Fengming, Rongguo Fu, Qiaoling Yu, Yanyan Yang, Yixin Zou, Fumeng Huang, and Zhengmou Wang. "Effect of Macrophage 2c on Human Renal Tubular Epithelial Cell Activation." Hong Kong Journal of Nephrology 17, no. 2 (October 2015): S85. http://dx.doi.org/10.1016/j.hkjn.2015.09.123.

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Hamilton, Kirk L., and Daniel C. Devor. "Basolateral membrane K+ channels in renal epithelial cells." American Journal of Physiology-Renal Physiology 302, no. 9 (May 1, 2012): F1069—F1081. http://dx.doi.org/10.1152/ajprenal.00646.2011.

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The major function of epithelial tissues is to maintain proper ion, solute, and water homeostasis. The tubule of the renal nephron has an amazingly simple structure, lined by epithelial cells, yet the segments (i.e., proximal tubule vs. collecting duct) of the nephron have unique transport functions. The functional differences are because epithelial cells are polarized and thus possess different patterns (distributions) of membrane transport proteins in the apical and basolateral membranes of the cell. K+ channels play critical roles in normal physiology. Over 90 different genes for K+ channels have been identified in the human genome. Epithelial K+ channels can be located within either or both the apical and basolateral membranes of the cell. One of the primary functions of basolateral K+ channels is to recycle K+ across the basolateral membrane for proper function of the Na+-K+-ATPase, among other functions. Mutations of these channels can cause significant disease. The focus of this review is to provide an overview of the basolateral K+ channels of the nephron, providing potential physiological functions and pathophysiology of these channels, where appropriate. We have taken a “K+ channel gene family” approach in presenting the representative basolateral K+ channels of the nephron. The basolateral K+ channels of the renal epithelia are represented by members of the KCNK, KCNJ, KCNQ, KCNE, and SLO gene families.

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Gao, Dongmei, Shun Yao, Yanhu Sun, Di Zheng, Quan Zhang, and Wenhua Li. "Astaxanthin attenuate iohexol-induced human proximal renal tubular epithelial cells injury via the ROS/NLRP3 inflammasome signal pathway." SDRP Journal of Food Science & Technology 4, no. 3 (2019): 687–95. http://dx.doi.org/10.25177/jfst.4.3.ra.503.

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Rastaldi, Maria P., Franco Ferrario, Laura Giardino, Giacomo Dell'Antonio, Carlo Grillo, Paolo Grillo, Frank Strutz, Gerhard A. Müller, Giuliano Colasanti, and Giuseppe D'Amico. "Epithelial-mesenchymal transition of tubular epithelial cells in human renal biopsies." Kidney International 62, no. 1 (July 2002): 137–46. http://dx.doi.org/10.1046/j.1523-1755.2002.00430.x.

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Peired, Anna Julie, Giulia Antonelli, Maria Lucia Angelotti, Marco Allinovi, Francesco Guzzi, Alessandro Sisti, Roberto Semeraro, et al. "Acute kidney injury promotes development of papillary renal cell adenoma and carcinoma from renal progenitor cells." Science Translational Medicine 12, no. 536 (March 25, 2020): eaaw6003. http://dx.doi.org/10.1126/scitranslmed.aaw6003.

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Acute tissue injury causes DNA damage and repair processes involving increased cell mitosis and polyploidization, leading to cell function alterations that may potentially drive cancer development. Here, we show that acute kidney injury (AKI) increased the risk for papillary renal cell carcinoma (pRCC) development and tumor relapse in humans as confirmed by data collected from several single-center and multicentric studies. Lineage tracing of tubular epithelial cells (TECs) after AKI induction and long-term follow-up in mice showed time-dependent onset of clonal papillary tumors in an adenoma-carcinoma sequence. Among AKI-related pathways, NOTCH1 overexpression in human pRCC associated with worse outcome and was specific for type 2 pRCC. Mice overexpressing NOTCH1 in TECs developed papillary adenomas and type 2 pRCCs, and AKI accelerated this process. Lineage tracing in mice identified single renal progenitors as the cell of origin of papillary tumors. Single-cell RNA sequencing showed that human renal progenitor transcriptome showed similarities to PT1, the putative cell of origin of human pRCC. Furthermore, NOTCH1 overexpression in cultured human renal progenitor cells induced tumor-like 3D growth. Thus, AKI can drive tumorigenesis from local tissue progenitor cells. In particular, we find that AKI promotes the development of pRCC from single progenitors through a classical adenoma-carcinoma sequence.

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Wilson, P. D., M. A. Dillingham, R. Breckon, and R. J. Anderson. "Defined human renal tubular epithelia in culture: growth, characterization, and hormonal response." American Journal of Physiology-Renal Physiology 248, no. 3 (March 1, 1985): F436—F443. http://dx.doi.org/10.1152/ajprenal.1985.248.3.f436.

