Renal epithelial cells

Endothelial cells are the major source of ET-1-synthesis. ET-1 is also produced by astrocytes, neurons, hepatocytes, bronchial epithelial cells, renal epithelial and mesangial cells. Physiological stimuli of ET-1-synthesis in endothelial cells are angiotensin II, catecholamines, thrombin, growth factors, insulin, hypoxia and shear stress. Inhibitors of ET-1 synthesis are atrial natriuretic peptide, prostaglandin E2 and prostacyclin. ET-2 is mainly synthesized in kidney, intestine, myocardium and placenta and ET-3 is predominantely produced by neurons, astrocytes and renal epithelial cells. 

Isolated perfused kidney/tubule Renal cortical slices Nephron segments Isolated renal epithelial cells Renal cell cultures... 

Sites of endothelin-receptor expression. ETA receptors are expressed in the smooth muscle cells of the vascular medial layer and the airways, in cardiac myocytes, lung parenchyma, bronchiolar epithelial cells and prostate epithelial cells. ETB receptors are expressed in endothelial cells, in bronchiolar smooth muscle cells, vascular smooth muscle cells of certain vessels (e.g. saphenous vein, internal mammary artety), in the renal proximal and distal tubule, the renal collecting duct and in the cells of the atrioventricular conducting system. 

OTRs are mainly expressed in myoepithelial cells of the galactiferus channels and the myometrium. The OTRs in vascular endothelial cells, renal epithelial cells (macula densa, proximal tubule) and cardiomyocytes induce the production of NO (vasodilation), natriuresis and release of ANP, respectively. The endometrium, ovary, amnion, testis, epididymis, prostate and thymus also express the OTR supporting a paracrine role of this peptide. Osteoblasts, osteoclasts, pancreatic islets cells, adipocytes, and several types of cancer cells also express OTRs. More over, expression of the OTR... 

Next, Reilly et al. [65] localized the Na /H exchanger gene product in renal epithelial cells where the distributions of the kinetic isoforms was well-established. The strategy was based on the observation that the resistant- and sensitive-types are restricted to the apical and basolateral membranes, respectively, in confluent LLC-PK]/Clone 4 cells [8]. Thus, if proteins encoded by the cloned cDNAs localized to the apical membrane this would indicate that they represent the resistant-type. Localization to the basolateral membrane would prove they were the sensitive-type and presence on both membranes would suggest that the two functional isoforms had identical primary structures. Na exchanger proteins were localized by... 

Large conductance CP-channels were described for renal epithelial cells such as MDCK-cells, urinary bladder, collecting duct and A6-cells [51-54] and in pulmonary alveolar cells [55]. 

Ueda, N. and Shah, S.V. (1992). Endonuclease-induced DNA damage and cell death in oxidant injury to renal tubular epithelial cells. J. Clin. Invest. 90, 2593-2597. 

Other plasminogen activator inhibitors are PAI-3, which is believed to be identical to the activated protein C inhibitor, and proteinase nexin 1, found in the renal epithelial cells, cytosol of fibroblasts, and cardiac myocytes (37, 42, 44, 45). 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

Colon adenocarcinoma epithelial cell line Rat renal proximal tubular epithelial cell line Tetrahydrofuranyl Valacyclovir hydrolase... 

Calcium oxalate monohydrate responsible for the formation of most kidney stones significantly increased mitochondrial superoxide production in renal epithelial cells [42], Recombinant human interleukin IL-(3 induced oxygen radical generation in alveolar epithelial cells, which was suppressed by mitochondrial inhibitors 4 -hydroxy-3 -methoxyacetophe-none and diphenylene iodonium [43]. Espositio et al. [44] found that mitochondrial oxygen radical formation depended on the expression of adenine nucleotide translocator Anti. Correspondingly, mitochondria from skeletal muscle, heart, and brain from the Antl-deficient mice sharply increased the production of hydrogen peroxide. 

Li+ also inhibits several hormone-stimulated adenylate cyclases which, in some cases, appear to be related to side effects of Li+ therapy. For instance, Li+ inhibits the hydro-osmotic action of vasopressin, the antidiuretic hormone which increases water resorption in the kidney [136]. This effect is associated with polyuria, a relatively harmless side effect sometimes experienced with Li+ treatment, which arises from the inability of the kidney to concentrate urine. Li+ has been shown to inhibit vasopressin-stimulated adenylate cyclase activity in renal epithelial cells. Additionally, Li+ is reported to enhance the vasopressin-induced synthesis of prostaglandin E2 (PGE2) in vitro in kidney. PGE2 inhibits adenylate cyclase activity by stimulation of Gj, and, therefore, this effect may contribute to the Li+-induced polyuria. 

Acute-, intermediate-, and chronic-duration oral exposures of male rats to doses of 10 mg/kg/day or greater were associated with renal tubular nephropathy (Gorzinski et al. 1985 NTP 1977, 1989 Weeks et al. 1979). Affected animals displayed tubular necrosis, hyaline droplets in tubular epithelial cells, regenerative tubular epithelium, interstitial nephritis, and fibrosis. The severity of the renal lesions varied with the dose and the duration of exposure. 

After peroral intake of nickel sulphate in mice, kidney damage appeared at the corticomedullary junction [296]. There was loss of renal tubular epithelial cells and protein loss, giving numerous hyaline casts in the renal tubules and collecting ducts, especially prominent in the renal papillae. 

One of the unique advantages of renal cell culture rests in making possible the study of the directional aspects of drug exposure and cellular injury that operate in vivo. The technology to grow renal epithelial cells on filter inserts for this purpose has recently been made available (Figure 17.4). This potential provides the opportunity to study compounds that interact or accumulate within the renal tubular epithelium in vivo via tubular reabsorption from the luminal surface or extraction... 

Gstraunthaler, G., Pfaller, W. and Kotanko, P. (1985). Biochemical characterization of renal epithelial cell cultures (LLC-PK and MDCK). Am. J. Physiol. 248 (Renal Fluid Electrolyte Physiol.) 17 F536-544. 

Rabito, C.A. and Karish, M.V (1982). Polarized amino acid transport by an epithelial cell line of renal origin (LLC-PKj). The hasolateral systems. J. Biol. Chem. 257 6802-6808. 

Renal 0.1 (cloudy swelling of tubule epithelial cells) ... 

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