Linked Life Data

17973244

Source:http://linkedlifedata.com/resource/pubmed/id/17973244

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-13
pubmed:abstractText
Macrophage infiltration is a common feature of the early phase of renal ischaemia/reperfusion injury. Indeed, it is generally regarded as the cause of tissue injury in this phase, although it is also clear that it can lead to tissue repair in other phases. In order to ascertain whether macrophages are directly involved in the repair/late phase, which follows the pro-inflammatory and injury process of renal ischaemia/reperfusion, we used two different approaches based on macrophage depletion. Firstly, we produced renal ischaemia in mice that were previously treated with clodronate liposome. Secondly, during reperfusion we re-injected RAW 264.7 to macrophage-depleted mice 24 h prior to sacrifice. The results showed that regeneration, as evaluated by stathmin and PCNA markers, was macrophage-dependent: it was blocked when macrophage depletion was provoked and recovered with macrophage re-injection. The cytokine profile revealed the influence of the inflammatory environment on kidney repair: pro-inflammatory cytokines (MCP-1, MIP-1alpha) increased during the early stages of reperfusion, coinciding with low regeneration, and the anti-inflammatory cytokine IL-10 increased during the longer periods of reperfusion when regeneration was more evident. We conclude that macrophages induce renal regeneration after ischaemia/reperfusion, depending on the inflammatory milieu.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-3417
pubmed:author
pubmed:issnType
Print
pubmed:volume
214
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
104-13
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Macrophage involvement in the kidney repair phase after ischaemia/reperfusion injury.
pubmed:affiliation
Department of Experimental Pathology, IIBB-CSIC, IDIBAPS, 08036, Barcelona, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't