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Individually microdissected nephron segments of defined epithelial origin from human kidneys were cultured in vitro in the present studies. Nephron segments of proximal convoluted tubule, proximal straight tubule, cortical thick ascending limb of Henle, and cortical collecting tubule were grown in defined media. Each cell type retained differentiated characteristics as assessed by ultrastructural morphology, marker enzyme profiles, and adenylate cyclase response to selected hormones. These studies demonstrate the feasibility of using primary cultures of well-defined segments of the human nephron to study human renal tubular epithelia in vitro.

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Du, J., and P. D. Wilson. "Abnormal polarization of EGF receptors and autocrine stimulation of cyst epithelial growth in human ADPKD." American Journal of Physiology-Cell Physiology 269, no. 2 (August 1, 1995): C487—C495. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c487.

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The underlying mechanism of the hyperproliferative response of human autosomal dominant polycystic kidney disease (ADPKD) epithelia was studied. Epidermal growth factor (EGF) protein is highly expressed in ADPKD cyst epithelia in vivo, and primary cultures are hyperesponsive to mitogenic stimulation by EGF in vitro. Doses of > 1 ng/ml EGF were highly mitogenic to ADPKD epithelia. 3H-labeled thymidine proliferation assays showed that cyst fluids and ADPKD epithelial cell-conditioned media also stimulated renal epithelial cell proliferation and contained EGF immunoreactivity (6, 30, and 37 kDa) as detected by Western blots. Radioimmunoassays detected mean levels of 2.87 and 1.4 ng/ml EGF in cyst fluids from early (proliferative) and end-stage ADPKD cysts, respectively. Scatchard analysis of 125I-labeled EGF binding to apical and basolateral membrane showed high-affinity binding to basolateral membranes of normal and ADPKD kidneys but additional unique high-affinity receptor binding to apical membranes of ADPKD but not normal kidneys. Cross-linking analysis and antiphosphotyrosine Western analysis demonstrated functionally active apical EGF receptors at 150-170 kDa. These results suggest mediation of cyst expansion via an autocrine loop involving EGF synthesis and processing by cyst epithelial cells, apical secretion into cyst lumens, and subsequent binding to and phosphorylation of apical membrane EGF receptors. These findings are consistent with a membrane protein polarization defect in ADPKD cyst epithelia.

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Simon, E. E., C. H. Liu, M. Das, S. Nigam, T. J. Broekelmann, and J. A. McDonald. "Characterization of integrins in cultured human renal cortical tubule epithelial cells." American Journal of Physiology-Renal Physiology 267, no. 4 (October 1, 1994): F612—F623. http://dx.doi.org/10.1152/ajprenal.1994.267.4.f612.

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We have characterized the integrins present on cultured tubule epithelial cells from human renal cortexes, enriched for proximal cells, using fluorescence microscopy, immunoprecipitation, and cell adhesion assays. By immunofluorescence, the alpha 3-integrin subunit stained most intensely and was present on all cells predominantly at cell-cell contacts. The alpha 6-subunit was present on all cells in a pattern consistent with extracellular matrix contacts. The alpha 5-subunit was present on most cells in a cell-matrix contact pattern; alpha V-subunit was weakly positive and occasionally seen in cell-matrix contacts. The alpha 2-subunit was present on clusters of distal tubule cells, predominantly at cell-cell contacts. Immunoprecipitation revealed the predominant integrin to be alpha 3 beta 1 with some alpha 2 beta 1, presumably contributed by distal cells. The alpha 5 beta 1-, alpha 6 beta 1-, alpha 6 beta 4-, and alpha V beta 3-integrins, as well as trace amounts of alpha 1 beta 1-integrins, were also present. The alpha 4 beta 1-integrin was not detected. Initial attachment to fibronectin was mediated by alpha V beta 3- and alpha 5 beta 1-integrins; initial attachment to laminin was mediated by the alpha 6 beta 1- and alpha 3 beta 1- integrins and, in some preparations, by an unidentified integrin; and initial attachment to collagen type IV was mediated by alpha V beta 3-integrin and an unidentified beta 1-integrin. After extensively immunodepleting membrane extracts with anti-alpha 1, -alpha 2, -alpha 3, -alpha 4, -alpha 5, -alpha 6, and -alpha V antibodies, an anti-beta 1 antibody still precipitated an integrin. Its electrophoretic mobility differs from the laminin-binding alpha 7 beta 1-integrin. Thus we have identified many of the integrins on cortical tubule cells and their role in mediating initial attachment to extracellular matrix. However, the cell adhesion assays and immunoprecipitations suggest the presence of an unidentified beta 1-integrin that may mediate renal tubule cell attachment to laminin and collagen.

