Research Article
Expression of calponin in periglomerular myofibroblasts of rat kidney with experimental chronic injuries
So-Young Lee, Jae-Youn Choi, Dong-Chan Jin, Jin Kim, Jung-Ho Cha
Published:
June 01, 2010
DOI:
10.5115/acb.2010.43.2.132
License:
Copyright © 2010. Anatomy and Cell Biology2010This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Our previous research demonstrated that calponin-immunoreactivity was localized in myofibroblasts of the periglomerular region of human kidney specimens obtained at the time of transplantation from organ recipients. In the present study we examined calponin expression in two chronic nephropathy models, puromycin aminonucleoside (PAN) nephropathy and subtotal nephrectomy (SNx), to investigate the role of calponin in chronic renal injury. Male Sprague-Dawley rats were used, and both nephropathy models were established at 1, 2, 4, and 8 weeks after surgery. There were no periglomerular calponin-positive cells in sham, PAN 1 and 2 week, and SNx 1, 2, and 4 week groups. In SNx 8 week and PAN 4 and 8 week groups, only a few glomeruli with periglomerular calponin-reactivity, which covered half or a very small part of the periglomerular space, were observed. All glomeruli with periglomerular calponin-reactivity showed sclerotic changes, especially thickening of parietal epithelial cells (PECs). In conjunction with our previous report, this data represents the first documentation of the expression of calponin in renal myofibroblasts. We suggest that interactions between PECs and calponin-positive myofibroblasts may play a key role in the late stage of glomerulosclerosis.