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PubMed1992

Localization of cGMP after infusion of ANP or nitroprusside in the maturing rat.

To determine the ontogeny of intrarenal distribution of guanosine 3',5'-cyclic monophosphate (cGMP) formation in response to atrial natriuretic peptide (ANP) or sodium nitroprusside (SNP), adult and neonatal Sprague-Dawley rats were anesthetized and infused for 60 s with rat ANP (5-2,500 micrograms/kg) or SNP (0.1-10.0 mg/kg). cGMP was identified by the immunoperoxidase technique using a specific antibody. In adult rats, infusion of ANP localized cGMP primarily to the glomerular podocytes, whereas stimulation by SNP increased cGMP in the mesangium only (P less than 0.01). In neonatal rats, although overall renal cGMP immunostaining was greater than in adults, specific localization to podocytes (ANP) or mesangium (SNP) resulted only with higher doses of agonists. Although basal generation of cGMP by isolated glomeruli was greater in neonatal rats, the threshold for stimulation by ANP was lower in glomeruli from adult rats. We conclude that in vivo ANP stimulates glomerular particulate guanylate cyclase primarily in the podocytes, whereas SNP stimulates soluble guanylate cyclase localized to the mesangial cells. There is a maturational increase in the sensitivity for activation of glomerular particulate and soluble guanylate cyclase.

Aging↗
PubMed1996

Localization of parathyroid hormone/parathyroid hormone-related peptide receptor mRNA in kidney.

In kidney, parathyroid hormone (PTH) exerts differential distal effects along the nephron. To define cells expressing receptors for PTH in kidney, we localized PTH/ PTH-related peptide (PTH/PTHrP) receptor mRNA in rat kidney by in situ hybridization. PTH/PTHrP receptor mRNA is localized to glomerular podocytes, convoluted and straight proximal tubules, the cortical portion of thick ascending limbs, and distal convoluted tubules, but was not detected in the thin limb of Henle's loop or in collecting ducts. Northern blot analysis showed that cultured human glomerular podocytes express a unique 4.0-kb PTH/PTHrP receptor transcript but do not express detectable levels of the common approximately 2.4-kb transcript found in whole kidney and in many other tissues. Whereas the tubular localization of PTH/PTHrP receptor mRNA coincides well with previously known sites of PTH action, the intense expression and the unique size of the PTH/PTHrP receptor transcript in glomerular podocytes suggest that PTH and/or PTHrP may play a role(s) in glomerular function.

Autoradiography↗
PubMed1978

Indomethacin and lysine acetylsalicylate in rats with autologous nephrotoxic serum nephritis. Biochemical and morphological studies.

The effects of indomethacin and lysine acetylsalicylate (L-ASA) were compared in rats in which autologous nephrotoxic serum nephritis had been induced. The aim of this study was to offer support to the hypothesis that indomethacin might reduce proteinuria through increased synthesis of glomerular basement membrane by the podocytes. Both drugs were injected intraperitoneally at the dosage of 4 mg/kg body weight daily during a 6-day period into 40 rats rendered nephritic by rabbit nephrotoxic serum injection. Rats treated with indomethacin showed a marked decrease of proteinuria (tested by the 3% sulfosalicylic aicd method) and a clear ultrastructural picture of hyperplasia and hypertrophy of podocytes. Rats given L-ASA showed only a slight correction of proteinuria and less specific ultrastructural modification. These observations suggest that indomethacin decreases proteinuria in nephritic rats not only through its anti-inflammatory activity, but possible also by a peculiar mechanism, namely an increase in podocytic basement membrane synthesis.

Animals↗
PubMed2003

Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases.