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Pleniceanu, Oren, Orit Harari-Steinberg, Dorit Omer, Yehudit Gnatek, Bat-El Lachmi, Osnat Cohen-Zontag, Eugenia Manevitz-Mendelson, et al. "Successful Introduction of Human Renovascular Units into the Mammalian Kidney." Journal of the American Society of Nephrology 31, no. 12 (August 4, 2020): 2757–72. http://dx.doi.org/10.1681/asn.2019050508.

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BackgroundCell-based therapies aimed at replenishing renal parenchyma have been proposed as an approach for treating CKD. However, pathogenic mechanisms involved in CKD such as renal hypoxia result in loss of kidney function and limit engraftment and therapeutic effects of renal epithelial progenitors. Jointly administering vessel-forming cells (human mesenchymal stromal cells [MSCs] and endothelial colony-forming cells [ECFCs]) may potentially result in in vivo formation of vascular networks.MethodsWe administered renal tubule–forming cells derived from human adult and fetal kidneys (previously shown to exert a functional effect in CKD mice) into mice, alongside MSCs and ECFCs. We then assessed whether this would result in generation of “renovascular units” comprising both vessels and tubules with potential interaction.ResultsDirectly injecting vessel-forming cells and renal tubule–forming cells into the subcutaneous and subrenal capsular space resulted in self-organization of donor-derived vascular networks that connected to host vasculature, alongside renal tubules comprising tubular epithelia of different nephron segments. Vessels derived from MSCs and ECFCs augmented in vivo tubulogenesis by the renal tubule–forming cells. In vitro coculture experiments showed that MSCs and ECFCs induced self-renewal and genes associated with mesenchymal–epithelial transition in renal tubule–forming cells, indicating paracrine effects. Notably, after renal injury, renal tubule–forming cells and vessel-forming cells infused into the renal artery did not penetrate the renal vascular network to generate vessels; only administering them into the kidney parenchyma resulted in similar generation of human renovascular units in vivo.ConclusionsCombined cell therapy of vessel-forming cells and renal tubule–forming cells aimed at alleviating renal hypoxia and enhancing tubulogenesis holds promise as the basis for new renal regenerative therapies.

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Haugen, Aage, Lovise Maehle, Steen Mollerup, Edgar Rivedal, and David Ryberg. "Nickel-Induced Alterations in Human Renal Epithelial Cells." Environmental Health Perspectives 102 (September 1994): 117. http://dx.doi.org/10.2307/3431773.

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31

Cooper, A. J. "Ammoniagenesis in cultured human renal cortical epithelial cells." American Journal of Physiology-Renal Physiology 257, no. 4 (October 1, 1989): F705—F706. http://dx.doi.org/10.1152/ajprenal.1989.257.4.f705.

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Haugen, A., L. Maehle, S. Mollerup, E. Rivedal, and D. Ryberg. "Nickel-induced alterations in human renal epithelial cells." Environmental Health Perspectives 102, suppl 3 (September 1994): 117–18. http://dx.doi.org/10.1289/ehp.94102s3117.

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Addla, Sanjai K., Mick D. Brown, Claire A. Hart, Vijay A. C. Ramani, and Noel W. Clarke. "Characterization of the Hoechst 33342 side population from normal and malignant human renal epithelial cells." American Journal of Physiology-Renal Physiology 295, no. 3 (September 2008): F680—F687. http://dx.doi.org/10.1152/ajprenal.90286.2008.

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The fundamental changes which predispose for renal cell carcinoma (RCC) are poorly characterized. It is hypothesized that “cancer stem cells” may be influential in carcinogenesis, and the epithelial side population (SP) is enriched for stemlike cells in other epithelial cancers. In this study, we have isolated and characterized the SP and non-SP (NSP) populations from normal (NK) and malignant (RCC) human kidney tissue. NK specimens were taken from patients undergoing non-renal cancer surgery and paired malignant and macroscopically normal tissue samples were taken from patients undergoing surgery for RCC. The Hoechst 33342 dye efflux technique was used to isolate epithelial SP and NSP from normal and malignant human renal tissue. Cellular subpopulations were phenotyped for lineage, cell cycle, and putative stem cell markers, and functionally characterized using in vitro colony-forming and proliferation assays. The SP constituted 3.8 ± 0.4 and 5.9 ± 0.9% of epithelial cells in NK and RCC, respectively, of which 14.1 ± 3.5 and 13.2 ± 3.6% were shown to be in G0. SP cells demonstrated greater proliferative potential in colony-forming efficiency, long-term culture, and spheroids assays and were shown to be maintained upon tissue culture passage. We have shown that the renal SP is enriched for quiescent cells, with a high proliferative capacity and stemlike properties. The population is, however, heterogeneous, confirming that the terms “SP cell” and “stem cell” cannot be used interchangeably.

