Injured podocytes proliferate in cellular focal segmental glomerulosclerosis (FSGS), collapsing FSGS and crescentic glomerulonephritis, where TGF-beta(1) is overexpressed in hyperplastic podocytes.
Beneficial effect of all-trans retinoic acid (ATRA) on glomerulosclerosis rats via the down-regulation of the expression of alpha-smooth muscle actin: a comparative study between ATRA and benazepril.
We evaluated the influence of TGF-beta(1) gene Arg(25)-->Pro, TNF alpha gene G-308A and IL-6 gene G-174C polymorphisms on the clinical manifestations of focal segmental glomerulosclerosis (FSGS).
We examined the expression patterns of TGF-beta 1, thrombospondin-1 (TSP-1), TGF-beta type II receptor (TGF-beta IIR), phosphorylated Smad2/Smad3, and podocyte-specific epitopes [Wilms' tumor protein-1 (WT-1) and glomerular epithelial protein-1 (GLEPP-1)] in 15 renal biopsy specimens with idiopathic FSGS and six renal biopsies with no detectable abnormalities by means of immunohistochemistry.
In patients with steroid-resistant NS, intrarenal TGF-beta1 gene expression showed a positive predictive value of 90% and a negative predictive value of 88% to identify FSGS (P < 0.0001).
The relationship between expression of TGF-beta 1 protein or TGF-beta 1 mRNA and tissue damage was investigated using the enzyme-antibody and in situ hybridization method in frozen slices of renal tissue from 30 patients: 25 with glomerulonephritis (18 with immunoglobulin A nephropathy; two with focal glomerulosclerosis, one with membranous nephropathy, one with crescentic glomerulonephritis and three with lupus nephritis) and five control patients with minimal change disease.