Kidney disease affects over 20 million people in the United States alone. Although the causes of renal failure are diverse, the glomerular filtration barrier is often the target of injury. Dysregulation of VEGF expression within the glomerulus has been demonstrated in a wide range of primary and acquired renal diseases, although the significance of these changes is unknown. In the glomerulus, VEGF-A is highly expressed in podocytes that make up a major portion of the barrier between the blood and urinary spaces. In this paper, we show that glomerular-selective deletion or overexpression of VEGF-A leads to glomerular disease in mice. Podocyte-specific heterozygosity for VEGF-A resulted in renal disease by 2.5 weeks of age, characterized by proteinuria and endotheliosis, the renal lesion seen in preeclampsia. Homozygous deletion of VEGF-A in glomeruli resulted in perinatal lethality. Mutant kidneys failed to develop a filtration barrier due to defects in endothelial cell migration, differentiation, and survival. In contrast, podocyte-specific overexpression of the VEGF-164 isoform led to a striking collapsing glomerulopathy, the lesion seen in HIV-associated nephropathy. Our data demonstrate that tight regulation of VEGF-A signaling is critical for establishment and maintenance of the glomerular filtration barrier and strongly supports a pivotal role for VEGF-A in renal disease.

Angiogenesis Inducing Agents↗
PubMed2000

Localization of S-adenosylhomocysteine hydrolase in the rat kidney.

S-adenosylhomocysteine (SAH) hydrolase is a cytosolic enzyme present in the kidney. Enzyme activities of SAH hydrolase were measured in the kidney in isolated glomeruli and tubules. SAH hydrolase activity was 0.62 +/- 0.02 mU/mg in the kidney, 0.32 +/- 0.03 mU/mg in the glomeruli, and 0.50 +/- 0.02 mU/mg in isolated tubules. Using immunohistochemical methods, we describe the localization of the enzyme SAH hydrolase in rat kidney with a highly specific antibody raised in rabbits against purified SAH hydrolase from bovine kidney. This antibody crossreacts to almost the same extent with the SAH hydrolase from different species such as rat, pig, and human. Using light microscopy, SAH hydrolase was visualized by the biotin-streptavidin-alkaline phosphatase immunohistochemical procedure. SAH hydrolase immunostaining was observed in glomeruli and in the epithelium of the proximal and distal tubules. The collecting ducts of the cortex and medulla were homogeneously stained. By using double immunofluorescence staining and two-channel immunofluorescence confocal laser scanning microscopy, we differentiated the glomerular cells (endothelium, mesangium, podocytes) and found intensive staining of podocytes. Our results show that the enzyme SAH hydrolase is found ubiquitously in the rat kidney. The prominent staining of SAH hydrolase in the podocytes may reflect high rates of transmethylation. (J Histochem Cytochem 48:211-218, 2000)

Adenosylhomocysteinase↗
PubMed1993

Nuclear localization of the protein encoded by the Wilms' tumor gene WT1 in embryonic and adult tissues.

The human Wilms' tumor gene WT1 encodes a putative transcription factor implicated in tumorigenesis and in specifying normal urogenital development. We have studied the distribution of WT1 protein and mRNA using immunohistochemistry and in situ hybridization. Monoclonal antibodies were raised against a peptide specific to the first alternative splice site of WT1. Two antibodies specifically reacted on Western blot to this WT1 isoform. Immunofluorescence localized WT1 protein to podocytes during mesonephric and metanephric development. In situ hybridization revealed a similar pattern of expression except that WT1 mRNA was also present in metanephric blastema and renal vesicles. Messenger RNA expression was most pronounced in the kidneys during early fetal development and declined thereafter. In contrast, WT1 protein was readily detectable in glomerular podocytes throughout adulthood. WT1 protein in Wilms' tumor was present in blastema and glomeruloid structures. Expression in the female gonad was linked to the different stages of granulosa cell development. In the male gonad, expression was restricted to Sertoli cells and their precursors, the embryonic tunica albuginea and the rete testis. The intracellular distribution of the WT1 protein was investigated by confocal laser microscopy and was demonstrated to be exclusively nuclear. The nuclear distribution and the selective pattern of expression support the proposed role of WT1 as a transcription factor active during urogenital development. The persistence of WT1 expression in the adult kidney suggests a role in homeostasis of the podocyte.

Blotting, Western↗
PubMed1999

The basic-helix-loop-helix protein pod1 is critically important for kidney and lung organogenesis.