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Achtstätter, T., R. Moll, B. Moore, and W. W. Franke. "Cytokeratin polypeptide patterns of different epithelia of the human male urogenital tract: immunofluorescence and gel electrophoretic studies." Journal of Histochemistry & Cytochemistry 33, no. 5 (May 1985): 415–26. http://dx.doi.org/10.1177/33.5.2580881.

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Intermediate filament proteins of normal epithelia of the human and the bovine male urogenital tract and of certain human renal and bladder carcinomas have been studied by immunofluorescence microscopy and by two-dimensional gel electrophoresis of cytoskeletal fractions from microdissected tissue samples. The patterns of expression of cytokeratin polypeptides differ in the various epithelia. Filaments of a cytokeratin nature have been identified in all true epithelial cells of the male urogenital tract, including renal tubules and rete testis. Simple epithelia of renal tubules and collecting ducts of kidney, as well as rete testis, express only cytokeratin polypeptides nos. 7, 8, 18, and 19. In contrast, the transitional epithelia of renal pelvis, ureter, bladder, and proximal urethra contain, in addition to those polypeptides, cytokeratin no. 13 and small amounts of nos. 4 and 5. Most epithelia lining the human male reproductive tract, including those in the epididymis, ductus deferens, prostate gland, and seminal vesicle, synthesize cytokeratin no. 5 in addition to cytokeratins nos. 7, 8, 18, and 19 (cytokeratin no. 7 had not been detected in the prostate gland). Cytokeratin no. 17 has also been identified, but in very low amounts, in seminal vesicle and epididymis. The cytokeratin patterns of the urethra correspond to the gradual transition of the pseudostratified epithelium of the pars spongiosa (cytokeratins nos. 4, 5, 6, 13, 14, 15, and 19) to the stratified squamous epithelium of the fossa navicularis (cytokeratins nos. 5, 6, 10/11, 13, 15, and 19, and minor amounts of nos. 1 and 14). The noncornified stratified squamous epithelium of the glans penis synthesizes cytokeratin nos. 1, 5, 6, 10/11, 13, 14, 15, and 19. In immunofluorescence microscopy, selective cytokeratin antibodies reveal differential staining of different groups or layers of cells in several epithelia that may relate to the specific expression of cytokeratin polypeptides. Human renal cell carcinomas show a simple cytokeratin pattern consisting of cytokeratins nos. 8, 18, and 19, whereas transitional cell carcinomas of the bladder reveal additional cytokeratins such as nos. 5, 7, 13, and 17 in various proportions. The results shows that the wide spectrum of histological differentiation of the diverse epithelia present in the male urogenital tract is accompanied by pronounced changes in the expression of cytokeratin polypeptides and suggest that tumors from different regions of the urogenital tract may be distinguished by their cytokeratin complements.

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35

Anderson, Robert J., Carla J. Ray, and Thomas J. Burke. "HUMAN RED BLOOD CELL HEMOLYSATE IS A POTENT MITOGEN FOR RENAL TUBULAR EPITHELIAL CELLS." Renal Failure 22, no. 3 (January 2000): 267–81. http://dx.doi.org/10.1081/jdi-100100871.

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CHAKRAVORTY, S. J., P. COCKWELL, J. GIRDLESTONE, C. J. BROOKS, and C. O. S. SAVAGE. "Fractalkine expression on human renal tubular epithelial cells: potential role in mononuclear cell adhesion." Clinical & Experimental Immunology 129, no. 1 (June 28, 2002): 150–59. http://dx.doi.org/10.1046/j.1365-2249.2002.01906.x.

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37

Parmar, Hema, Peter Young, Joanne T. Emerman, Richard M. Neve, Shanaz Dairkee, and Gerald R. Cunha. "A Novel Method for Growing Human Breast Epithelium in Vivo Using Mouse and Human Mammary Fibroblasts." Endocrinology 143, no. 12 (December 1, 2002): 4886–96. http://dx.doi.org/10.1210/en.2002-220570.

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Abstract A novel system is described for studying the growth of normal human mammary epithelium in vivo as grafts in athymic nude mice. The key feature of this model is reconstitution of the epithelial-stromal interactions required for normal growth and differentiation of the human mammary epithelium, which produces ducts that are comparable to those in the normal human mammary gland. Human breast epithelial organoids were combined with mammary fibroblasts from mouse or human origin in collagen gels, which were subsequently transplanted under the renal capsule of female nude mice hosts. The resulting grafts showed an increase in the ductal density compared with that observed previously. These ducts expressed appropriate markers for luminal and myoepithelial cells and steroid receptors. Treatment of the host with diethylstilbestrol or estradiol and progesterone significantly increased the number of ducts observed and increased cell proliferation. The grafts also displayed production of β-casein and milk fat globule membrane protein when the hosts were allowed to become pregnant. This model allows for a variety of epithelial and stromal cells to be used in combination, which would aid in understanding key factors that regulate normal human mammary gland development.

