Anat Cell Biol.  2010 Jun;43(2):132-139. 10.5115/acb.2010.43.2.132.

Expression of calponin in periglomerular myofibroblasts of rat kidney with experimental chronic injuries

• Lee SY
• Choi JY
• Jin DC
• Kim J
• Cha JH

• KMID: 2168886
• DOI: http://doi.org/10.5115/acb.2010.43.2.132

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.

Keyword

Chronic renal failure; rat; calponin; immunohistochemistry; renal myofibroblasts

MeSH Terms

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
Calcium-Binding Proteins
Microfilament Proteins
Puromycin Aminonucleoside
Salicylamides

Figure

• 

  Fig. 1 Light microscopic findings of glomeruli representing glomeruloscrelosis lesions at each time point of disease rat. (A) SNx model sham, (B) SNx model 8 weeks, (C) PAN model sham, (D) PAN model 8 weeks. Note periglomerular and tubulointerstitial fibrosis in blue (B & D) with Masson's trichrome stain. Scale bar is 200 um.

• 

  Fig. 2 Light microscopic findings of glomeruli representing glomeruloscrelosis lesions at each time point of disease rat. (A) SNx model sham, (B) SNx model 8 weeks, (C) PAN model sham, (D) PAN model 8 weeks. Glomeruli in B & D show segmental glomerulosclerotic change. Arrows indicate the infiltrated cells. Masson's trichrome stain. Scale bar is 100 um.

• 

  Fig. 3 Five serial sections (A to E, F to J) stained with periodic acid-methenamine silver method (A, F), alpha-smooth muscle actin (ASMA) antiserum (B, G), calponin antiserum (C, H), periodic acid-Schiff method (D, I) and vimentin antiserum (E, J) from the subtotal nephrectomy and puromycin model 8 weeks after operation. Almost basement membrane of Bowman's capsules (arrows in A, F) was intact. Calponinpositive cells (arrows in C, H) were also ASMA- and vimentin positive. Note the thickened membrane (arrows in D, I) covered by calponin-positive cells compared with the thin membrane of the glomerulus (G in H) without periglomerular calponin-positivity. Focal segemental glomerulosclerosis is shown (open arrowhead in D). Scale bar is 100 um.

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