An immunohistochemical study of developing glomeruli in human fetal kidneys, See Editorial by Oliver and Al-Awqati, p. 2167

Naruse, Keishi; Fujieda, Mikiya; Miyazaki, Eriko; Hayashi, Yoshihiro; Toi, Makoto; Fukui, Takayuki; Kuroda, Naoto; Hiroi, Makoto; Kurashige, Takanobu; Enzan, Hideaki

doi:10.1046/j.1523-1755.2000.00033.x

Cited by 52 publications

(55 citation statements)

References 20 publications

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“…Moreover, nestin/vimentin doublelabeled cells clearly resembled podocytes, displaying long immunoreactive primary processes ( Figures 1G-1I). Double-labeling experiments carried out using nestin and the endothelial marker CD31 (Naruse et al 2000) showed that the relationships occurring between nestinpositive cells and endothelial cells were those expected between podocytes and the glomerular capillaries ( Figures 1J-1L).…”

Section: Adult Kidneymentioning

confidence: 69%

“…For this reason, in a single section of fetal kidney it is possible to appreciate all the stages of glomerular development in a sort of gradient of maturation going from the surface to the depth of the organ. The steps of glomerular maturation are morphologically divided into the following stages: vesicle (V), S-shaped body (S), capillary loop (C), and maturing glomerulus (M) (Naruse et al 2000;Pavenstä dt et al 2003). At low magnification, nestin staining on fetal kidney sections clearly appeared located in glomeruli at all the maturation stages ( Figure 4A).…”

Section: Fetal Kidneymentioning

confidence: 99%

“…As a mesangial marker, we chose a-smooth muscle actin (a-SMA), which has been reported to be expressed in activated and fetal mesangial cells (Alpers et al 1992;Naruse et al 2000), whereas we used CD34 as a marker for the endothelium (Fina et al 1990;Ito et al 1995;Naruse et al 2000). a-SMA was constantly expressed in the S (Figure 5B …”

Section: Fetal Kidneymentioning

confidence: 99%

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Nestin Expression in Adult and Developing Human Kidney

Bertelli

Regoli

Fonzi

et al. 2006

J Histochem Cytochem.

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S U M M A R Y Nestin is considered a marker of neurogenic and myogenic precursor cells. Its arrangement is regulated by cyclin-dependent kinase 5 (CDK5), which is expressed in murine podocytes. We investigated nestin expression in human adult and fetal kidney as well as CDK5 presence in adult human podocytes. Confocal microscopy demonstrated that adult glomeruli display nestin immunoreactivity in vimentin-expressing cells with the podocyte morphology and not in cells bearing the endothelial marker CD31. Glomerular nestin-positive cells were CDK5 immunoreactive as well. Western blotting of the intermediate filamentenriched cytoskeletal fraction and coimmunoprecipitation of nestin with anti-CDK5 antibodies confirmed these results. Nestin was also detected in developing glomeruli within immature podocytes and a few other cells. Confocal microscopy of experiments conducted with antibodies against nestin and endothelial markers demonstrated that endothelial cells belonging to capillaries invading the lower cleft of S-shaped bodies and the immature glomeruli were nestin immunoreactive. Similar experiments carried out with antibodies raised against nestin and a-smooth muscle actin showed that the first mesangial cells that populate the developing glomeruli expressed nestin. In conclusion, nestin is expressed in the human kidney from the first steps of glomerulogenesis within podocytes, mesangial, and endothelial cells. This expression, restricted to podocytes in mature glomeruli, appears associated with CDK5. (J Histochem Cytochem 55:411-421, 2007)

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Section: Adult Kidneymentioning

confidence: 69%

Section: Fetal Kidneymentioning

confidence: 99%

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Nestin Expression in Adult and Developing Human Kidney

Bertelli

Regoli

Fonzi

et al. 2006

J Histochem Cytochem.

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“…46 During normal postnatal renal development in rats, the α-SMA cytoskeletal protein is expressed more intensely in the glomeruli, interstitium and peritubular capillaries, but α-SMA expression is restricted to arteriole and artery walls when the above mentioned structures mature. 47 Madsen et al 48 showed that the treatment of rats with the AT 1 antagonist candesartan for two weeks after birth reduced the total length, volume and surface area of capillaries in both cortex and medulla and disrupted vasa recta bundle organizations. These animals exhibited α-SMA-positive spindle-shaped cells that predominantly populated the outer medullary interstitium and the cortical medullary rays.…”

Section: Discussionmentioning

confidence: 99%

The role of oxidative stress in renal injury induced in rats by losartan exposure during lactation

