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Collecting Duct (collecting + duct)
Terms modified by Collecting Duct Selected AbstractsModification of epithelial cell barrier permeability and intercellular junctions by Clostridium sordellii lethal toxinsCELLULAR MICROBIOLOGY, Issue 7 2006Catherine Boehm Summary Clostridium sordellii lethal toxin (LT) is a glucosyltransferase which inactivates small GTPases from the Rho and Ras families. In the present work, we studied the effects of two variants, LT82 and LT9048, on the integrity of epithelial cell barrier using polarized MCCD (Mouse Cortical Collecting Duct) and MDCK (Madin-Darby Canine Kidney) cells. Our results demonstrate for the first time that LTs have very limited effects on tight junctions. In contrast, we show that both toxins modified the paracellular permeability within 2,4 h. Concomitantly LT82 and LT9048 induced a disorganization of basolateral actin filaments, without modifying apical actin. Both toxins mainly altered adherens junctions by removing E-cadherin-catenin complexes from the membrane to the cytosol. Similar effects on adherens junctions have been observed with other toxins, which directly or indirectly depolymerize actin. Thereby, Rac, a common substrate of both LTs, might play a central role in LT-dependent adherens junction alteration. Here, we show that adherens junction perturbation induced by LTs results neither from a direct effect of toxins on adherens junction proteins nor from an actin-independent Rac pathway, but rather from a Rac-dependent disorganization of basolateral actin cytoskeleton. This further supports that a dynamic equilibrium of cortical actin filaments is essential for functional E-cadherin organization in epithelia. [source] EndothelinA (ETA) and ETB receptor-mediated regulation of nitric oxide synthase 1 (NOS1) and NOS3 isoforms in the renal inner medullaACTA PHYSIOLOGICA, Issue 4 2007J. C. Sullivan Abstract Aim:, Our laboratory and others have shown that endothelin (ET)-1 directly stimulates nitric oxide (NO) production in inner medullary collecting duct (IMCD) cells. The goal of this study was to determine which NO synthase (NOS) isoforms in IMCD are sensitive to ET-1, and the role of ETA and ETB receptor activation in vivo and in vitro. Methods:, NOS enzymatic activity and NOS isoform protein expression were examined in cultured IMCD-3 cells and isolated renal inner medulla. ETB receptor-deficient homozygous rats (sl/sl) have elevated levels of circulating ET-1 and lack a functional ETB signalling pathway in kidneys, and furthermore provides a unique model to study ETA receptor signalling in the renal inner medulla in vivo. Results:, Incubation of IMCD-3 cells with exogenous ET-1 (50 nm) resulted in ETA -dependent increased NOS1 protein expression in IMCD-3 cells with no effect on NOS2 or NOS3 expression. ETB receptor antagonism has no effect on NOS expression in IMCD-3 cells. Consistent with in vitro results, cytosolic NOS1 protein expression was significantly greater in the renal inner medulla of sl/sl rats compared with heterozygous (sl/+) controls, with no alteration in NOS3 expression. In contrast to protein expression data, NOS1- and NOS3-specific enzymatic activities decreased in the cytosolic fraction from the renal inner medulla of sl/sl compared with sl/+. Conclusion:, These results provide evidence that both ETA and ETB receptors regulate NOS isoform activity in the renal inner medulla and specifically support the hypothesis that ETA receptor activation increases NOS1 expression. [source] The diagnostic utility of MOC31, BerEP4, RCC marker and CD10 in the classification of renal cell carcinoma and renal oncocytoma: an immunohistochemical analysis of 328 casesHISTOPATHOLOGY, Issue 5 2004C-C Pan Aims:, To demonstrate the diagnostic utility of MOC31, BerEP4, renal cell carcinoma marker (RCC Ma) and CD10 in the classification of RCC and renal oncocytoma, based upon a comprehensive immunohistochemical analysis. Methods and results:, Immunohistochemistry was performed on 328 samples consisting of 256 clear cell/conventional, 27 papillary, 28 chromophobe, five collecting duct, five unclassified RCCs and seven renal oncocytomas using antibodies MOC31, BerEP4 and antibodies against cytokeratins (KL-1, CAM5.2, 34,E12, cytokeratin 7), RCC Ma, epithelial membrane antigen, E-cadherin, CD10, CD15 and vimentin. Multivariate analysis showed that MOC31, BerEP4, RCC Ma and CD10 have discriminatory value. MOC31 