We are analyzing https://link.springer.com/article/10.1007/s11010-008-9991-2.

Title:
Up regulation of the GRP-78 and GADD-153 and down regulation of Bcl-2 proteins in primary glomerular diseases: a possible involvement of the ER stress pathway in glomerulonephritis | Molecular and Cellular Biochemistry
Description:
The role of endoplasmic reticulum (ER) stress in kidney diseases is not well elucidated. Fifty patients with primary glomerular diseases (PGD): minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN), membranoproliferative glomerulonephritis (MPGN), and crescentic glomerulonephritis, n = 10 (each group) were enrolled. MCD, FSGS, and MGN patients were sub-grouped as nonproliferative glomerulonephritis (NPGN) and MPGN, RPGN as proliferative glomerulonephritis (PGN). Glucose regulated proteins (GRP-78), growth arrest and DNA damage inducible proteins (GADD-153), and Bcl-2 protein expression was analyzed by Western blotting, immunofluorescence and immunohistochemistry in the kidney biopsy. Up regulation of GADD-153, GRP-78, with more pronounced expression in PGN vs. NPGN (P < 0.05) and down regulation of Bcl-2 proteins was observed in the GN (PGD excluding MCD) as compared to MCD (P < 0.05). Our results suggest that renal injury in PGD is associated with ER stress and ER stress may be involved in the rapid progression of PGN to renal failure.
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Topics {✒️}

focal segmental glomerulosclerosis glucose regulated proteins ccaat/enhancer-binding protein family chronic glomerular diseases month download article/chapter growth arrest primary glomerular diseases endoplasmic reticulum-golgi stress membranoproliferative glomerulonephritis based nonproliferative glomerulonephritis proliferative glomerulonephritis ranjana walker minz harbir singh kohli glomerular epithelial cells human iga nephropathy membranoproliferative glomerulonephritis endoplasmic reticulum stress full article pdf hypertensive nephropathy reveals glomerular disease endoplasmic reticulum dysfunction idiopathic membranous nephropathy kidney diseases privacy choices/manage cookies progressive glomerular injury minimal change disease cellular redox state unfolded-protein response unfolded protein response article markan related subjects madhu khullar renal epithelial cells /ebp homology protein article molecular european economic area cellular biochemistry aims presenilin-1 mutations downregulate renal disease antioxidant defense mechanism dos santos ea post graduate institute poor renal prognosis endoplasmic reticulum conditions privacy policy cell cycle control congenital nephrotic syndrome er stress pathway gadd153 sensitizes cells degenerative diseases

Schema {🗺️}

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         headline:Up regulation of the GRP-78 and GADD-153 and down regulation of Bcl-2 proteins in primary glomerular diseases: a possible involvement of the ER stress pathway in glomerulonephritis
         description:The role of endoplasmic reticulum (ER) stress in kidney diseases is not well elucidated. Fifty patients with primary glomerular diseases (PGD): minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN), membranoproliferative glomerulonephritis (MPGN), and crescentic glomerulonephritis, n = 10 (each group) were enrolled. MCD, FSGS, and MGN patients were sub-grouped as nonproliferative glomerulonephritis (NPGN) and MPGN, RPGN as proliferative glomerulonephritis (PGN). Glucose regulated proteins (GRP-78), growth arrest and DNA damage inducible proteins (GADD-153), and Bcl-2 protein expression was analyzed by Western blotting, immunofluorescence and immunohistochemistry in the kidney biopsy. Up regulation of GADD-153, GRP-78, with more pronounced expression in PGN vs. NPGN (P < 0.05) and down regulation of Bcl-2 proteins was observed in the GN (PGD excluding MCD) as compared to MCD (P < 0.05). Our results suggest that renal injury in PGD is associated with ER stress and ER stress may be involved in the rapid progression of PGN to renal failure.
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            Primary glomerular diseases
            Nonproliferative glomerulonephritis
            Proliferative glomerulonephritis
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            Growth arrest and DNA damage inducible proteins
            Apoptosis
            Biochemistry
            general
            Cardiology
            Cancer Research
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      headline:Up regulation of the GRP-78 and GADD-153 and down regulation of Bcl-2 proteins in primary glomerular diseases: a possible involvement of the ER stress pathway in glomerulonephritis
      description:The role of endoplasmic reticulum (ER) stress in kidney diseases is not well elucidated. Fifty patients with primary glomerular diseases (PGD): minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulonephritis (MGN), membranoproliferative glomerulonephritis (MPGN), and crescentic glomerulonephritis, n = 10 (each group) were enrolled. MCD, FSGS, and MGN patients were sub-grouped as nonproliferative glomerulonephritis (NPGN) and MPGN, RPGN as proliferative glomerulonephritis (PGN). Glucose regulated proteins (GRP-78), growth arrest and DNA damage inducible proteins (GADD-153), and Bcl-2 protein expression was analyzed by Western blotting, immunofluorescence and immunohistochemistry in the kidney biopsy. Up regulation of GADD-153, GRP-78, with more pronounced expression in PGN vs. NPGN (P < 0.05) and down regulation of Bcl-2 proteins was observed in the GN (PGD excluding MCD) as compared to MCD (P < 0.05). Our results suggest that renal injury in PGD is associated with ER stress and ER stress may be involved in the rapid progression of PGN to renal failure.
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      dateModified:2008-12-24T00:00:00Z
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         Endoplasmic reticulum stress
         Primary glomerular diseases
         Nonproliferative glomerulonephritis
         Proliferative glomerulonephritis
         Glucose regulated proteins
         Growth arrest and DNA damage inducible proteins
         Apoptosis
         Biochemistry
         general
         Cardiology
         Cancer Research
         Medical Biochemistry
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