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Fernandez Miyakawa, Mariano E., Osvaldo Zabal, and Claudia Silberstein. "Clostridium perfringens epsilon toxin is cytotoxic for human renal tubular epithelial cells." Human & Experimental Toxicology 30, no. 4 (May 20, 2010): 275–82. http://dx.doi.org/10.1177/0960327110371700.

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Clostridium perfringens epsilon toxin (ETX) is responsible for a fatal enterotoxemia in different animal species, producing extensive renal damage, neurological disturbance and edema of lungs, heart and kidneys. However, there is no information about the susceptibility of humans to ETX. Here, we report that primary cultures of human renal tubular epithelial cells (HRTEC) exposed to ETX showed a marked swelling with subsequent large blebs surrounding most cells. The incubation of HRTEC with ETX produced a reduction of cell viability in a dose- and time-dependent manner. The CD50 after 1-hour and 24-hour incubation were 3 µg/mL and 0.5 µg/mL, respectively. The pulse with ETX for 3 min was enough to produce a significant cytotoxic effect on HRTEC after 1-hour incubation. ETX binds to HRTEC forming a large complex of about 160 kDa similar to what was found in the Madin-Darby canine kidney (MDCK) cell line. The HRTEC could be a useful cell model to improve the understanding of the mechanisms involved on the cell damage mediated by ETX.

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Fuller, C. M., M. S. Awayda, M. P. Arrate, A. L. Bradford, R. G. Morris, C. M. Canessa, B. C. Rossier, and D. J. Benos. "Cloning of a bovine renal epithelial Na+ channel subunit." American Journal of Physiology-Cell Physiology 269, no. 3 (September 1, 1995): C641—C654. http://dx.doi.org/10.1152/ajpcell.1995.269.3.c641.

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A bovine homologue of the rat and human epithelial Na+ channel subunits, alpha-rENaC and alpha-hENaC, was cloned. The cDNA clone, termed alpha-bENaC, was isolated from a bovine renal papillary collecting duct cDNA expression library. The bovine cDNA is 3,584 base pairs (bp) long, has an open reading frame of 2,094 bp encoding a 697-amino acid protein, and is 75-85% homologous to its rat and human counterparts. In vitro translation of the transcribed cRNA yields an 80-kDa polypeptide and one at 92 kDa in the presence of pancreatic microsomes. The clone exhibits consensus sequences for N-linked glycosylation and for phosphorylation by protein kinase C, but not for protein kinase A. After expression in Xenopus laevis oocytes, a small amiloride-sensitive Na+ conductance that exhibited inward rectification and a reversal potential greater than +30 mV, consistent with the predicted equilibrium potential for Na+, was identified. The expressed alpha-bENaC-associated Na+ current was not responsive to elevations in adenosine 3',5'-cyclic monophosphate but could be stimulated by phorbol 12-myristate 13-acetate, an activator of protein kinase C. alpha-bENaC also formed amiloride-sensitive chimeric channels when coexpressed with the rat beta- and gamma-ENaC subunits in Xenopus oocytes. alpha-bENaC therefore represents a novel isoform of a growing family of epithelial Na+ channels.

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Sramkova, Monika, Katarina Kozics, Vlasta Masanova, Iveta Uhnakova, Filip Razga, Veronika Nemethova, Petra Mazancova, et al. "Kidney nanotoxicity studied in human renal proximal tubule epithelial cell line TH1." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 845 (September 2019): 403017. http://dx.doi.org/10.1016/j.mrgentox.2019.01.012.

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41

Loghman-Adham, Mahmoud, Surya M. Nauli, Carlos E. Soto, Barbara Kariuki, and Jing Zhou. "Immortalized epithelial cells from human autosomal dominant polycystic kidney cysts." American Journal of Physiology-Renal Physiology 285, no. 3 (September 2003): F397—F412. http://dx.doi.org/10.1152/ajprenal.00310.2002.