and BerEP4 chiefly labelled distal tubules of normal kidney while RCC Ma and CD10 labelled the proximal tubules. Twenty-three chromophobe RCCs (82%) were reactive for MOC31, while only four clear cell RCCs and three papillary RCCs were positive for this marker. Clear cell RCCs were characterized by a high positive rate for CD10 (82%) and a low positive rate for BerEP4 (27%). Papillary RCCs frequently coexpressed RCC Ma and BerEP4 (51%). All renal oncocytomas were negative for MOC31 and CD10. Conclusions:, MOC31 has diagnostic merit in discerning chromophobe RCC. The CD10+/BerEP4, profile and RCC Ma+/BerEP4+ profile achieve moderate sensitivity and good specificity for clear cell RCC and papillary RCC, respectively. The non-reactivity for both MOC31 and CD10 is helpful in distinguishing renal oncocytoma from RCC. When properly selected, antibodies have immunohistochemical diagnostic utility for the classification of renal cortical epithelial tumours. [source] Low-grade renal epithelial tumor originating from the distal nephronINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2004NOBORU HARA Abstract, There are few published reports of low-grade renal epithelial tumor originating from the distal nephron. However, it should not be disregarded clinically, because the actual number of patients with such tumors may be higher than expected. We investigated the immunohistochemical profile of a histologically distinct subtype of such a tumor in detail, in addition to the clinical course and imaging studies. The present study demonstrated that both glandular and spindle cell components of this tumor have a persistent characteristic of an epithelial tumor arising from the distal tubule or collecting duct. This tumor is a benign complex neoplasm that can be treated successfully with radical surgery. Beta-catenin and E-cadherin are suggested to play a crucial role in tumorigenesis and the biphasic arrangement of this neoplasm, concerning the expression of epithelial membrane antigen and carbohydrate antigen 19-9. We suggest that the term ,distal nephron epithelioma' is appropriate for classifying such rare but clinicopathologically distinct tumors. [source] Collecting duct carcinoma with long survival treated by partial nephrectomyINTERNATIONAL JOURNAL OF UROLOGY, Issue 7 2001Hiroaki Matsumoto Abstract A case is reported of collecting duct carcinoma of the left kidney treated with partial nephrectomy. A 57-year-old woman presented for evaluation of the left renal mass, which was detected by screening ultrasonography. A computed tomography scan and magnetic resonance imaging showed a solid mass at the upper pole of the left kidney. The renal tumor biopsy revealed a low-grade renal cell carcinoma or a tubulopapillary adenoma. Subsequently, left partial nephrectomy was performed. Microscopically, the tumor showed tubulopapillary proliferation with a fibrous capsule. Histochemically, the tumor cells reacted with lectins or antibodies against the collecting duct. Twenty-four months after partial nephrectomy, the patient is alive and has no distant metastatic lesions. We review the literature on collecting duct carcinoma, in addition to the case of partial nephrectomy. [source] Alterations in renal cilium length during transient complete ureteral obstruction in the mouseJOURNAL OF ANATOMY, Issue 2 2008Leanne Wang Abstract The renal cilium is a non-motile sensory organelle that has been implicated in the control of epithelial phenotype in the kidney. The contribution of renal cilium defects to cystic kidney disease has been the subject of intense study. However, very little is known of the behaviour of this organelle during renal injury and repair. Here we investigate the distribution and dimensions of renal cilia in a mouse model of unilateral ureteral obstruction and reversal of ureteral obstruction. An approximate doubling in the length of renal cilia was observed throughout the nephron and collecting duct of the kidney after 10 days of unilateral ureteral obstruction. A normalization of cilium length was observed during the resolution of renal injury that occurs following the release of ureteral obstruction. Thus variations in the length of the renal cilium appear to be a previously unappreciated indicator of the status of renal injury and repair. Furthermore, increased cilium length following renal injury has implications for the specification of epithelial phenotype during repair of the renal tubule and