Induction of antioxidant enzymes in murine podocytes precedes injury by puromycin aminonucleoside

Vega-Warner, Virginia; Ransom, Richard F.; Vincent, Andrea M.; Brosius, Frank C.; Smoyer, William E.

doi:10.1111/j.1523-1755.2004.00962.x

Cited by 39 publications

(36 citation statements)

References 33 publications

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“…6B). As shown previously (16), there was no indication of overall cell death at the 48-h time point in PAN-treated cells (data not shown).…”

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Asupporting

confidence: 53%

“…7, A and B). Cytoskeleton changes similar to PAN, such as increase in stress fibers close to the cell periphery (16,36) and gradual loss of Neph1 from the junctions, were noted in the Ang II-treated cells. In contrast, the distribution of Neph1 at the junctions was significantly higher (p Ͻ 0.05) in TAT-Neph1CD-transduced podocytes as compared with the untransduced cells (Fig.…”

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Amentioning

confidence: 91%

“…5, A and B). It is to be noted that the TAT-GFP-transduced cells treated with PAN (48 h) failed to make efficient cell-cell contacts as noted previously (16,17) and also demonstrated by the staining of podocyte cell membrane using Vybrantô DiI cell-labeling dye (Invitrogen catalog number V-22885). To quantitatively assess the ability of cells to form cell-cell junctions, we estimated the number of cells involved in making cell-cell contacts in treated and untreated cells.…”

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Amentioning

confidence: 99%

“…One of the most common podocyte injury-inducing agents that has been used under both in vitro and in vivo conditions is PAN. 3 Treatment of PAN in cultured podocytes has been shown to induce the disassembly of cell-cell junctions, actin cytoskeleton rearrangement, and the retraction of cellular processes (13)(14)(15)(16)(17). In the rat model, PAN treatment has been shown to induce podocyte effacement, a characteristic of actin reorganization, and loss of podocyte function associated with proteinuria (12,18).…”

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confidence: 99%

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Slit Diaphragm Protein Neph1 and Its Signaling

Arif

Rathore

Kumari

et al. 2014

Journal of Biological Chemistry

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Background: Neph1 is a podocyte protein that is critical for maintaining renal function. Results: Inhibiting Neph1 signaling preserves podocyte structure and function in response to glomerular injury-inducing agents. Conclusion: Maintaining a robust expression of Neph1 at the podocyte cell membrane protects podocytes from renal injury. Significance: This is the first report demonstrating that Neph1 signaling is a therapeutic target for preventing podocyte damage.

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“…6B). As shown previously (16), there was no indication of overall cell death at the 48-h time point in PAN-treated cells (data not shown).…”

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Asupporting

confidence: 53%

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Amentioning

confidence: 91%

Section: Transduction Of Tat-neph1cd Protects Podocytes From Panand Amentioning

confidence: 99%

mentioning

confidence: 99%

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Slit Diaphragm Protein Neph1 and Its Signaling

Arif

Rathore

Kumari

et al. 2014

Journal of Biological Chemistry

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“…It is very interesting that mRNA expression of SV2B is already dramatically downregulated 1 h after PAN administration and was recovered at the peak of proteinuria. Although the initiation mechanism of PAN nephropathy is uncertain, it has been reported that PAN treatment induces significant early changes in reactive oxygen species in podocyte (37). The downregulation of SV2B might be mediated by reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

Synaptic Vesicle Protein 2B Is Expressed in Podocyte, and Its Expression Is Altered in Proteinuric Glomeruli

Miyauchi

Saito²,

Karasawa³

et al. 2006

Journal of the American Society of Nephrology

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Synaptic vesicle protein 2B (SV2B) was identified by the subtraction hybridization technique as a molecule of which mRNA expression was decreased in puromycin aminonucleoside (PAN) nephropathy by glomerular cDNA subtraction assay. The expression of SV2B was detected in glomerular lysate with Western blot analysis. Dual-labeling immunofluorescence studies with glomerular cell markers demonstrated that SV2B is expressed in glomerular visceral epithelial cells (podocytes). The expression of SV2B is detected also in cultured podocyte and in human kidney section as podocytic pattern. The decrease of SV2B mRNA was already detected before the onset of proteinuria in PAN nephropathy. The mRNA expression of SV2B clearly is altered not only in PAN nephropathy but also in another proteinuric state that is caused by an antibody against nephrin, a functional molecule of the slit diaphragm. The decreased intensity in SV2B staining was already detected before the peak of proteinuria in both models with immunofluorescence study. A reduced amount of SV2B was detected in both models also with Western blot analysis. CD2AP, another functional molecule of the slit diaphragm, was observed in cytoplasm, including the processes area of the cultured podocyte, and when the podocyte was treated with small interfering RNA for SV2B, CD2AP staining at the process area was not detected. These results suggest that SV2B is a functional molecule of podocyte, and SV2B may play a role in the expression and proper localization of CD2AP.

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Peroxidase expression is decreased by palmitate in cultured podocytes but increased in podocytes of advanced diabetic nephropathy

Lee¹,

Lee²

2018

Journal Cellular Physiology

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High levels of serum free fatty acids (FFAs) are associated with lipotoxicity and type 2 diabetes. Palmitic acid (PA) is the predominant circulating saturated FFA. PA induces mitochondrial superoxide and hydrogen peroxide (H O ) generation in cultured podocytes. To elucidate the role of PA in antioxidant defense systems in diabetic nephropathy (DN), cultured podocytes were exposed to 250 μM PA for 1-24 hr, and protein expressions of catalase, peroxiredoxins (Prxs), and glutathione peroxidase (GPx) were examined by western blot analysis. PA induced an early transient increase in the Prx1, Prx2, and GPx1 levels in podocytes, but not catalase. Long-term exposure of PA to podocytes significantly decreased the protein levels of Prx1, Prx2, GPx1, and catalase. Coincubation of PA-treated cells with oleic acid, however, restored the expression of these proteins. In advanced human diabetic glomeruli, H O generation was elevated as shown by increased fluorescence of dichlorofluorescein. Strong immunostaining for Prx1, Prx2, GPx1, and catalase was observed in the podocytes of advanced human DN, wherein transforming growth factor-β1 staining was also positive. These results suggest that podocytes are susceptible to PA-induced oxidative damage with impaired peroxidase activity and that peroxidases have futile antioxidant effects in the podocytes in the late stages of DN. Given this, PA-induced podocyte injury via inadequate peroxidase response to H O appears to play an important role in the pathogenesis of DN.

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Induction of antioxidant enzymes in murine podocytes precedes injury by puromycin aminonucleoside

Cited by 39 publications

References 33 publications

Slit Diaphragm Protein Neph1 and Its Signaling

Slit Diaphragm Protein Neph1 and Its Signaling

Synaptic Vesicle Protein 2B Is Expressed in Podocyte, and Its Expression Is Altered in Proteinuric Glomeruli

Peroxidase expression is decreased by palmitate in cultured podocytes but increased in podocytes of advanced diabetic nephropathy

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