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Autosomal dominant polycystic kidney disease (ADPKD) is the result of mutations in one allele of the PKD1 or PKD2 genes, followed by “second hit” somatic mutations of the other allele in renal tubule cells. Continued proliferation of clonal cells originating from different nephron segments leads to cyst formation. In vitro studies of the mechanisms of cyst formation have been hampered by the scarcity of nephrectomy specimens and the limited life span of cyst-derived cells in primary culture. We describe the development of a series of immortalized epithelial cell lines from over 30 individual renal cysts obtained from 11 patients with ADPKD. The cells were immortalized with either wild-type (WT) or temperature-sensitive (TS) recombinant adeno-simian virus (SV)40 viruses. SV40 DNA integration into the cell genome was verified by PCR analysis. The cells have been passaged over 50 times with no apparent phenotypic change. By light microscopy, the cells appear pleomorphic but mostly polygonal and resemble the primary cultures. Transmission electron microscopy shows polarized epithelia with tight junctions. The SV40 large T antigen was detected by immunocytochemistry and by Western blot analysis at 37°C in the WT cell lines and at 33°C in the TS cell lines. It disappeared in TS cells 72 h following transfer to 39°C. The majority ( 29 ) of the cell lines show binding of Dolichos biflorus lectin, suggesting distal tubule origin. Three cell lines show binding of Lotus tetragonolobus lectin or express aminopeptidase N, suggesting proximal tubule origin. Three cell lines were derived from a mixture of cysts and express features of both tubules. The PKD1 and PKD2 mRNA and protein were detected in all cells by RT-PCR and by immunocytochemistry. The majority of the cells tested also express the epidermal growth factor receptor, cystic fibrosis transmembrane conductance regulator, epithelial sodium channel, and renin. These new series of cyst-derived cell lines represent useful and readily available in vitro models for studying the cellular and molecular biology of ADPKD.

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42

Kreft, B., W. J. Jabs, T. Laskay, M. Klinger, W. Solbach, S. Kumar, and G. van Zandbergen. "Polarized Expression of Tamm-Horsfall Protein by Renal Tubular Epithelial Cells Activates Human Granulocytes." Infection and Immunity 70, no. 5 (May 2002): 2650–56. http://dx.doi.org/10.1128/iai.70.5.2650-2656.2002.

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ABSTRACT In renal bacterial infections granulocytes are of major importance in the primary immune defense against invading pathogens. However, the mechanisms of granulocytic activation in renal interstitial invasion have not been clarified. Renal tubular epithelial cell mechanisms inducing granulocytic activation and bacterial killing may include tubular cell expression of Tamm-Horsfall protein (THP), a urinary protein that is known to enhance cytokine expression in monocytes. We studied the role of THP in granulocytic activation. A strong binding of THP to human granulocytes was demonstrated by fluorescence-activated cell sorter analysis. Urinary THP and supernatants of THP-expressing cultured tubular epithelial cells (MDCK) enhanced interleukin-8 (IL-8) expression by human granulocytes. Renal tubular cells growing polarized on polycarbonate membranes were used to study apical versus basal THP expression. By electron microscopy THP immunoreactivity was exclusively found on the apical surfaces of tubular cells and was absent on the basolateral cell membrane. In the apical cell culture compartment we found significantly more stimulatory activity for granulocytic IL-8 expression. CD62L, a selectin less expressed in activated granulocytes, was decreased in granulocytes incubated with urinary THP and in supernatants of THP-producing renal tubular cells but not in supernatants from THP-negative cells. Again, the effect on CD62L expression was found only in apical culture media and was absent in the basal compartment. In summary our data give evidence that renal tubular cell THP expression may be relevant in kidney diseases since THP is a potent activator of human granulocytes. The regulation of apical versus basal THP expression and release in vivo may be crucial in the induction of the inflammatory response, e.g., in bacterial renal diseases.

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43

Bijuklic, Klaudija, Paul Jennings, Jordan Kountchev, Julia Hasslacher, Sonia Aydin, Daniel Sturn, Walter Pfaller, Josef R. Patsch, and Michael Joannidis. "Migration of leukocytes across an endothelium-epithelium bilayer as a model of renal interstitial inflammation." American Journal of Physiology-Cell Physiology 293, no. 1 (July 2007): C486—C492. http://dx.doi.org/10.1152/ajpcell.00419.2006.

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Interstitial inflammation has emerged as a key event in the development of acute renal failure. To gain better insight into the nature of these inflammatory processes, the interplay between tubular epithelial cells, endothelial cells, and neutrophils (PMN) was investigated. A coculture transmigration model was developed, composed of human dermal microvascular endothelial (HDMEC) and human renal proximal tubular cells (HK-2) cultured on opposite sides of Transwell growth supports. Correct formation of an endoepithelial bilayer was verified by light and electron microscopy. The model was used to study the effects of endotoxin (LPS), tumor necrosis factor (TNF)-α, and α-melanocyte-stimulating hormone (α-MSH) by measuring PMN migration and cytokine release. To distinguish between individual roles of microvascular endothelial and epithelial cells in transmigration processes, migration of PMN was investigated separately in HK-2 and HDMEC monolayers. Sequential migration of PMN through endothelium and epithelium could be observed and was significantly increased after proinflammatory stimulation with either TNF-α or LPS (3.5 ± 0.58 and 2.76 ± 0.64-fold vs. control, respectively). Coincubation with α-MSH inhibited the transmigration of PMN through the bilayer after proinflammatory stimulation with LPS but not after TNF-α. The bilayers produced significant amounts of IL-8 and IL-6 mostly released from the epithelial cells. Furthermore, α-MSH decreased LPS-induced IL-6 secretion by 30% but had no significant effect on IL-8 secretion. We established a transmigration model showing sequential migration of PMN across microvascular endothelial and renal tubular epithelial cells stimulated by TNF-α and LPS. Anti-inflammatory effects of α-MSH in this bilayer model are demonstrated by inhibition on PMN transmigration and IL-6 secretion.

