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Up-regulation of alpha(1)-microglobulin by hemoglobin and reactive oxygen species in hepatoma and blood cell lines.

Gram, Magnus LU ; Allhorn, Maria LU ; Olofsson, Tor LU and Åkerström, Bo LU (2007) In Free Radical Biology & Medicine 42(6). p.842-851
Abstract
alpha(1)-Microglobulin is a 26-kDa glycoprotein synthesized in the liver, secreted to the blood, and rapidly distributed to the extravascular compartment of all tissues. Recent results show that alpha(1)-microglobulin has heme-binding and heme-degrading properties and it has been suggested that the protein is involved in the defense against oxidation by heme and reactive oxygen species. In the present study the influence of hemoglobin and reactive oxygen species (ROS) on the cellular expression of alpha(1)-microglobulin was investigated. Oxy- and methemoglobin, free heme, and Fenton reaction-induced hydroxyl radicals induced a dose-dependent up-regulation of alpha(1)-microglobutin on both mRNA and protein levels in hepatoma cells and an... (More)
alpha(1)-Microglobulin is a 26-kDa glycoprotein synthesized in the liver, secreted to the blood, and rapidly distributed to the extravascular compartment of all tissues. Recent results show that alpha(1)-microglobulin has heme-binding and heme-degrading properties and it has been suggested that the protein is involved in the defense against oxidation by heme and reactive oxygen species. In the present study the influence of hemoglobin and reactive oxygen species (ROS) on the cellular expression of alpha(1)-microglobulin was investigated. Oxy- and methemoglobin, free heme, and Fenton reaction-induced hydroxyl radicals induced a dose-dependent up-regulation of alpha(1)-microglobutin on both mRNA and protein levels in hepatoma cells and an increased secretion of alpha(1)-microglobulin. The up-regulation was reversed by the addition of catalase and ascorbate, and by reacting hemoglobin with cyanide which prevents redox reactions. Furthermore, the blood cell lines U937 and K562 expressed alpha(1)-microglobulin at low levels, and this expression increased up to 11-fold by the addition of hemoglobin. These results suggest that a-l-microglobulin expression is induced by ROS, arising from redox reactions of hemoglobin or from other sources and are consistent with the hypothesis that alpha(1)-microglobulin participates in the defense against oxidation by hemoglobin, heme, and reactive oxygen species. (c) 2007 Elsevier Inc. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
ROS, up-regulated expression, alpha(1)-microglobulin, hemoglobin, hepatoma cells, blood cells
in
Free Radical Biology & Medicine
volume
42
issue
6
pages
842 - 851
publisher
Elsevier
external identifiers
  • wos:000244795900011
  • scopus:33847081645
ISSN
0891-5849
DOI
10.1016/j.freeradbiomed.2006.12.017
language
English
LU publication?
yes
id
7dfdee1d-81d2-45ce-8175-ce13bcdf9a14 (old id 165466)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17320766&dopt=Abstract
date added to LUP
2007-07-09 13:48:09
date last changed
2017-05-14 03:40:16
@article{7dfdee1d-81d2-45ce-8175-ce13bcdf9a14,
  abstract     = {alpha(1)-Microglobulin is a 26-kDa glycoprotein synthesized in the liver, secreted to the blood, and rapidly distributed to the extravascular compartment of all tissues. Recent results show that alpha(1)-microglobulin has heme-binding and heme-degrading properties and it has been suggested that the protein is involved in the defense against oxidation by heme and reactive oxygen species. In the present study the influence of hemoglobin and reactive oxygen species (ROS) on the cellular expression of alpha(1)-microglobulin was investigated. Oxy- and methemoglobin, free heme, and Fenton reaction-induced hydroxyl radicals induced a dose-dependent up-regulation of alpha(1)-microglobutin on both mRNA and protein levels in hepatoma cells and an increased secretion of alpha(1)-microglobulin. The up-regulation was reversed by the addition of catalase and ascorbate, and by reacting hemoglobin with cyanide which prevents redox reactions. Furthermore, the blood cell lines U937 and K562 expressed alpha(1)-microglobulin at low levels, and this expression increased up to 11-fold by the addition of hemoglobin. These results suggest that a-l-microglobulin expression is induced by ROS, arising from redox reactions of hemoglobin or from other sources and are consistent with the hypothesis that alpha(1)-microglobulin participates in the defense against oxidation by hemoglobin, heme, and reactive oxygen species. (c) 2007 Elsevier Inc. All rights reserved.},
  author       = {Gram, Magnus and Allhorn, Maria and Olofsson, Tor and Åkerström, Bo},
  issn         = {0891-5849},
  keyword      = {ROS,up-regulated expression,alpha(1)-microglobulin,hemoglobin,hepatoma cells,blood cells},
  language     = {eng},
  number       = {6},
  pages        = {842--851},
  publisher    = {Elsevier},
  series       = {Free Radical Biology & Medicine},
  title        = {Up-regulation of alpha(1)-microglobulin by hemoglobin and reactive oxygen species in hepatoma and blood cell lines.},
  url          = {http://dx.doi.org/10.1016/j.freeradbiomed.2006.12.017},
  volume       = {42},
  year         = {2007},
}