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논문분류	춘계학술대회 초록집
제목	Agonistic cMet Antibody Prevents Kidney Fibrosis in Acute Kidney Disease Mice Model
저자	Jeonghwan Lee, Lilin Li, Young Wook Choi, Jung Nam An, Yoon Kyu Oh, Chun Soo Lim, Seung Hee Yang, Yon Su Kim, Jung Pyo Lee
출판정보	2019; 2019(1):
키워드	agonistic cMet Antibody \| kidney fibrosis \| acute kidney disease model
초록	We aimed to investigate whether treatment with agnostic cMet antibody can prevent kidney fibrosis in the acute kidney disease mice model. Unilateral ischemic-reperfusion injury at left kidney was introduced in 7-week0old male C57BL/6 mice (n = 14) and raised for up to 28 days to induce acute kidney disease model. Agnostic cMet antibody (20 mg/kg) was injected via tail vein at a schedule of day -1, 0, 1, 3, and twice weekly thereafter in the treatment group (n = 7). Vehicle (saline) was injected via tail vein at the same schedule in the control group (n = 7). Left kidney weight per total body weight was significantly higher in the treatment group (0.63 ± 0.21% vs. 0.43 ± 0.22%, P = 0.022). In the histopathologic specimen of Masson's trichrome stain, areas of kidney interstitial fibrosis attenuated in the treatment group. In the western-blot analysis, protein abundance of α-smooth muscle actin (22.5% of control, P = 0.03), fibronectin (16.4% of control, P = 0.03), TGF-β (33.3% of control, P = 0.05), total (6.6% of control, P = 0.03) and phospho-smad2/3 (10.1% of control, P = 0.03) decreased significantly, and protein abundance of e-cadherin increased (912.4% of control, P = 0.03) significantly in the treatment group. In the real-time PCR analysis, mRNA expression of α-smooth muscle actin (11.5% of control, P = 0.006), collagen 1 (11.6% of control, P = 0.01), fibronectin (11.2% of control, P = 0.01), TGF-β (21.3% of control, P = 0.01) decreased significantly in the treatment group. Agonistic cMet antibody attenuates kidney fibrosis in the mice unilateral ischemic reperfusion induced acute kidney disease model, and TGF-β and smad2/3 pathway involved in the kidney fibrosis are effectively suppressed in the treatment of agonistic cMet antibody.
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