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Wang, Bohan, Gaofei He, Gang Xu, Jiaming Wen, and Xiao Yu. "miRNA-34a inhibits cell adhesion by targeting CD44 in human renal epithelial cells: implications for renal stone disease." Urolithiasis 48, no. 2 (September 10, 2019): 109–16. http://dx.doi.org/10.1007/s00240-019-01155-9.

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Guay-Woodford, L. M., O. Platt, and H. W. Harris. "Toad urinary bladder epithelial cells contain an analogue of cytoskeletal protein 4.1." American Journal of Physiology-Cell Physiology 260, no. 6 (June 1, 1991): C1308—C1314. http://dx.doi.org/10.1152/ajpcell.1991.260.6.c1308.

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Epithelial cell polarity and vectorial transport require cytoskeletal proteins that maintain local cell membrane structure and mediate cytoplasmic vesicle movement. The cytoskeleton of leaky epithelia, such as the intestinal mucosa and renal proximal tubule cells, has been extensively studied. However, cytoskeletal studies in tight epithelia such as the mammalian collecting duct and toad urinary bladder generally have been confined to ultrastructural investigation. Recent research in nonepithelial cell types has identified an interesting family of cytoskeletal proteins. Present in multiple cell types, these protein 4.1 analogues share a number of similar functional characteristics, yet are structurally diverse. They are multiply phosphorylated by several different kinases, and phosphorylation regulates their associations with other cytoskeletal constituents, integral membrane components, and cytoplasmic vesicles. Using a combination of immunochemical and immunofluorescent techniques, we have demonstrated that toad bladder epithelial cells contain a 65-kDa analogue of human erythrocyte protein 4.1. Toad bladder epithelial cell protein 4.1 is structurally similar to its erythrocyte counterpart and is phosphorylated. This protein 4.1 species is present throughout the toad bladder granular cell cytoplasm, suggesting that it participates in multiple granular cell functions.

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Adler, Lior, Edna Efrati, and Israel Zelikovic. "Molecular mechanisms of epithelial cell-specific expression and regulation of the human anion exchanger (pendrin) gene." American Journal of Physiology-Cell Physiology 294, no. 5 (May 2008): C1261—C1276. http://dx.doi.org/10.1152/ajpcell.00486.2007.

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Pendrin, a Cl−/anion exchanger encoded by the gene PDS, is highly expressed in the kidney, thyroid, and inner ear epithelia and is essential for bicarbonate secretion, iodide accumulation, and endolymph ion balance, respectively. This study aimed to define promoter regulatory elements essential for renal, thyroid, and inner ear epithelial cell-specific expression of human PDS (hPDS) and to explore the effect of ambient pH and aldosterone on hPDS promoter activity. Endogenous pendrin mRNA and protein were detected in renal HEK293, thyroid LA2, and inner ear VOT36 epithelial cell lines, but not in the fibroblast cell line, NIH3T3. A 4.2-kb hPDS 5′-flanking DNA sequence and consecutive 5′-deletion products were cloned into luciferase reporter vectors and transiently transfected into the above cell lines. Distinct differences in expression/activity of deduced positive/negative regulatory elements within the hPDS promoter between HEK293, LA2, and VOT36 cells were demonstrated, with only basal activity in NIH3T3 cells. Acidic pH (7.0–7.1) decreased and alkaline pH (7.6–7.7) increased hPDS promoter activity in transfected HEK293 and VOT36, but not in LA2 cells. Aldosterone (10−8 M) reduced hPDS promoter activity in HEK293 but had no effect in LA2 and VOT36 cells. These pH and aldosterone-induced effects on the hPDS promoter occurred within 96-bp and 89-bp regions, respectively, which likely contain distinct response elements to these modulators. Acidic pH and aldosterone decreased, and alkaline pH increased, endogenous pendrin mRNA level in HEK293 cells. In conclusion, pendrin-mediated HCO3− secretion in the renal tubule and anion transport in the endolymph may be regulated transcriptionally by systemic pH and aldosterone.

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Shen, Rulong, and Ping Wen. "Clear Cell Renal Cell Carcinoma With Syncytial Giant Cells: A Case Report and Review of the Literature." Archives of Pathology & Laboratory Medicine 128, no. 12 (December 1, 2004): 1435–38. http://dx.doi.org/10.5858/2004-128-1435-ccrccw.

