| Angiotensin II Inhibition Increases Epithelial to Mesenchymal Transition in Neonatal Rat Kidney |
| Hyung Eun Yim, Kee Hwan Yoo, In Sun Bae, Young Sook Hong, Joo Won Lee |
| Korea Univ Guro Hospital, Department of Paediatrics, Seoul, Korea, South |
| 바로잡습니다 : 온라인 혈액투석여과법의 효용성과 안전성 |
| 임형은, 유기환, 배인선, 홍영숙, 이주원 |
| 고려대학교 구로병원 소아청소년과 |
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| Abstract |
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Renin-angiotensin system is markedly activated during renal development and neonatal interruption of angiotensin II induces renal growth impairment that is linked to renal papillary atrophy and persistent tubulointerstitial damage. Epithelial to mesenchymal transition (EMT) is a critical developmental process and has important implications in renal fibrosis. Nestin, a classical stem cell marker, is expressed during kidney development and recent studies show that it could be a novel marker for tubulointerstitial injury. To investigate the effects of angiotensin II inhibition on EMT in developing kidney, we tested the expression of EMT markers and nestin in the angiotensin converting enzyme (ACE) inhibitor-treated kidney. Newborn rat pups were treated with enalapril (30 mg/kg/d) or vehicle for 7 days. Immunohistochemistry for the expression of α-smooth muscle actin (SMA), E-cadherin, vimentin, and nestin was performed. The number of positive-stained cells was determined under 100 magnification at 10 random fields. In the enalapril-treated group, the number of α-SMA-positive cells significantly increased in both renal cortex and medulla, which were mainly expressed in the dilated tubular epithelial cells (p<0.05). The expression of E-cadherin-positive cells was dramatically reduced in the cortical and medullary tubular epithelial cells in the enalapril-treated group, compared with the control group (p<0.05). The number of vimentin- and nestin-positive cells was not different in cortex between the two groups, however, their expression increased in the medullary tubulointerstitail cells in the enalapril-treated group (p<0.05). Our results show that ACE inhibition in the developing rat kidney increases renal EMT by upregulating the expression of α-SMA and downregulating that of E-cadherin. Enalapril-treated rats also demonstrated increased expression of vimentin and nestin in renal medulla, suggesting that renal medullary changes in the process of EMT could be more prominent and ACE inhibition might differentially modulate the expressions of EMT markers in the developing rat kidney. |
| Key Words:
안지오텐신, 세포 전이, 발달, Angiotensin, Cell transdifferentiation, Development |
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