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Göteborgs universitets publikationer

Mesangial cells from patients with IgA nephropathy have increased susceptibility to galactose-deficient IgA1

Författare och institution:
Kerstin Ebefors (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Peidi Liu (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Emelie Lassén (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Johannes Elvin (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Emma Candemark (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi); Kristina Levan (Institutionen för kliniska vetenskaper, sektionen för kvinnors och barns hälsa, Avdelningen för obstetrik och gynekologi); Börje Haraldsson (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Jenny Nyström (Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi)
Publicerad i:
Bmc Nephrology, 17 s. 40
ISSN:
1471-2369
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2016
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
Background: IgA nephropathy (IgAN) is the most common glomerulonephritis in the world, affecting close to a million people. Circulating galactose-deficient IgA (gd-IgA), present in patients with IgAN, form immune complex deposits in the glomerular mesangium causing local proliferation and matrix expansion. Intriguing though, individuals having gd-IgA deposits in the kidneys do not necessarily have signs of glomerular disease. Recurrence of IgAN only occurs in less than half of transplanted patients with IgAN, indicating that gd-IgA is not the only factor driving the disease. We hypothesize that, in addition to IgA complexes, patients with IgAN possess a subtype of mesangial cells highly susceptible to gd-IgA induced cell proliferation. Methods: To test the hypothesis, we designed a technique to culture primary mesangial cells from renal biopsies obtained from IgAN patients and controls. The cell response to gd-IgA treatment was then measured both on gene and protein level and the proliferation rate of the cells in response to PDGF was investigated. Results: When treated with gd-IgA, mesangial cells from patients with IgAN express and release more PDGF compared to controls. In addition, the mesangial cells from patients with IgAN were more responsive to treatment with PDGF resulting in an increased proliferation rate of the cells compared to control. Mesangial cells cultured from patients with IgAN expressed and released more IL-6 than controls and had a higher expression of matrix genes. Both mesangial cells derived from patients with IgAN and controls increased their expressed TGF beta 1 and CCL5 when treated with gd-IgA. Conclusion: We conclude that mesangial cells derived from IgAN patients have a mesangioproliferative phenotype with increased reactivity to IgA and that these cellular intrinsic properties may be important for the development of IgA nephropathy.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Klinisk medicin
Nyckelord:
Mesangial cells, IgA nephropathy, PDGF, growth-factor-beta, renal-transplantation, immune-complexes, pdgf-bb, expression, recurrence, glomeruli, glomerulonephritis, immunoglobulin, proliferation, Urology & Nephrology
Postens nummer:
235226
Posten skapad:
2016-04-26 13:59
Posten ändrad:
2016-06-27 16:13

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