duct. [source] Chromophobe renal cell carcinoma: Clinical, pathological and molecular biological aspectsPATHOLOGY INTERNATIONAL, Issue 11 2000Yoji Nagashima Chromophobe renal cell carcinoma (RCC), a newly established subtype of renal neoplasm, is composed of tumor cells with characteristically cloudy, weakly eosinophilic and reticular cytoplasm. The tumor should be distinguished from the common clear cell RCC, because of the unique clinicopathological and molecular biological features. The tumor does not show gender bias. Patient ages are similar to those of clear cell RCC, but might occur in the 20- to 40-year-old age group. Grossly, the tumor tends to be beige in color, which is different from the yellowish color of common RCC. Electron microscopy and immunohistochemistry indicate the intercalated cell of the collecting duct as the cellular origin. Cytogenetic study shows non-random multiple chromosome loss, with mitochondrial DNA rearrangement. Alteration of the von Hippel,Lindau (VHL) gene, a cancer suppressor gene relating with clear cell RCC, has not yet been observed. In order to adopt the most appropriate treatment, including gene therapy, recognition and correct pathological diagnosis of chromophobe RCC are extremely important. [source] Differential expression of heat shock protein 27 and 70 in renal papillary collecting duct and interstitial cells , implications for urea resistanceTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Wolfgang Neuhofer The adaptation of renal medullary cells to their hyperosmotic environment involves the accumulation of compatible organic osmolytes and the enhanced synthesis of heat shock proteins (HSP) 27 and 70. While the mechanisms leading to osmolyte accumulation are similar in papillary collecting duct (PCD) and papillary interstitial (PI) cells, the present data demonstrate that HSP27 and HSP70 are expressed differentially in these cells both in vivo and in vitro. HSP70 is abundant in PCD, but not expressed in PI cells in the papilla in situ, while HSP27 is expressed in both PCD and PI cells. These observations could be reproduced by non-permeant solutes in cultured cells. Osmotic stress strongly induced HSP70 in MDCK cells (as a model for PCD cells), but not in PI cells, while HSP27 was constitutively expressed in MDCK cells and was up-regulated in PI cells. Since prior hypertonic stress (NaCl addition) protects MDCK against subsequent exposure to high urea concentrations, this effect was also assessed in PI cells. In both cell lines, hypertonic pretreatment prior to urea exposure (400 mm) strongly attenuated caspase-3 activation. Inhibition of HSP27 expression by antisense transfection diminished the protective effect of hypertonic preconditioning in PI cells, while attenuation of HSP70 expression in MDCK cells diminished the protective effect of hypertonic preconditioning in these cells. These observations indicate that PCD and PI cells employ cell-specific mechanisms for protection against high urea concentrations as present in the renal papilla during antidiuresis. [source] Effects of nominally selective inhibitors of the kinases PI3K, SGK1 and PKB on the insulin-dependent control of epithelial Na+ absorptionBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2010Morag K Mansley BACKGROUND AND PURPOSE Insulin-induced Na+ retention in the distal nephron may contribute to the development of oedema/hypertension in patients with type 2 diabetes. This response to insulin is usually attributed to phosphatidylinositol-3-kinase (PI3K)/serum and glucocorticoid-inducible kinase 1 (SGK1) but a role for protein kinase B (PKB) has been proposed. The present study therefore aimed to clarify the way in which insulin can evoke Na+ retention. EXPERIMENTAL APPROACH We examined the effects of nominally selective inhibitors of PI3K (wortmannin, PI103, GDC-0941), SGK1 (GSK650394A) and PKB (Akti-1/2) on Na+ transport in hormone-deprived and insulin-stimulated cortical collecting duct (mpkCCD) cells, while PI3K, SGK1 and PKB activities were assayed by monitoring the phosphorylation of endogenous proteins. KEY RESULTS Wortmannin substantially inhibited basal Na+ transport whereas PI103 and GDC-0941 had only very small effects. However, these PI3K inhibitors all abolished insulin-induced Na+ absorption and inactivated PI3K, SGK1 and PKB fully. GSK650394A and Akti-1/2 also inhibited insulin-evoked Na+ absorption and while GSK650394A inhibited SGK1 without affecting PKB, Akti-1/2 inactivated