Takayuki Shindo, Hiroki Kurihara, Kouji Kuno, Hitoshi Yokoyama, Takashi Wada, Yukiko Kurihara, Tomihiko Imai, Yuhui Wang, Masafumi Ogata, Hiroaki Nishimatsu, Nobuo Moriyama, Yoshio Oh-hashi, Hiroyuki Morita, Takatoshi Ishikawa, Ryozo Nagai, Yoshio Yazaki, Kouji Matsushima
J Clin Invest.
2000;
105(10):1345–1352
doi:10.1172/JCI8635
This article Copyright © 2000, The American Society for Clinical Investigation
Abstract
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disintegrin and metalloproteinase (ADAM) represents a protein family possessing both metalloproteinase and disintegrin domains. ADAMTS-1, an ADAM family member cloned from cachexigenic colon adenocarcinoma, is unusual in that it contains thrombospondin type I motifs and anchors to the extracellular matrix. To elucidate the biological role of ADAMTS-1, we developed ADAMTS-1–null mice by gene targeting. Targeted disruption of the mouse ADAMTS-1 gene resulted in growth retardation with adipose tissue malformation. Impaired female fertilization accompanied by histological changes in the uterus and ovaries also resulted. Furthermore, ADAMTS-1–/– mice demonstrated enlarged renal calices with fibrotic changes from the ureteropelvic junction through the ureter, and abnormal adrenal medullary architecture without capillary formation. ADAMTS-1 thus appears necessary for normal growth, fertility, and organ morphology and function. Moreover, the resemblance of the renal phenotype to human ureteropelvic junction obstruction may provide a clue to the pathogenesis of this common congenital disease.
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