Limits...
Podocin is translocated to cytoplasm in puromycin aminonucleoside nephrosis rats and in poor-prognosis patients with IgA nephropathy.

Fukuda H, Hidaka T, Takagi-Akiba M, Ichimura K, Oliva Trejo JA, Sasaki Y, Wang J, Sakai T, Asanuma K, Tomino Y - Cell Tissue Res. (2015)

Bottom Line: Surprisingly, the gap is also significantly increased (p < 0.05) in human kidney biopsy specimens of poor-prognosis IgA nephropathy patients.This suggests that the podocin gap could be a useful marker for classifying the prognosis of IgA nephropathy and indicating the translocation of podocin to the cytoplasm.Interestingly, podocin is also translocated to the cytoplasm in poor-prognosis human IgA nephropathy.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.

ABSTRACT
Podocytes serve as the final barrier to urinary protein loss through a highly specialized structure called a slit membrane and maintain foot process and glomerular basement membranes. Podocyte injury results in progressive glomerular damage and accelerates sclerotic changes, although the exact mechanism of podocyte injury is still obscure. We focus on the staining gap (podocin gap) defined as the staining difference between podocin and synaptopodin, which are normally located in the foot process. In puromycin aminonucleoside nephrosis rats, the podocin gap is significantly increased (p < 0.05) and podocin is translocated to the cytoplasm on days 7 and 14 but not on day 28. Surprisingly, the gap is also significantly increased (p < 0.05) in human kidney biopsy specimens of poor-prognosis IgA nephropathy patients. This suggests that the podocin gap could be a useful marker for classifying the prognosis of IgA nephropathy and indicating the translocation of podocin to the cytoplasm. Next, we find more evidence of podocin trafficking in podocytes where podocin merges with Rab5 in puromycin aminonucleoside nephrosis rats at day 14. In immunoelectron microscopy, the podocin positive area was significantly translocated from the foot process areas to the cytoplasm (p< 0.05) on days 7 and 14 in puromycin aminonucleoside nephrosis rats. Interestingly, podocin is also translocated to the cytoplasm in poor-prognosis human IgA nephropathy. In this paper, we demonstrate that the translocation of podocin by endocytosis could be a key traffic event of critical podocyte injury and that the podocin gap could indicate the prognosis of IgA nephropathy.

No MeSH data available.


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a–c Immunoelectron microscopy of podocin in the control and IgAN-poor group. Podocin was translocated from the slit diaphragm area to the cytoplasmic area in the IgAN-poor group. Scale bars (a, a’, c’) 500 nm, (b, b’, c) 2 μm. Normal glomerulus: minor glomerular abnormalities. Left low-magnification images (×8000), right high- magnification images (×30,000)
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Fig5: a–c Immunoelectron microscopy of podocin in the control and IgAN-poor group. Podocin was translocated from the slit diaphragm area to the cytoplasmic area in the IgAN-poor group. Scale bars (a, a’, c’) 500 nm, (b, b’, c) 2 μm. Normal glomerulus: minor glomerular abnormalities. Left low-magnification images (×8000), right high- magnification images (×30,000)

Mentions: We next performed immunoelectron microscopy using an anti-podocin antibody in kidney biopsy specimens of minor glomerular injury and IgAN-poor specimens (Fig. 5a–c). Podocin was located in the SD area of the control specimen. On the other hand, in the IgAN-poor biopsy specimens, the structure of the foot processes was destroyed and podocin was translocated to the cytoplasm area (Fig. 5b, c, IgAN-poor).Fig. 5


Podocin is translocated to cytoplasm in puromycin aminonucleoside nephrosis rats and in poor-prognosis patients with IgA nephropathy.

Fukuda H, Hidaka T, Takagi-Akiba M, Ichimura K, Oliva Trejo JA, Sasaki Y, Wang J, Sakai T, Asanuma K, Tomino Y - Cell Tissue Res. (2015)

a–c Immunoelectron microscopy of podocin in the control and IgAN-poor group. Podocin was translocated from the slit diaphragm area to the cytoplasmic area in the IgAN-poor group. Scale bars (a, a’, c’) 500 nm, (b, b’, c) 2 μm. Normal glomerulus: minor glomerular abnormalities. Left low-magnification images (×8000), right high- magnification images (×30,000)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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Fig5: a–c Immunoelectron microscopy of podocin in the control and IgAN-poor group. Podocin was translocated from the slit diaphragm area to the cytoplasmic area in the IgAN-poor group. Scale bars (a, a’, c’) 500 nm, (b, b’, c) 2 μm. Normal glomerulus: minor glomerular abnormalities. Left low-magnification images (×8000), right high- magnification images (×30,000)
Mentions: We next performed immunoelectron microscopy using an anti-podocin antibody in kidney biopsy specimens of minor glomerular injury and IgAN-poor specimens (Fig. 5a–c). Podocin was located in the SD area of the control specimen. On the other hand, in the IgAN-poor biopsy specimens, the structure of the foot processes was destroyed and podocin was translocated to the cytoplasm area (Fig. 5b, c, IgAN-poor).Fig. 5

Bottom Line: Surprisingly, the gap is also significantly increased (p < 0.05) in human kidney biopsy specimens of poor-prognosis IgA nephropathy patients.This suggests that the podocin gap could be a useful marker for classifying the prognosis of IgA nephropathy and indicating the translocation of podocin to the cytoplasm.Interestingly, podocin is also translocated to the cytoplasm in poor-prognosis human IgA nephropathy.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.

ABSTRACT
Podocytes serve as the final barrier to urinary protein loss through a highly specialized structure called a slit membrane and maintain foot process and glomerular basement membranes. Podocyte injury results in progressive glomerular damage and accelerates sclerotic changes, although the exact mechanism of podocyte injury is still obscure. We focus on the staining gap (podocin gap) defined as the staining difference between podocin and synaptopodin, which are normally located in the foot process. In puromycin aminonucleoside nephrosis rats, the podocin gap is significantly increased (p < 0.05) and podocin is translocated to the cytoplasm on days 7 and 14 but not on day 28. Surprisingly, the gap is also significantly increased (p < 0.05) in human kidney biopsy specimens of poor-prognosis IgA nephropathy patients. This suggests that the podocin gap could be a useful marker for classifying the prognosis of IgA nephropathy and indicating the translocation of podocin to the cytoplasm. Next, we find more evidence of podocin trafficking in podocytes where podocin merges with Rab5 in puromycin aminonucleoside nephrosis rats at day 14. In immunoelectron microscopy, the podocin positive area was significantly translocated from the foot process areas to the cytoplasm (p< 0.05) on days 7 and 14 in puromycin aminonucleoside nephrosis rats. Interestingly, podocin is also translocated to the cytoplasm in poor-prognosis human IgA nephropathy. In this paper, we demonstrate that the translocation of podocin by endocytosis could be a key traffic event of critical podocyte injury and that the podocin gap could indicate the prognosis of IgA nephropathy.

No MeSH data available.


Related in: MedlinePlus