Invasion of Calponin-positive Glomerular Parietal Epithelial Cells into Glomerular Tuft Is Related to the Development of Glomerulosclerosis
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We previously have reported that periglomerular calponin expression of the glo-merulosclerotic glomeruli in the chronic nephropathy. To investigate the role of calponin during glomerulosclerosis, we examined the detailed localization pattern of calponin in chronic nephropathy rat model using serial morphometric analysis. Male Sprague-Dawley rats were used, and chronic nephropathy models were established at 8 and 12 weeks after single intraperitoneal injection of adriamycin (10 mg/kg body weight; n=5). In nephropathy models, 16.3% (8 weeks) and 23.4% (12 weeks) glomeruli showed calponin-positivity at glomerular area. In all these glomeruli, showing various sclerotic changes, calponin-immunoreactivities were present only both the glomerular parietal epithelial cells (PECs) and periglomerular myoἀbroblasts (PMFs). However, in the glomeruli with weak calponin-positive, immunoreactivity was mostly detected in PECs, suggesting that calponin may be expressed in PECs earlier than in PMFs in the glomerulosclerotic change. Some calponin-positive PECs invaded glomerular tuft with loop-shaped projection, and around this projection, nestin expression of glomerular tuft were much reduced. These results suggested that calponin-positive PECs may play a key role in the development of glomerulosclerosis, and direct contact with PECs and glomerular tuft may be more important to degenerative changes of glomeruli.
Abstract
We previously have reported that periglomerular calponin expression of the glo-merulosclerotic glomeruli in the chronic nephropathy. To investigate the role of calponin during glomerulosclerosis, we examined the detailed localization pattern of calponin in chronic nephropathy rat model using serial morphometric analysis. Male Sprague-Dawley rats were used, and chronic nephropathy models were established at 8 and 12 weeks after single intraperitoneal injection of adriamycin (10 mg/kg body weight; n=5). In nephropathy models, 16.3% (8 weeks) and 23.4% (12 weeks) glomeruli showed calponin-positivity at glomerular area. In all these glomeruli, showing various sclerotic changes, calponin-immunoreactivities were present only both the glomerular parietal epithelial cells (PECs) and periglomerular myoἀbroblasts (PMFs). However, in the glomeruli with weak calponin-positive, immunoreactivity was mostly detected in PECs, suggesting that calponin may be expressed in PECs earlier than in PMFs in the glomerulosclerotic change. Some calponin-positive PECs invaded glomerular tuft with loop-shaped projection, and around this projection, nestin expression of glomerular tuft were much reduced. These results suggested that calponin-positive PECs may play a key role in the development of glomerulosclerosis, and direct contact with PECs and glomerular tuft may be more important to degenerative changes of glomeruli.
참고문헌 (16)
- Bohle A, Mackensen-Haen S, "Significance of tubulointerstitial changes in the renal cortex for the excretory function and concentration ability of the kidney: a morphometric contribution", Am. J. Nephrol, 7, pp.421~433 (1987)
- Cha J H, "Hydration status affects nuclear distribution of transcription factor tonicity responsive enhancer binding protein in rat kidney", J. Am. Soc. Nephrol, 12, pp.2221~2230 (2001)
- de Mik S M L, "Pathophysiology and treatment of focal segmental glomerulosclerosis: the role of animal models", BMC Nephrology, 14, pp.74~83 (2013)
- Dijkman H, "The parietal epithelial cell is crucially involved in human idiopathic focal segmental glomerulosclerosis", Kidney Int, 68, pp.1562~1572 (2005)
- El Nahas A M, "Glomerulosclerosis: intrinsic and extrinsic pathways", Nephrol. Dial. Transplant, 11, pp.773~777 (1996)
- Guan N, "Key molecular events in puromycin aminonucleoside nephrosis rats", Pathol. Int, 54, pp.703~711 (2004)
- Kelly D J, "Tranilast attenuates structural and functional aspects of renal injury in the remnant kidney model", J. Am. Soc. Nephrol, 15, pp.2619~2629 (2004)
- So-Young Lee, "Expression of calponin in periglomerular myofi broblasts of rat kidney with experimental chronic injuries", Anatomy and Cell Biology, 43(2), pp.132~139 (2010), 대한해부학회
- Lee V W, "Adriamycin nephropathy: a model of focal segmental glomerulosclerosis", Nephrology (Carlton), 16, pp.30~38 (2011)
- Liu W, "The expression of intermediate filament protein nestin and its association with cyclin-dependent kinase 5 in the glomeruli of rats with diabetic nephropathy", Am. J. Med. Sci, 345, pp.470~477 (2013)
- Ohse T, "De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular disease", Am. J. Physiol. Renal. Physiol, 298, pp.F702~F711 (2010)
- Okamoto T, "Prevalence of CD44-positive glomerular parietal epithelial cells reflects podocyte injury in adriamycin nephropathy", Nephron. Exp. Nephrol, 124, pp.11~18 (2013)
- Pippin J W, "Inducible rodent models of acquired podocyte diseases", Am. J. Physiol. Renal. Physiol, 296, pp.F213~F229 (2009)
- Smeets B, "The parietal epithelial cell: a key player in the pathogenesis of focal segmental glomerulosclerosis in Thy-1.1 transgenic mice", J. Am. Soc. Nephrol, 15, pp.928~939 (2004)
- Zhang J, "Retinoids augment the expression of podocyte proteins by glomerular parietal epithelial cells in experimental glomerular disease", Nephron. Exp. Nephrol, 121, pp.e23~e37 (2012)
- Zivotić M, "Glomerular nestin expression: possible predictor of outcome of focal segmental glomerulosclerosis in children", Pediatr. Nephrol, 30, pp.79~90 (2015)