Expression of calponin in periglomerular myofibroblasts of rat kidney with experimental chronic injuries.
10.5115/acb.2010.43.2.132
- Author:
So Young LEE
1
;
Jae Youn CHOI
;
Dong Chan JIN
;
Jin KIM
;
Jung Ho CHA
Author Information
1. Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Korea. jhcha@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Chronic renal failure;
rat;
calponin;
immunohistochemistry;
renal myofibroblasts
- MeSH:
Animals;
Calcium-Binding Proteins;
Epithelial Cells;
Humans;
Immunohistochemistry;
Kidney;
Kidney Failure, Chronic;
Male;
Microfilament Proteins;
Myofibroblasts;
Nephrectomy;
Puromycin Aminonucleoside;
Rats;
Rats, Sprague-Dawley;
Salicylamides;
Transplants
- From:Anatomy & Cell Biology
2010;43(2):132-139
- CountryRepublic of Korea
- Language:English
-
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.