Epithelial-mesenchymal interactions are required for the development of all solid organs but few molecular mechanisms that underlie these interactions have been identified. Pod1 is a basic-helix-loop-helix (bHLH) transcription factor that is highly expressed in the mesenchyme of developing organs that include the lung, kidney, gut and heart and in glomerular visceral epithelial cells (podocytes). To determine the function of Pod1 in vivo, we have generated a lacZ-expressing null Pod1 allele. Null mutant mice are born but die in the perinatal period with severely hypoplastic lungs and kidneys that lack alveoli and mature glomeruli. Although Pod1 is exclusively expressed in the mesenchyme and podocytes, major defects are observed in the adjacent epithelia and include abnormalities in epithelial differentiation and branching morphogenesis. Pod1 therefore appears to be essential for regulating properties of the mesenchyme that are critically important for lung and kidney morphogenesis. Defects specific to later specialized cell types where Pod1 is expressed, such as the podocytes, were also observed, suggesting that this transcription factor may play multiple roles in kidney morphogenesis.

Alleles↗
PubMed1998

Morphological studies of glomeruli in obstructive kidneys by confocal laser scanning microscopy and quick-freezing replica method.

Morphological changes of glomeruli in obstructive kidneys were studied by using confocal laser scanning microscopy (CLSM), and quick-freezing and deep-etching (QF-DE) method. Twenty-one rabbits were divided into three groups, consisting of control, 6-hr bilateral ureteral obstruction (BUO) and 24-hr BUO. In the experimental groups, the attenuation of cell bodies, the lengthening and stretching of major processes, the cystic formation in the cytoplasm and the fusion of foot processes were observed on conventional ultrathin sections. These changes in the 24-hr BUO group were more clearly observed than those in the 6-hr BUO group. By the CLSM, cell bodies and foot processes of podocytes in the experimental groups were more intensely immunostained with anti-alpha-tubulin antibody and phalloidin-FITC. By the QF-DE method, cytoskeletons in the podocyte cell bodies and major processes were composed of numerous intermediate filaments, but distinct changes of actin filaments and microtubules were not observed in the control and experimental groups. Considering the physiological changes in BUO, the mechanical stress appeared to be brought about by hemodynamic factors rather than the change of intratubular pressure, resembling the morphological changes in experimental animals with hyperfiltration and the homeostatic adaptation of podocytes under the BUO condition.

Animals↗
PubMed1984

Scanning and transmission electron microscopy of cysts in the renal cortex of the macaque monkey.

Renal cysts in the cortex of the monkey kidney were observed by scanning and transmission electron microscopy, in an attempt to determine the three-dimensional structures of the epithelial cells in these cysts. The cysts were composed of a thin wall which limited a large spherical space containing a jelly-like substance and some wandering cells. Rudimentary tufts of glomerular capillaries and/or a mound-like swelling were present on the inner surface of the cyst wall, and the inner surface of the cysts was lined with an epithelium with pedicles. The epithelial cells were podocytes, whose surface structure was similar to that on the glomerular capillary in the normal renal corpuscle. The terminal foot processes were characteristically interdigitated not only on the glomerular capillaries, but also on the mound-like swelling and concave surface of the parietal portion of the cyst. A discrete, smooth-surfaced area was found on the side opposite to the glomerulus or swelling. This area was covered by squamous epithelial cells. At the peripheral zone of the smooth-surfaced area, elongated epithelial cells were demonstrated. Our findings indicate that the podocyte layer of the cyst corresponds to the internal leaflet of Bowman's capsule, and the squamous cell layer to the external leaflet. The mound-like swelling covered by podocytes is considered to represent a stage of possible evagination of the tufts of glomerular capillaries. There was no evidence of an opening of the urinary tubule in the cyst wall.

Animals↗
PubMed2005

Molecular pathomechanisms of membranous nephropathy: from Heymann nephritis to alloimmunization.

Membranous nephropathy (MN), the most common cause of idiopathic nephrotic syndrome in white adults, is characterized by an accumulation of immune deposits on the outer aspect of the glomerular basement membrane. In Heymann nephritis, the rat experimental model for MN, megalin--the target antigen of the nephritogenic antibodies--is expressed on the surface of podocytes, where immune complexes are formed, leading to complement activation and nephrotic-range proteinuria. However, megalin cannot be held responsible for human MN because it has not been found in human podocytes or detected in subepithelial immune deposits in patients with MN. Several potential antigens have been identified in so-called secondary forms of MN, but there is no real proof that these antigens are pathogenic. In a subgroup of infants with antenatal MN, neutral endopeptidase (NEP) has been identified as the first protein target on human podocytes of nephritogenic antibodies. The infants' mothers became immunized during pregnancy against NEP expressed on syncytiotrophoblastic cells because they were NEP deficient as a result of truncating mutations in the MME gene. Severity of neonatal renal disease was determined by the mothers' IgG response that led to the formation of the membrane attack complex of complement in the subepithelial deposits. Alloimmunization against NEP is a novel pathomechanism of MN that might also account for some cases of MN after renal or bone marrow transplantation. Other types of alloimmunization should be investigated in MN but also in other renal and nonrenal diseases, particularly those that affect the pediatric age.

