Abstract
The aim of the present study was to investigate the expression of alpha-smooth muscle actin (alpha-SM-actin) and proliferating cell nuclear antigen (PCNA) in renal cortex from patients with focal segmental glomerulosclerosis (FSGS) and their correlations with parameters of renal disease progression. We analyzed renal biopsies from 41 patients with idiopathic FSGS and from 14 control individuals. The alpha-SM-actin immunoreaction was evaluated using a score that reflected the changes in the extent and intensity of staining in the glomerular or cortical area. The PCNA reaction was quantified by counting the labeled cells of the glomeruli or renal cortex. The results, reported as median +/- percentile (25th; 75th), showed that the alpha-SM-actin scores in the glomeruli and tubulointerstitium from the renal cortex were 2.0 (2.0; 4.0) and 3.0 (3.0; 4.0), respectively, in patients with FSGS, and 0.5 (0.0; 1.0) and 0.0 (0.0; 0.5) in the controls. The number of PCNA-positive cells per glomerulus and graded field of tubulointerstitium from the renal cortex was 0.2 (0.0; 0.4) and 1.1 (0.3; 2.2), respectively, for patients with FSGS, and 0.0 (0.0; 0.5) and 0.0 (0.0; 0.0) for controls. The present data showed an increase of alpha-SM-actin and PCNA expression in glomeruli and renal cortex from FSGS patients. The extent of immunoreaction for alpha-SM-actin in the tubulointerstitial area was correlated with the intensity of proteinuria. However, there was no correlation between the kidney expression of these proteins and the reciprocal of plasma creatinine level or renal fibrosis. These findings suggest that the immunohistochemical alterations may be reversible.
Highlights
The progression of renal disease depends, among other factors, on the interaction between kidney cells and cytokines [1]
The extent of immunoreaction for a-SM-actin in the tubulointerstitial area was correlated with the intensity of proteinuria
Increased renal content and production of these polypeptides have been observed in several glomerular diseases [1,14,17,18,19,20,21,22], probably induced by glomerular hypertension or hypertrophy, macrophage infiltration, high renal levels of angiotensin and proteinuria observed in these patients [1,14,23,24,25,26]
Summary
The progression of renal disease depends, among other factors, on the interaction between kidney cells and cytokines [1]. Cytokines act on renal cells (tubular cells, mesangial cells and fibroblasts) by inducing proliferation and modifying their phenotypes. These cells start to express a-smooth muscle actin (a-SM-actin) and increase the production of collagen and other extracellular matrix components [1,2,3]. The a-SM-actin isoform is normally expressed by vascular smooth muscle cells but interstitial fibroblasts and mesangial and tubular cells can express this protein in a variety of glomerular diseases. PCNA is an acidic nuclear protein whose levels are increased from the late G1 to the S phase of the cell cycle and whose detection parallels other standard methods of assessing cell proliferation such as BrdU labeling and Ki-67 staining [12,13]. The aim of the present study was to investigate the expression of a-SM-actin and PCNA in renal cortex from patients with focal segmental glomerulosclerosis (FSGS) and from control individuals and their correlations with parameters of renal disease progression
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