both kinases. CONCLUSION AND IMPLICATIONS While studies undertaken using PI103 and GDC-0941 show that hormone-deprived cells can absorb Na+ independently of PI3K, PI3K seems to be essential for insulin induced Na+ transport. Akti-1/2 does not act as a selective inhibitor of PKB and data obtained using this compound must therefore be treated with caution. GSK650394A, on the other hand, selectively inhibits SGK1 and the finding that GSK650394A suppressed insulin-induced Na+ absorption suggests that this response is dependent upon signalling via PI3K/SGK1. [source] Perinatal development of the rat kidney: Apoptosis and epidermal growth factorCONGENITAL ANOMALIES, Issue 3 2003Toshiya Okada ABSTRACT, Localization of apoptotic cells in the kidney of perinatal rats was examined by the terminal deoxynucleotidyl transferase,mediated d,UTP,biotin nick end labeling (TUNEL) method and electron microscopy. Perinatal changes in the percentage of kidney cells with DNA fragmentation were determined by flow cytometric analysis. Through observation of two successive sections, the relationship between the localization of the epidermal growth factor receptor (EGFR) positive cells and TUNEL positive cells in the kidney was determined. From fetal day 18 to neonatal day 5, TUNEL positive cells were noted in immature glomeruli, collecting ducts and interstitium. Electron microscopically, chromatin condensed nuclei and apoptotic bodies were seen in the same tissue component as the TUNEL positive cells. The percentage of DNA fragmented cells significantly increased from fetal days 18 to 20 and significantly decreased from fetal days 20 to 22, while they still remained low in the neonatal period. The TUNEL positive cells in immature glomeruli and collecting ducts were not reactive to the EGFR antibody. The TUNEL positive cells were not observed in the proximal tubular cells, which were positive to EGFR antibody. These results indicate that apoptotic cells are present in the kidney throughout the perinatal period in the rat and that EGF plays an important role in perinatal development of the rat kidney. [source] Trefoil factor family 3 expression in the oral cavityEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 6 2009T. Storesund This study examined the expression, in oral keratinocytes and in the major and minor salivary glands, of Trefoil factor family 3 (TFF3) peptide. Trefoil factor family 3 messenger RNA (mRNA) and peptide were detected in cultures of normal oral keratinocytes by quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. Trefoil factor family 3 was found, by immunohistochemical analyses, to be expressed in the basal layers of the oral mucosal epithelium. In salivary glands, immunohistochemical staining showed that TFF3 peptide expression was strongest in the mucous acini of the submandibular and the small salivary glands. Serous cells in the same glands showed weak staining. In the parotid gland, many serous acini showed weak positive staining, while other areas did not. In all glands examined, the intercalated, striated, and collecting ducts were moderately TFF3-positive. Double immunostaining confirmed that mucous (MUC5B positive) cells were moderately or strongly positive for TFF3 and that some serous (MUC7 positive) cells showed restricted TFF3 expression, mostly in a granular pattern. The prevalence of the TFF3 peptide in the salivary secretions of healthy volunteers was detected by western blotting of saliva from minor salivary glands (four of five) and the parotid gland (one of five) and of mixed submandibular/sublingual saliva (five of five). In conclusion, the submandibular and small salivary glands appear to be the major producers of oral TFF3, but duct cells of all glands and keratinocytes of the oral mucosa may also contribute as sources of TFF3 in the oral cavity. [source] Histological study of fetal kidney with urethral obstruction and vesicoureteral reflux: A consideration on the etiology of congenital reflux nephropathyINTERNATIONAL JOURNAL OF UROLOGY, Issue 10 2003KENJI SHIMADA Purpose: A recent subject of interest regarding reflux nephropathy is the presence of renal abnormalities in neonates and infants who have no history of urinary tract infections. Debates have centered on the etiology of this renal abnormality , congenital reflux nephropathy; regarding whether it is the result of abnormal ureteral budding or of back pressure effect from sterile reflux. We examined the renal pathology