Glomerulonephritis↗
PubMed2006

Glomerular localization and expression of Angiotensin-converting enzyme 2 and Angiotensin-converting enzyme: implications for albuminuria in diabetes.

Angiotensin-converting enzyme 2 (ACE2) expression has been shown to be altered in renal tubules from diabetic mice. This study examined the localization of ACE and ACE2 within the glomerulus of kidneys from control (db/m) and diabetic (db/db) mice and the effect of chronic pharmacologic ACE2 inhibition. ACE2 co-localized with glomerular epithelial cell (podocyte) markers, and its localization within the podocyte was confirmed by immunogold labeling. ACE, by contrast, was seen only in glomerular endothelial cells. By immunohistochemistry, in glomeruli from db/db mice, strong ACE staining was found more frequently than in control mice (db/db 64.6 +/- 6.3 versus db/m 17.8 +/- 3.4%; P < 0.005). By contrast, strong ACE2 staining in glomeruli from diabetic mice was less frequently seen than in controls (db/db 4.3 +/- 2.4 versus db/m 30.6 +/- 13.6%; P < 0.05). For investigation of the significance of reduced glomerular ACE2 expression, db/db mice were treated for 16 wk with a specific ACE2 inhibitor (MLN-4760) alone or combined with telmisartan, a specific angiotensin II type 1 receptor blocker. At the end of the study, glomerular staining for fibronectin, an extracellular matrix protein, was increased in both db/db and db/m mice that were treated with MLN-4760. Urinary albumin excretion (UAE) increased significantly in MLN-4760-treated as compared with vehicle-treated db/db mice (743 +/- 200 versus 247 +/- 53.9 microg albumin/mg creatinine, respectively; P < 0.05), and the concomitant administration of telmisartan completely prevented the increase in UAE associated with the ACE2 inhibitor (161 +/- 56; P < 0.05). It is concluded that ACE2 is localized in the podocyte and that in db/db mice glomerular expression of ACE2 is reduced whereas glomerular ACE expression is increased. The finding that chronic ACE2 inhibition increases UAE suggests that ACE2, likely by modulating the levels of glomerular angiotensin II via its degradation, may be a target for therapeutic interventions that aim to reduce albuminuria and glomerular injury.

Albuminuria↗
PubMed2001

Temporally compartmentalized expression of ephrin-B2 during renal glomerular development.

Glomerular development proceeds through the spatially ordered and sequential recruitment, proliferation, assembly, and differentiation of endothelial, mesangial, and epithelial progenitors. The molecular determinants of cell-cell recognition and targeting in this process have yet to be defined. The Eph/ephrin family of membrane receptors and counter-receptors are critical participants of developmental vascular assembly in extrarenal sites. Renal expression patterns of ephrin-B2 and EphB4 were investigated using mice expressing beta-galactosidase under control of ephrin-B2 or EphB4 promoters. The earliest glomerular expression of ephrin-B2 was identified in a subset of differentiating comma-stage glomerular epithelial cells (podocyte progenitors) adjacent to the vascular cleft where endothelial progenitors are subsequently recruited. Epithelial ephrin-B2 expression was accompanied by expression in endothelial and mesangial cells as capillary assembly progressed. At or near completion of glomerular maturation, epithelial ephrin-B2 expression was extinguished, with persistence in glomerular endothelial cells. Throughout development, one of several ephrin-B2 receptors, EphB4, was persistently and exclusively expressed in endothelial cells of venous structures. The findings show sequential ephrin-B2 expression across glomerular lineages, first in a distinct subset of podocyte progenitors and subsequently in endothelial cells of the developing glomerulus. Given targeting functions for Eph/ephrin family proteins, the findings suggest that ephrin-B2 expression marks podocyte progenitors at the site of vascular cleft formation, where expression may establish an "address" to which endothelial and mesangial progenitors are recruited. Thus, the present results suggest that ephrin-B2 and EphB interactions play an important role in glomerular microvascular assembly.