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Abstract Renal cell carcinoma with syncytial giant cells (SGCs) is rare; to our knowledge, there are only 3 cases reported in the English literature. We report on a case that, unlike previous reports, was associated with higher grade renal cell carcinoma and an aggressive behavior. A 63-year-old man with gross hematuria was found to have a large left renal mass and no evidence of metastasis. The nephrectomy specimen contained a 14.8-cm mass that was confined within the renal capsule. Microscopically, a 1.8-cm area of SGCs was noted in a background of clear cell renal cell carcinoma of Fuhrman nuclear grades 2 to 4. The SGCs had voluminous cytoplasm, multiple large nuclei with prominent nucleoli, and focal emperipolesis. Identical to the background mononuclear tumor cells, the SGCs were positive for AE1/AE3, vimentin, and epithelial membrane antigen and negative for CD68, β-human chorionic gonadotropin, and mucin. Three months after surgery, the patient developed metastases in the liver, right kidney, and lungs.

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Omer, Dorit, Orit Harari-Steinberg, Ella Buzhor, Sally Metsuyanim, Oren Pleniceanu, Adi Zundelevich, Einav Nili Gal-Yam, and Benjamin Dekel. "Chromatin-Modifying Agents Reactivate Embryonic Renal Stem/Progenitor Genes in Human Adult Kidney Epithelial Cells but Abrogate Dedifferentiation and Stemness." Cellular Reprogramming 15, no. 4 (August 2013): 281–92. http://dx.doi.org/10.1089/cell.2012.0087.

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Twite, Nicolas, Graciela Andrei, Caroline Kummert, Catherine Donner, David Perez-Morga, Rita De Vos, Robert Snoeck, and Arnaud Marchant. "Sequestration of human cytomegalovirus by human renal and mammary epithelial cells." Virology 460-461 (July 2014): 55–65. http://dx.doi.org/10.1016/j.virol.2014.04.032.

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Devocelle, Aurore, Lola Lecru, Hélène François, Christophe Desterke, Cindy Gallerne, Pierre Eid, Oberlin Estelle, Bruno Azzarone, and Julien Giron-Michel. "Inhibition of TGF-β1 Signaling by IL-15: A Novel Role for IL-15 in the Control of Renal Epithelial-Mesenchymal Transition: IL-15 Counteracts TGF-β1-Induced EMT in Renal Fibrosis." International Journal of Cell Biology 2019 (July 7, 2019): 1–15. http://dx.doi.org/10.1155/2019/9151394.

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Abstract:

Renal tubulointerstitial fibrosis is the final common pathway in end-stage renal disease and is characterized by aberrant accumulation of extracellular matrix (ECM) components secreted by myofibroblasts. Tubular type 2 EMT, induced by TGF-β, plays an important role in renal fibrosis, by participating directly or indirectly in myofibroblasts generation. TGF-β1-induced apoptosis and fibrosis in experimental chronic murine kidney diseases are concomitantly associated with an intrarenal decreased expression of the IL-15 survival factor. Since IL-15 counteracts TGF-β1 effects in different cell models, we analyzed whether (1) human chronic inflammatory nephropathies evolving towards fibrosis could be also characterized by a weak intrarenal IL-15 expression and (2) IL-15 could inhibit epithelial-mesenchymal transition (EMT) and excess matrix deposition in human renal proximal tubular epithelial cells (RPTEC). Our data show that different human chronic kidney diseases are characterized by a strong decreased expression of intrarenal IL-15, which is particularly relevant in diabetic nephropathy, in which type 2 tubular EMT plays an important role in fibrosis. Moreover, primary epithelial tubular cultures deprived of growth supplements rapidly produce active TGF-β1 inducing a “spontaneous” EMT process characterized by the loss of membrane-bound IL-15 (mbIL-15) expression. Both “spontaneous” EMT and recombinant human (rh) TGF-β1-induced EMT models can be inhibited by treating RPTEC and HK2 cells with rhIL-15. Through a long-lasting phospho-c-jun activation, IL-15 inhibits rhTGF-β1-induced Snail1 expression, the master inducer of EMT, and blocks TGF-β1-induced tubular EMT and downstream collagen synthesis. In conclusion, our data suggest that intrarenal IL-15 could be a natural inhibitor of TGF-β in human kidney able to guarantee epithelial homeostasis and to prevent EMT process. Thus, both in vivo and in vitro an unbalance in intrarenal IL-15 and TGF-β1 levels could render RPTEC cells more prone to undergo EMT process. Exogenous IL-15 treatment could be beneficial in some human nephropathies such as diabetic nephropathy.

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Journal articles on the topic 'Human renal epithelial cell'

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