Abstract
Aims/hypothesis. Inflammation and fibrosis are pathological
mechanisms that are partially regulated by cell
signalling through the p38 mitogen-activated protein
kinase (MAPK) pathway. Elements of the diabetic milieu
such as high glucose and advanced glycation endproducts
induce activation of this pathway in renal
cells. Therefore, we examined whether p38 MAPK
signalling is associated with the development of human
and experimental diabetic nephropathy.
Methods. Immunostaining identified phosphorylated
(active) p38 MAPK in human biopsies with no abnormality
(n=6) and with Type 2 diabetic nephropathy
(n=12). Changes in kidney levels of phosphorylated
p38 were assessed by immunostaining and western
blotting in mice with streptozotocin-induced Type 1
diabetes that had been killed after 0.5, 2, 3, 4 and
8 months, and in Type 2 diabetic db/db mice at 2, 4, 6
and 8 months of age.
Original language | English |
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Pages (from-to) | 1210 - 1222 |
Number of pages | 13 |
Journal | Diabetologia |
Volume | 47 |
Issue number | 7 |
DOIs | |
Publication status | Published - 2004 |