of fetuses with urethral obstruction and vesicoureteral reflux, and we suggest herein a possible etiology of congenital reflux nephropathy. Methods: The renal pathology of seven autopsied fetuses with vesicoureteral reflux was studied. Reflux was demonstrated at autopsy by slow injection of contrast medium into the bladder. Severe urethral obstruction, either atresia or urethral valves, was evident in six of the subjects. Results: In six subjects, abnormality of the urinary tracts was detected by prenatal ultrasonography. Of these six subjects, three revealed characteristics of prune belly syndrome. Reflux was graded as moderate in five subjects, and severe in two. In three subjects autopsied at 21 weeks gestation or earlier, the kidneys were well-developed with normal corticomedullary configuration, and nephrogenesis was retained. In three cases autopsied at over 25 weeks of gestation, the kidneys were grossly cystic, and the nephrogenic zone was completely absent. Contrast medium was observed not only in the dilated ducts and tubules, but also in the subcapsular cysts. Extravasation of the contrast medium was seen in the peritubular space. In the last subject with normal lower urinary tract, abnormal segments among normal cortical structures were observed. Conclusion: Our findings of renal pathology in fetuses with reflux are quite similar to those seen in fetal hydronephrosis. Back pressure from reflux probably damages the developing kidney leading to a degeneration of the ampullae and a reduction in the number of nephrons. Both dilatation of the collecting ducts and tubules, and extravasation of the urine may result in interstitial fibrosis. We postulate that one of the important etiologies of congenital reflux nephropathy may be the result of back pressure from sterile reflux. [source] Extracellular signal-regulated kinase-dependent interstitial macrophage proliferation in the obstructed mouse kidneyNEPHROLOGY, Issue 5 2008YINGJIE HAN SUMMARY: Aim: A number of growth factors have been shown to induce proliferation of renal cell types in animal models of kidney disease. In vitro studies suggest that many such growth factors induce renal cell proliferation through the extracellular signal-regulated kinase (ERK) pathway. The aim of this study was to determine the functional role of ERK signalling in cell proliferation in the obstructed kidney. Methods: Unilateral ureteric obstruction was induced in C57BL/6J mice which then received an ERK inhibitor drug (U0126 100 mg/kg t.i.d.), vehicle (DMSO) or no treatment, starting at day 2 after unilateral ureteric obstruction surgery and continuing until animals were killed on day 5. Cell proliferation was assessed by uptake of bromodeoxyuridine (BrdU). Results: In normal mice, phosphorylation (activation) of ERK (p-ERK) was restricted to collecting ducts. Western blotting identified a marked increase in p-ERK in the obstructed kidney in the no-treatment and vehicle-treated groups. Immunostaining showed strong p-ERK staining in many tubules and in interstitial cells. U0126 treatment inhibited ERK phosphorylation as assessed by western blot and immunostaining. The number of BrdU+ cortical tubular cells was reduced by vehicle treatment but was not further changed by U0126 treatment. In contrast, interstitial cell proliferation in the obstructed kidney was unaltered by vehicle treatment, but this was significantly inhibited by U0126. This was associated with a reduction in interstitial macrophage accumulation, but no effect was seen upon interstitial accumulation of ,-SMA+ myofibroblasts. Renal fibrosis, as assessed by collagen deposition, was unaffected by U0126 or vehicle treatment. Conclusion: These studies show that accumulation of interstitial macrophages in the obstructed kidney is, in part, dependent upon the ERK signalling pathway. [source] Histopathological and immunohistochemical characterization of canine prostate cancerTHE PROSTATE, Issue 5 2008Chen-Li Lai Abstract Background In this study we try to identify the origin of canine prostate cancer (cPC) by classifying the tumors histological subtypes and relate these subtypes to their combined expressional characteristics of several tissue specific and differentiation markers. Methods cPCs were examined histomorphologically and by immunohistochemical detection of the cytokeratin markers CK14, HMWCK, CK5, CK18, and CK7, and of the markers UPIII, PSA and PSMA. Results Histopathologically, six growth patterns could