Transforming growth factor-beta 1 inhibits scavenger receptor activity in THP-1 human macrophages.
作者： L.A. Bottalico , R.E. Wager , L.B. Agellon , R.K. Assoian , I. Tabas
DOI: 10.1016/S0021-9258(18)54434-3
关键词:
摘要: The macrophage scavenger receptor, a 220-kDa trimeric membrane glycoprotein, mediates the internalization of modified forms low density lipoprotein (LDL) such as acetyl-LDL and oxidized-LDL thus is likely to play key role in atheroma foam cell formation. In addition, recent evidence suggests that receptor may be an important binding site for lipopolysaccharide involved scavenging by macrophages. However, little known about regulation this receptor. We now report induction activity (as measured stimulation intracellular cholesterol esterification) seen phorbol ester-differentiated THP-1 human macrophages was completely suppressed level undifferentiated monocytes picomolar concentrations transforming growth factor-beta 1 (TGF-beta 1). 125I-Acetyl-LDL degradation inhibited dose-dependent manner TGF-beta 1, with maximal inhibition (approximately 70%) occurring at 24 pM 1. Scatchard analysis revealed treatment resulted approximately 2-fold decrease number, Northern blot RNA isolated from differentiated demonstrated less mRNA 1-treated cells compared not treated Since thought present both atherosclerotic inflammatory lesions, above findings have physiological relevance regarding formation and/or clearance
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