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논문분류	춘계학술대회 초록집
제목	Lysyl oxidase-like 2 expression is related with the progression of renal tubulointerstitial fibrosis
저자	Sung-Eun Choi* 1, Nara Jeon1, Hoon Young Choi2, Hyeong Cheon Park2, Beom Jin Lim
출판정보	2016; 2016(1):
키워드	animal model, lysyl oxidase-like 2, therapeutic target, transforming growth factor-beta, tubulointerstitial fibrosis
초록	Background: Tubulointerstitial fibrosis is a common end point of chronic kidney diseases. Preventing the progression of tubulointerstitial fibrosis is a key to prevent renal failure. Transforming growth factor-β (TGF-β) and accompanying molecules have been demonstrated to be responsible for tubulointerstitial fibrosis, but effective therapy has not been established yet. Lysyl oxidase-like 2 (LOXL2) is a molecule known to be related with invasive growth and metastasis of malignant neoplasm. Recently, it is reported that LOXL2 is also responsible for hepatic and pulmonary fibrosis. In this study, we investigated the expression of LOXL2 in human and mice kidneys, and demonstrate the change of expression in experimentally induced tubulointerstitial fibrosis. Methods: We measured the expression of LOXL2 with immunohistochemistry in biopsied human renal tissue and mice kidney. The markers of proximal tubule or distal tubule were double stained with anti-LOXL2 antibody to determine the exact location of expression. Tubulointerstitial fibrosis was induced by intraperitoneal injection of folic acid in CD1 mice. Protein expression and mRNA level were measured by western blot and real time RT-PCR in vehicle-treated and folic acid-treated mice. Results: LOXL2 was normally expressed in cytoplasm of some proximal and distal tubular epithelial cells. After inducing tubulointerstitial fibrosis, LOXL2 mRNA showed more than 5-fold increase compared to normal kidney. By immunohistochemistry, more tubular epithelial cells show LOXL2 expression with higher intensity after induction of tubulointerstitial fibrosis. Conclusion: LOXL2 is normally expressed in human and mice renal tubular epithelial cells. Expression of LOXL2 markedly increased after tubulointerstitial fibrosis. The function of LOXL2 in tubulointerstitial fibrosis and its interaction with TGF-β should be further investigated.
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