Premium
Transforming growth factor β isoforms in human glomerulonephropathies
Author(s) -
HASAN Qurratulain,
DUNBAR P Rod,
MURRAYMCINTOSH Rosalind P,
NEALE T James
Publication year - 1998
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1998.tb00371.x
Subject(s) - gene isoform , transforming growth factor , fibrosis , messenger rna , kidney , mesangial cell , transforming growth factor beta , cytokine , biology , pathological , microbiology and biotechnology , medicine , immunology , pathology , gene , endocrinology , genetics
SUMMARY: Transforming growth factor β (TGFβ) is a multifunctional cytokine for which three isoforms, TGFβ1, ‐2 and ‐3 have been characterized in mammals. Several reports suggest an involvement of TGFβ in the cellular and molecular basis of renal fibrosis. Most of these studies have focused exclusively on TGFβ1. Here we demonstrate using reverse transcriptase polymerase chain reaction (RT‐PCR) that transcripts from all three isoforms of TGFβ were detected in 31 renal biopsies, control tissue and cultured human mesangial cells. A novel alternative transcript of TGFβ2 was identified in renal tissue. the variation in transcript levels detected using this technique did not exhibit a striking correlation with any specific disease type. In addition, complement deposition and localization (i.e. mesangial or capillary wall) does not appear to have any direct correlation with the occurrence of a particular TGFβ isoform transcript. It is likely that dynamic changes in all TGFβ transcript levels occur in normal and diseased kidneys as a response to physiological and pathological demands. Most investigations have focused on one TGFβ isoform neglecting the contribution of the others. Studies which analyse all known isoforms and their alternative transcripts may establish the interplay between these during the progression of renal disease.