Linked Life Data

21719609

Source:http://linkedlifedata.com/resource/pubmed/id/21719609

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-8-17
pubmed:abstractText
Our previous study on immune-related changes in the aged liver described immune cell infiltration and elevation of inflammation with age. Levels of interferon (IFN)-?, a known cell cycle inhibitor, were elevated in the aging liver. Here, we determine the role played by IFN-? in the delayed regenerative response observed in the aged livers. We observed elevated IFN signaling in both aged hepatocytes and regenerating livers post-partial hepatectomy. In vivo deletion of the major IFN-? producers-the macrophages and the natural killer cells, leads to a reduction in the IFN-? levels accompanied with the restoration of the DNA synthesis kinetics in the aged livers. Eighteen-month-old IFN-?-/- mice livers, upon resection, exhibited an earlier entry into the cell cycle compared with age-matched controls. Thus, our study strongly suggests that an age-related elevation in inflammatory conditions in the liver often dubbed as "inflammaging" has a detrimental effect on the regenerative response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1758-535X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
944-56
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Elevated interferon gamma signaling contributes to impaired regeneration in the aged liver.
pubmed:affiliation
Department of Dermatology, Columbia University Medical Center, 1150 St. Nicholas Avenue, New York, NY 10032, USA. pallavi.singh02@gmail.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural