Abstract:
:The release of hepatic lipase (HTGL), which is responsible for the hydrolysis of lipoprotein triacylglyceride, produced by heparin from the isolated rat hepatocytes in primary culture has been examined. Tyrosine kinase (TK) inhibitors (ST-638 and biochanin A) inhibited the heparin-stimulated release of HTGL activity. The activity of partially purified TK preparation from the hepatocytes was found to be increased following incubation with heparin in a manner which was both time- and dose-dependent. An intracellular Ca(2+)-chelator (Quin2/AM), a calmodulin inhibitor (W-7) and a Ca(2+)/calmodulin-dependent protein kinase II (CaMK-II) inhibitor (KN-93) suppressed the release of HTGL activity by heparin. In addition, CaMK-II activity in the hepatocytes incubated with heparin was recognized to elevate in a time- and dose-dependent manner. The increase in CaMK-II activity by heparin was markedly reduced in the presence of the inhibitors of TK. These results suggest that the release of HTGL activity from the hepatocytes by heparin is, in part, caused through a pathway involving an activation of CaMK-II associated with an increase in membrane TK activity.
journal_name
Biol Pharm Bulljournal_title
Biological & pharmaceutical bulletinauthors
Tagashira H,Nakahigashi S,Kerakawati R,Motoyashiki T,Morita Tdoi
10.1248/bpb.28.409subject
Has Abstractpub_date
2005-03-01 00:00:00pages
409-12issue
3eissn
0918-6158issn
1347-5215pii
JST.JSTAGE/bpb/28.409journal_volume
28pub_type
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