Linked Life Data

19058853

Source:http://linkedlifedata.com/resource/pubmed/id/19058853

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-12-26
pubmed:abstractText
The generation of animals lacking Smad proteins has made it possible to explore the contribution of the TGF-beta-Smad signaling to immune activity in vivo. And there have been related issues actively pursued by many laboratories. Here we report that, in contrast to the markedly enhanced inflammatory response, Smad3 gene knockout (Smad3(ex8/ex8)) mice paradoxically show suppressed hepatic acute phase response to the injury induced by lipopolysaccharide (LPS) compared with wild-type mice, characterized by significantly weaker reaction of several typical acute phase proteins in mRNA level. The increase of positive acute phase proteins, e.g. alpha1-acid glycoprotein (alpha1-AGP), haptoglobin (HP) and C-reaction protein (CRP), and the decrease of negative acute phase proteins, including albumin (ALB) and transferrin (TRF), were both repressed according to the expression in liver estimated by optimized RT-PCR. Smad3(ex8/ex8) mice also exhibited lower survival rate as stimulated by LPS, which was probably on account of the suppressed acute phase response. These data are, to our knowledge, the first to implicate Smad3 in specific pathways of acute phase response in the liver.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
362-5
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Suppressed acute phase response to LPS-induced hepatic injury in Smad3-deficient mice.
pubmed:affiliation
Burn Institute of Chinese PLA, Department of Burn Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China. lijiahui0609@hotmail.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't