Animals↗
PubMed1995

Structure-stabilizing forces in the glomerular tuft.

The glomerular tuft is constantly exposed to considerable expansile forces resulting from high capillary pressures. Counterforces must be generated in order to maintain structural stability. This review analyzes those structures of the glomerular tuft capable of developing such stabilizing forces. Two systems are described. A basic system consists of the glomerular basement membrane (GBM) and the mesangium. The GBM represents the main skeletal element of the glomerular tuft. In general, opposing portions of the GBM are bridged by contractile mesangial cell processes, generating inwardly directed forces that balance the expansile forces resulting from pressure gradients across the GBM. A second structure-stabilizing role of the podocytes appears to be superimposed on this system. Podocytes are attached to the GBM by numerous foot processes that contain a contractile system. The foot process attachments probably stabilize small patches of the underlying GBM, counteracting local elastic distension. In addition, podocytes may contribute to the stabilization of the folding pattern of the tuft by linking neighboring capillary loops to each other.

Animals↗
PubMed1981

Distribution of anionic groups in the glomerular capillary wall in rat nephrotoxic nephritis and aminonucleoside nephrosis.

It is widely believed that polyanionic plasma proteins, such as albumin, are normally prevented from penetrating the glomerular capillary wall by the presence of intrinsic fixed negative charges in the wall. There is also strong support for the corollary that proteinuria occurs in glomerular disease as a result of loss of such charges. Morphologic studies using cationic 'stains' have indicated that anionic groups can be detected in normal glomeruli and that, in proteinuric states, there is an apparent reduction in such staining. Because most of the latter claims are based largely upon light microscopic studies, critical reassessment at the electron microscopic level is necessary, particularly using the recently developed technique of in situ drip-fixation of superficial glomeruli during good blood flow. In normal rats, this technique results in heavy cationic colloidal iron staining of podocytic epithelial surfaces but little or no staining in the basement membrane or within endothelial fenestrae. In two experimental proteinuric models, rat nephrotoxic nephritis and aminonucleoside nephrosis, there was no loss of colloidal iron staining on podocytic epithelial surfaces at any stage. There was, however, a striking alteration in glomerular architecture in each model, particularly affecting podocytic epithelium. Thus, there was extensive replacement of foot processes by flattened expanses of epithelial cytoplasm, associated with scattered focal gaps in the epithelial covering of the basement membrane. It therefore appears that the reduction of glomerular polyanion seen by light microscopy in glomerular disease results simply from a decrease in visceral epithelial surface area rather than a loss of intrinsic polyanion from the filtering portion of the glomerular capillary wall.

Animals↗
PubMed1992

Effects of epidermal growth factor on calf renal glomerular cells in vitro.

Epidermal growth factor (EGF) stimulates the mitosis and differentiation of a variety of cellular types. It also delays the cell senescence in vitro. Because of its multiple functions, the effects of EGF on cells from isolated, explanted calf renal glomeruli have been studied. The cell types emerging from glomeruli cultured with and without EGF were compared and identified by morphological, immunofluorescence and electron microscopy criteria. Two cell types: visceral epithelial cells or podocytes (type I) and mesangial cells (type II) emerged from glomeruli cultivated without EGF. A third cell type, called type III cells, appeared only in the presence of EGF. These cells divided, were mobile and had prolonged lifespan in culture. They appeared pavement-like, and acquired progressively the morphological features and cytoskeletal components of type I cells. They also showed certain characteristics of podocytes in vivo. We suggest that type III epithelial-like cells are precursor cells of podocytes, that EGF triggers their emergence from glomeruli and their subsequent proliferation and differentiation in vitro. EGF also prolongs their lifetime in culture.

Animals↗
PubMed1978

Polycation-induced dislocation of slit diaphragms and formation of cell junctions in rat kidney glomeruli: the effects of low temperature, divalent cations, colchicine, and cytochalasin B.