be differentiated. The most frequent patterns were solid, cribriform and micropapillary growth patterns, while sarcomatoid, small acinar/ductal, and tubulo-papillary growth patterns were less frequent present. Solid growth patterns were significantly (P,=,0.027) more often seen in castrated dogs. Immunohistochemically, about half of the cPC cases showed expression of PSA (8/20) and PSMA (10/20); 85% and 60% of the cPC expressed UPIII (17/20) and CK7 (12/20), while 13 and 12 cPC expressed CK5 and CK14, respectively; all cPC expressed CK18. CK14 was significantly more often and UPIII less frequent expressed in the solid growth patterns than in the micropapillary and cribriform patterns, respectively. Conclusions Canine prostate cancer appear to be more aggressive and of a less differentiated type than most common human prostate cancers. Comparing the expression patterns of the markers in cPC to those in normal canine prostate tissue, cPC most likely originates from the collecting ducts rather than from the peripheral acini. Given also the fact that canine prostate cancer is unresponsive to androgen withdrawal therapy, canine prostate cancer mostly resembles human, androgen refractory, poorly differentiated prostate cancer. Prostate 68: 477,488, 2008. © 2008 Wiley-Liss, Inc. [source] The Development of the Metanephric Kidney in the PigANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005H. Bragulla Aims:, The metanephric kidneys of the pig are used as xenotransplants in human medicine. In order for transplants to fit within the host organisms, the subcapsular blastema and blood vessels are crucial for the development of new nephrons to sustain the organ functions. The aim of this study is to obtain data concerning the post-natal development of metanephric nephrons in the porcine kidney. Materials and Methods:, The metanephric kidneys of six porcine fetuses with a crown-rump length ranging from 40 mm to 220 mm of eight piglets aged between 6 to 10 weeks and of three adult pigs were studied. Eight lectins as well as anti-actin and anti-myosin antibodies were used for lectin- and immunohistochemistry to study the subcapsular metanephric blastema, to visualize the blood-urine barrier in the nephrons and collecting tubules, and to study the blood vessels in both the renal cortex and marrow. Results and Conclusions:, A subcapsular metanephric blastema was still present in the kidney of 10-week-old piglets. Dense condensation of mesenchymal cells surrounded the terminal branches of the collecting ducts and showed first signs of mesenchymal-epithelial transformation. Characteristic comma-shaped and s-shaped bodies were found in and underneath the subcapsular blastema. In the fibrous renal capsule of six-week-old piglets, a first faint binding reaction of anti-actin was visible and intensified in the fibrous renal capsule in ten-week-old piglets and in adult pigs. In addition, the smooth-muscle layers of the blood vessels were stained by the anti-actin and anti-myosin antibodies. The lectins showed various affinities to the endothelium of blood vessels and to the epithelial cells lining of the capsules of the metanephric renal corpuscles, the various parts of the renal tubules, as well as the collecting tubules and the renal pelvis. The affinity of the epithelial cells to a specific lectin varies in neighbouring cells, indicating different cell activities or cell cycles. [source] Vasopressin receptor antagonists: pharmacological tools and potential therapeutic agentsAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 2 2006J. O. Streefkerk Summary 1 The present survey deals with the development and applications of non-peptidergic vasopressin receptor antagonists. 2 The existence of at least three vasopressin receptors (V1, V2 and V3 respectively) is firmly established. 3 V1 -receptors play a relevant role in the regulation of vascular tone, whereas V2 -receptors are known to mediate the antidiuretic activity of vasopressin at the level of the renal collecting ducts. The V3 -receptor appears to be involved in the release of the adreno-corticotropic hormone. 4 Vasopressin receptor antagonists which are peptides have been known for several decades, more recently, both V1 - and V2 -receptor blockers which are non-peptidergic have been introduced, as well as agents with affinity for both V1 - and V2 -receptor subtypes. A survey of these non-peptidergic antagonists is presented here. Such compounds are useful as pharmacological tools, and they can also be thought of as therapeutic agents as therapeutic agents in cardiovascular and renal diseases. 