title: Plasma lysophosphatidic acid level and serum autotaxin activity are increased in liver injury in rats in relation to its severity.
abstract: Lysophosphatidic acid (LPA) is a lipid mediator with multiple biological actions. We have reported that LPA stimulates hepatic stellate cell proliferation and inhibits DNA synthesis in hepatocytes, suggesting that LPA might play some role in the liver. We have found that plasma LPA level and serum autotaxin (ATX) activity were increased in patients with chronic hepatitis C. However, the clinical significance of LPA and its synthetic enzyme, autotaxin (ATX), is still unclear. To determine whether the increase of plasma LPA level and serum ATX activity might be found generally in liver injury, we examined the possible modulation of them in the blood in rats with various liver injuries. Plasma LPA level and serum ATX activity were increased in carbon tetrachloride-induced liver fibrosis correlatively with fibrosis grade, in dimethylnitrosamine-induced acute liver injury correlatively with serum alanine aminotransferase level or in 70% hepatectomy as early as 3 h after the operation. Plasma LPA level was correlated with serum ATX activity in rats with chronic and acute liver injury. ATX mRNA in the liver was not altered in carbon tetrachloride-induced liver fibrosis. Plasma LPA level and serum ATX activity are increased in various liver injuries in relation to their severity. Whether increased ATX and LPA in the blood in liver injury is simply a result or also a cause of the injury should be further clarified.
authors.affiliation: Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Tokyo 113-8655, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Watanabe
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ikeda
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Nakamura
authors.forename: Ryunosuke
authors.initials: R
authors.lastname: Ohkawa
authors.forename: Yukio
authors.initials: Y
authors.lastname: Kume
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Tomiya
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Tejima
authors.forename: Takako
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Masahiro
authors.initials: M
authors.lastname: Arai
authors.forename: Mikio
authors.initials: M
authors.lastname: Yanase
authors.forename: Junken
authors.initials: J
authors.lastname: Aoki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Arai
authors.forename: Masao
authors.initials: M
authors.lastname: Omata
authors.forename: Kenji
authors.initials: K
authors.lastname: Fujiwara
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Yatomi
mesh_terms: D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity; D006498:Hepatectomy; D008099:Liver / Q000187:drug effects*; D008246:Lysophospholipids / Q000097:blood*; D008297:Male; D010727:Phosphoric Diester Hydrolases / Q000097:blood* / Q000235:genetics; D011755:Pyrophosphatases / Q000097:blood* / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D000099189:Lysophospholipase D
chemical_list: D002251:Carbon Tetrachloride; D008246:Lysophospholipids; D010727:Phosphoric Diester Hydrolases; D011755:Pyrophosphatases; D012333:RNA, Messenger; D000099189:Lysophospholipase D; C032881:lysophosphatidic acid