Injured kidney cells express SM22α (transgelin): Unique features distinct from α-smooth muscle actin (αSMA)

ABSTRACT Aim: SM22α (transgelin) has been focused upon as a player in the process of phenotypic changes of types of cells. The SM22α expression in the rat anti‐glomerular basement membrane (GBM) nephritis model and differences from an established phenotypic marker for the myofibroblast, α‐smooth muscle actin (αSMA), were investigated. Methods: The rat kidney tissues were processed for histological studies, immunohistochemical and immunoelectronmicroscopy analyses on days 0, 7, 28, 42 and 56 after injection of rabbit anti‐GBM serum for the disease induction. Results: Immunohistochemistry with anti‐SM22α antibodies (Ab) revealed that kidneys of the nephritic rats on day 7 expressed SM22α in podocytes, crescentic cells and epithelial cells of Bowman's capsule. After 28 days, SM22α was also expressed in peritubular interstitial cells. Double immunofluorescence with anti‐SM22α Ab and anti‐αSMA Ab showed that SM22α was preferentially expressed in podocytes, whereas αSMA was positive in mesangial cells on day 7. After day 28, both molecules became positive in peritubular interstitial cells. Conclusion: SM22α was expressed in epithelial cells of inflamed glomeruli in the early phase, and then also in peritubular interstitial cells in the later phase of anti‐GBM nephritis model. SM22α presented unique kinetics of expression distinct from αSMA. This manuscript describes de novo expression of the actin‐associated protein SM22α (also known as transgelin) by injured podocytes in a rat model of crescentic glomerulonephritis. Immuno‐EM localized SM22α to effaced, but not intact, foot processes in podocytes suggest a role for this molecule in reorganization of the actin cytoskeleton following podocyte injury.