Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-50422
Sen, K; Lindenmeyer, M T; Gaspert, A; Eichinger, F; Neusser, M A; Kretzler, M; Segerer, S; Cohen, C D (2011). Periostin is induced in glomerular injury and expressed de novo in interstitial renal fibrosis. American Journal of Pathology, 179(4):1756-1767.
PDF - Registered users only
View at publisher
Matricellular proteins participate in the pathogenesis of chronic kidney diseases. We analyzed glomerular gene expression profiles from patients with proteinuric diseases to identify matricellular proteins contributing to the progression of human nephropathies. Several genes encoding matricellular proteins, such as SPARC, THBS1, and CTGF, were induced in progressive nephropathies, but not in nonprogressive minimal-change disease. Periostin showed the highest induction, and its transcript levels correlated negatively with glomerular filtration rate in both glomerular and tubulointerstitial specimen. In well-preserved renal tissue, periostin localized to the glomerular tuft, the vascular pole, and along Bowman's capsule; no signal was detected in the tubulointerstitial compartment. Biopsies from patients with glomerulopathies and renal dysfunction showed enhanced periostin expression in the mesangium, tubular interstitium, and sites of fibrosis. Periostin staining correlated negatively with renal function. α-smooth muscle actin-positive mesangial and interstitial cells localized close to periostin-positive sites, as indicated by co-immunofluorescence. In vitro stimulation of mesangial cells by external addition of TGF-β1 resulted in robust induction of periostin. Addition of periostin to mesangial cells induced cell proliferation and decreased the number of cells expressing activated caspase-3, a marker of apoptosis. These human data indicate for the first time a role of periostin in glomerular and interstitial injury in acquired nephropathies.
0 downloads since deposited on 31 Oct 2011
0 downloads since 12 months
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Surgical Pathology|
|Dewey Decimal Classification:||610 Medicine & health|
|Deposited On:||31 Oct 2011 09:39|
|Last Modified:||06 Dec 2013 07:57|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page