5 Selective V1 - and V2 -receptor antagonists were used to study the interaction between vasopressin receptors and sympathetic neurones. Depending on the experimental model used this interaction can occur at either the pre- or postsynaptic sites. In both cases predominantly V1 -receptors are involved. 6 A brief survey is given of the potential use of V-receptor antagonists in the drug therapy of syndrome of inappropriate antidiuretic hormone secretion and other water retaining disorders, congestive heart failure and certain forms of hypertension (in particular in the Negroid hypertensive patients). [source] Altered expression of aquaporin-2 in human explants with chronic renal allograft dysfunctionBJU INTERNATIONAL, Issue 7 2005Kossen M.T. Ho OBJECTIVE To investigate the distribution of aquaporins, a recently discovered family of transmembrane water channels, in human renal explants, with specific reference to chronic renal allograft dysfunction (CRAD). MATERIALS AND METHODS Immunohistochemistry for aquaporin-1 and -2 was used in 11 explants, of which five had clinically and histologically confirmed CRAD. Controls were taken from the six explants unaffected by CRAD and from histologically normal areas of six kidneys excised for renal tumours. RESULTS In the renal tumour control group, aquaporin-1 immunoreactivity was detected in the glomerular endothelium, Bowman's capsule, the proximal convoluted tubules and the thin limb of the loop of Henle, whereas immunoreactivity for aquaporin-2 was detected in the collecting ducts only. Of the explants without CRAD, where architecture was preserved, immunoreactivity for aquaporin-1 and -2 was the same as in the renal tumour controls. In the two explants with no CRAD and loss of collecting ducts, there was no aquaporin-2 immunoreactivity. In five explants with CRAD, immunoreactivity for aquaporin-2 was decreased or absent from the medulla to the cortex. The apparent decreased immunoreactivity of aquaporin-1 in this group was secondary to a decrease in the number of viable proximal tubules. CONCLUSION There was less aquaporin-2 immunoreactivity in human renal explants diagnosed with CRAD, starting from the medullary region. In explants with no CRAD and viable collecting ducts, or in normal controls, aquaporin-2 immunoreactivity remained unchanged. Aquaporins might be useful as markers for CRAD. [source] DIFFERENTIAL REGULATION OF ANGIOTENSIN II RECEPTORS DURING RENAL INJURY AND COMPENSATORY HYPERTROPHY IN THE RATCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2005Emma Joly SUMMARY 1.,The renin-angiotensin system may be involved in the compensatory adaptations occurring after the reduction of renal mass and during the consecutive changes leading to chronic renal failure. We therefore investigated the regulation of angiotensin II receptors in two models of renal hypertrophy in the rat: hypertrophy following uninephrectomy (UNx) or subtotal nephrectomy (STNx). The level of angiotensin type 1 (AT1A -R and AT1B -R) and type 2 (AT2 -R) receptor mRNA was quantified by competitive reverse transcription-polymerase chain reaction (RT-PCR) in specific renal zones and the intrarenal distribution of angiotensin II receptors was analysed by immunohistochemistry. 2.,In the UNx rats, AT1 -R mRNA expression was not modified in the cortex or in the inner stripe of the outer medulla of the residual kidney at any time after the surgery (1, 4 and 12 weeks). In contrast, AT1 -R mRNA expression was significantly reduced in these zones in STNx rats (,33% and ,40%, respectively). This downregulation was organ-specific, as AT1 -R mRNA levels were not modified in the liver. The proportions of AT1 -R subtype (AT1A and AT1B) mRNA were unchanged by UNx or STNx. Very low levels of AT2 -R mRNA were found in the cortex of all groups. Immunostaining revealed a similar localization of AT1 -R in mesangial cells, proximal tubule, basolateral membrane of thick ascending limb, in both models of hypertrophy. AT1 -R labelling was also detected in the apical membrane of intercalated cells of cortical collecting ducts. 3.,This differential mRNA expression of angiotensin II receptors during compensatory hypertrophy and renal injury suggests that the development of renal hypertrophy is independent of AT1 -R and AT2 -R gene expression levels. [source] | ||||||||||||||||||||||||||||