Marin

Francescato

Costa

et al. 2013

J Renin Angiotensin Aldosterone Syst

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Introduction: Rats exposed to angiotensin II (AII) receptor antagonists during lactation present progressive disturbances in renal development that lead to progressive alterations in renal function and structure. This study evaluates the role of oxidative stress in the renal changes induced by exposure to losartan, a type 1 AII receptor antagonist, in rats during lactation. Materials and methods: Male Wistar pups were divided into: Control, pups of dams that received 2% sucrose solution; Control-tempol, pups of dams that received tempol (0.34 g/l), a superoxide dismutase mimetic compound; Losartan, pups of dams that received losartan (100 mg/kg/day), and Losartan-tempol, pups of dams that received losartan and tempol. Losartan and/or tempol were administered during lactation. Blood and urine samples were collected at 21 or 60 days, and the kidneys were removed. Results: Losartan-treated pups exhibited disturbances in renal function and structure that persisted into adulthood. Tempol treatment reduced oxidative stress and attenuated the changes induced by losartan in the glomerular filtration rate, desmin expression at the glomerular edge, vimentin in tubular cells, as well as apoptosis and inflammatory infiltration in the renal cortex. Conclusion: Oxidative stress contributes at least in part to the renal injury observed in pups exposed to losartan during lactation.

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“…However, in various types of glomerular injury, the mesangial cell may acquire characteristics of a myofibroblast, which may in fact be injurious to the glomerulus. In human glomerulogenesis, mesangial cells gradually lose fetal phenotypes identified by alpha-smooth muscle actin [24]. However, with certain pathogenic stimulators, such as platelet-derived growth factor, mesangial cells may acquire smooth-muscle-like properties, characterised by the de novo expression of alpha-smooth muscle actin, and by the development of fibroblast-like properties, characterised by the production of interstitial collagens in addition to normal mesangial matrix constituents [25].…”

Section: Mouse Model Of Type 2 Diabetesmentioning

confidence: 99%

Glomerular structural and functional changes in a high-fat diet mouse model of early-stage Type 2 diabetes

Wei

Lane

et al. 2004

Diabetologia

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Aims/hypothesis. Type 2 diabetes often results in diabetic nephropathy, which is preceded by an elevated glomerular filtration rate (GFR). This study was designed to develop a mouse model of Type 2 diabetes and to elucidate the glomerular events in the early stages of diabetic nephropathy. Methods. Four-week-old mice were fed a normal or high-fat (42% of total calories from fat) diet, and body weight, blood glucose, insulin, leptin, lipids and GFR were monitored from 9 to 21 weeks or longer after the feeding programme. Mesangial cell dedifferentiation was accessed by alpha-smooth muscle actin staining. Glomerular hypertrophy was determined using image analysis with haematoxylin-eosin staining. Matrix deposition was determined by type IV collagen staining. Results. After 9 weeks, mice fed a high-fat diet weighed more than mice fed a normal diet (30.5±1.2 vs 22.3±0.5 g, p<0.05), and mice fed a high-fat diet were hyperinsulinaemic (283.9±69.7 vs 102.9±36.4 pmol/l, p<0.05), hyperglycaemic (8.0±0.6 vs 6.5±0.2 mmol/l, p<0.05) and their leptin levels were increased six-fold (1.48±0.45 vs 0.25±0.03 ng/ml, p<0.05). After 13 weeks, mice fed a high-fat diet showed hyperfiltration (GFR; 440±60 vs 210±10 µl/min, p<0.05). During the early stages of diabetic nephropathy, mesangial cell dedifferentiation was evident, shown by increased expression of alpha-smooth muscle actin in the glomeruli. After 9 weeks, mice fed a high-fat diet already demonstrated increased type IV collagen deposition. After 13 weeks, they developed enlarged glomerular tufts compared with those of their age-matched controls. Conclusions/interpretation. The results of this study suggest that collagen IV deposition precedes the hyperfiltration and enlargement of glomeruli in early-stage diabetic nephropathy. Dedifferentiation of mesangial cells may be associated with collagen IV deposition.

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An immunohistochemical study of developing glomeruli in human fetal kidneys, See Editorial by Oliver and Al-Awqati, p. 2167

Cited by 52 publications

References 20 publications

Nestin Expression in Adult and Developing Human Kidney

Nestin Expression in Adult and Developing Human Kidney

The role of oxidative stress in renal injury induced in rats by losartan exposure during lactation

Glomerular structural and functional changes in a high-fat diet mouse model of early-stage Type 2 diabetes

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