Neutralization of negatively charged groups in the glomerular capillary wall by polycations causes extensive loss of podocyte footplates, formation of tight and gap junctions, and dislocation of slit diaphragms within a few minutes (M. W. Seiler, M. A. Venkatachalam, and R. S. Cotran: Science 189:390, 1975). This study attempts to elucidate further the development of podocyte abnormalities by quantitating the effects of inhibitors of microfilaments, microtubules, and cellular metabolism. The decrease in the number of footplates per micrometer of basement membrane caused by the polycationic chemical protamine sulfate (PS) was determined after in situ perfusion of the left kidney of rats. An approximate 50 per cent amelioration of this effect of PS was observed when in addition to perfusion with PS: (1) perfusion was performed in the cold (6 degrees C.); (2) the perfusate contained cytochalasin B; (3) the perfusate lacked Ca2+; and (4) the perfusate contained ethylenediaminetetraacetic acid. In contrast, colchicine did not affect PS-induced footplate loss. It was concluded that the PS-induced footplate retraction observed in scanning micrographs, is partially an active process involving podocyte actin filaments. Intact microtubuli are obviously not necessary. Formation of tight and gap junctions between foot processes and dislocation of slit diaphragms were not influenced by any of the inhibitory conditions listed above.

Animals↗
PubMed2001

Repulsive charge mechanism serve to maintain lumens and cavities. An histochemical study of rat serosa and kidney.

The free surface of the rat peritoneum was covered with a rich negative-charged substance which is distinctly stained with cationic colloidal iron (pH 1.5). Neuraminidase digestion erased this iron stain. Treatment with Limax flavus agglutinin (LFA), which has specific affinity to sialic acid, interferred with iron staining on the serosal surface. Transmission electron microscopy of the peritoneal samples stained with colloidal iron showed that colloidal particles were deposited on the free surface of the mesothelial cells. At pH 1.5, the colloidal particles aggregated in a dotted fashion; in those stained at pH 7.0, the particles arranged in fine strands (100-300 nm in length). This difference may occur as a structural transformation due to pH level changes. The string like structure seemed to correspond well to membrane associated sialomucin. The urinary surface of the rat glomerular podocytes possessed negatively charged sites detectable with cationic colloidal iron even at pH 1.5. Neuraminidase and LFA treatments erased iron staining. Substance containing sialic acid such as podocalyxin on the podocyte surface may be stained. This study shows that negatively charged sites of the substance covering the free surface of these regions repulse each other to maintain the serosal cavities or the podocyte end-feet slits.

Animals↗
PubMed2001

Immunohistochemical analysis of human serum sickness glomerulonephritis.

AIM: To analyze pathological and immunohistochemical characteristics of glomerulonephritis in human serum sickness. METHODS: Renal biopsy specimens from two female patients with serum sickness that ensued after application of anti-lymphocyte horse globulin for aplastic anemia were analyzed by light microscopy, immunofluorescence, and electron microscopy. To prove the depositions of foreign protein, frozen sections were incubated with fluorescein-conjugated anti-horse protein serum. Immunohistochemical analysis was performed on B5-fixed paraplast-embedded tissue or frozen acetone-fixed sections with the primary antibodies for molecules/cell markers CD35, CD43, CD45RO, CD68, CD2, lysozime, L26, and S100. RESULTS: Diffuse proliferating and necrotizing glomerulonephritis with crescents was found. There were coarse granular mesangial, subepithelial, subendothelial, and intramembranaceous deposits of mainly horse globulin, C3, and IgG. Most mesangium infiltrating cells were macrophages and T-lymphocytes. Electron microscopy revealed hypertrophy of podocytes, but immunohistochemistry did not show their normal CD35 (C3b-receptor) staining. Apart from epithelial cells, main crescent forming cells were macrophages and T-lymphocytes. Rare dendritic cells and abundant infiltration of macrophages, T-lymphocytes, and neutrophiles were found in the interstitium. CONCLUSION: In severe serum sickness, glomeruli and tubuli are destroyed beyond the range usually seen in other types of glomerulonephritis caused by immune complexes, except in cases with widespread crescents. Hypertrophy of podocytes and loss of their normal C3b-receptor staining has not yet been described in the literature. C3b-receptors on podocytes could play a role in pathogenesis of glomerular injury caused by immune complexes.

Adult↗