Protection of α3 integrin-mediated podocyte shape by superoxide dismutase in the puromycin aminonucleoside nephrosis rat

Kojima, Kenichiro; Matsui, Katsuyuki; Nagase, Mitsumasa

doi:10.1016/s0272-6386(00)70056-4

Cited by 32 publications

(30 citation statements)

References 25 publications

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“…Anti-β1 integrin antibodies lead to an increase of albumin permeability in isolated glomeruli (19). Reduced expression of α3β1 integrin in podocytes has been demonstrated in both humans with FSGS (6) and in diabetic (20) and PAN model rats (21). Podocyte foot processes are anchored to the GBM via α3β1 integrin (22) and α/β-DG (23).…”

Section: Discussionmentioning

confidence: 99%

1,25-Dihydroxyvitamin D3 Ameliorates Podocytopenia in Rats with Adriamycin-induced Nephropathy

Min-shu

Zhou

et al. 2010

Intern. Med.

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Objective To investigate the role of α3β1 integrin and α/β-dystroglycan in protective effects of 1,25(OH)2D3 on podocytes in rats with adriamycin-induced nephropathy. Methods Sprague-Dawley rats were randomly divided into three groups: control group (NC), nephropathy group (NE), and nephropathy+1,25(OH)2D3 group (ND). Rats in NE and ND group were injected intravenously with adriamycin (0.1 mg/10 g body weight) to induce nephropathy, and those in ND group were then subcutaneously treated with 1,25(OH)2D3 for 8 weeks. Urinary protein level, number of urine podocytes, foot process width and glomerulosclerotic index were determined. Nephrin and podocin mRNA and protein expressions were determined by RT-PCR and western blot, respectively. Podocyte density and expressions of α3β1 integrin and α/β-dystroglycan (DG) were analyzed by immunohistochemistry and western blot, respectively. Results The increase in proteinuria, podocyturia and width of foot process in NE group were ameliorated after treatment with 1,25(OH)2D3 for 8 weeks. The glomerulosclerotic index was significantly decreased in ND group when compared with NE group. The podocyte density in ND group (10.3 ± 1.64 cells/glomerulus) was significantly higher than that in NE group (8.43 ± 1.75 cells/glomerulus) (p=0.008). 1,25(OH)2D3 treatment could significantly up-regulate the mRNA and protein expressions of nephrin and podocin, and the protein expressions of α3β1 integrin and α/β-DG. Conclusion The expressions of nephrin, podocin, α3β1 integrin and α/β-DG were decreased in rats with nephropathy. However, 1,25(OH)2D3 treatment could significantly up-regulate the expressions of nephrin, podocin, α3β1 integrin and α/β-DG proteins which might suppress podocyte detachment and podocytopenia.

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Section: Discussionmentioning

confidence: 99%

1,25-Dihydroxyvitamin D3 Ameliorates Podocytopenia in Rats with Adriamycin-induced Nephropathy

Min-shu

Zhou

et al. 2010

Intern. Med.

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“…These findings led to the hypothesis that changes in podocyte integrins could correlate with proteinuria by interfering with the dynamic of foot process anchoring in the GBM. However, several studies examining integrin expression in a variety of glomerular diseases and in vitro systems produced conflicting results concerning ␣ 3 ␤ 1 -integrin distribution or levels (26,28,60,184,196,203,216,228,365,366,426). These data could be reconciled by a modification of integrin function without changes in the overall integrin levels in the framework of integrin inside-out signaling (see below).…”

Section: Transmembrane Matrix Receptorsmentioning

confidence: 99%

“…In puromycin nephrosis, phosphatidylcholinebound superoxide dismutase, which has a higher affinity to the cell membrane than recombinant human superoxide dismutase, decreased proteinuria to the control level and improved podocyte density. Puromycin induced a decrease of ␣ 3 -integrin expression and a change of polarity of its site of expression, which was preserved by phosphatidylcholine-bound superoxide dismutase (216). In biopsies of patients with membranous nephropathy, Grone et al (148) demonstrated oxidatively modified proteins in podocytes, mesangial cells, and basal membranes (148).…”

Section: A Rosmentioning

confidence: 99%

Cell Biology of the Glomerular Podocyte

Pavenstädt

Kriz

Kretzler

2003

Physiological Reviews

1,305

1,278

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Glomerular podocytes are highly specialized cells with a complex cytoarchitecture. Their most prominent features are interdigitated foot processes with filtration slits in between. These are bridged by the slit diaphragm, which plays a major role in establishing the selective permeability of the glomerular filtration barrier. Injury to podocytes leads to proteinuria, a hallmark of most glomerular diseases. New technical approaches have led to a considerable increase in our understanding of podocyte biology including protein inventory, composition and arrangement of the cytoskeleton, receptor equipment, and signaling pathways involved in the control of ultrafiltration. Moreover, disturbances of podocyte architecture resulting in the retraction of foot processes and proteinuria appear to be a common theme in the progression of acquired glomerular disease. In hereditary nephrotic syndromes identified over the last 2 years, all mutated gene products were localized in podocytes. This review integrates our recent physiological and molecular understanding of the role of podocytes during the maintenance and failure of the glomerular filtration barrier.

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“…Some evidence indicates that the increase in angiotensinogen expression is signaled by intracellular reactive oxygen species (ROS) (74). Oxidative stress is a leading initiator of cellular dysfunction in diabetes complications (76,77), and increased ROS generation can induce podocyte dysfunction (78,79).…”

Section: Role Of Ang II In Nephrin Expression and Podocyte Injurymentioning

confidence: 99%

From the Periphery of the Glomerular Capillary Wall Toward the Center of Disease

2005

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Protection of α3 integrin-mediated podocyte shape by superoxide dismutase in the puromycin aminonucleoside nephrosis rat

Cited by 32 publications

References 25 publications

1,25-Dihydroxyvitamin D3 Ameliorates Podocytopenia in Rats with Adriamycin-induced Nephropathy

1,25-Dihydroxyvitamin D3 Ameliorates Podocytopenia in Rats with Adriamycin-induced Nephropathy

Cell Biology of the Glomerular Podocyte

From the Periphery of the Glomerular Capillary Wall Toward the Center of Disease

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