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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2005-11-8
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pubmed:abstractText |
Hemin upregulates heme oxygenase-1 (HO-1), a stress-induced enzyme implicated in protection from a variety of injuries while its related isoform HO-2 is constitutively expressed. The role of hemin or HO-1 in the pancreas and their potential modulation of pancreatic injury are unknown. We show that HO-1 is induced in pancreatitis caused by caerulein and more prominently in severe pancreatitis caused by feeding a choline-deficient diet (CDD). Intraperitoneal hemin administration dramatically increases peritoneal and pancreas macrophages that overexpress HO-1 in association with pancreatic induction of the chemoattractants monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha but not RANTES or macrophage inflammatory protein-2. Hemin administration before CDD feeding protected 8 of 8 mice from lethality while 7 of 16 controls died. Protection is mediated by HO-1-overexpressing macrophages since hemin-primed macrophages home to the pancreas after transfer to naive mice and protect from CDD-induced pancreatitis. Suppression of hemin-primed peritoneal cell HO-1 using HO-1-specific small interfering RNA prior to cell transfer abolishes protection from CDD-induced pancreatitis. Similarly, hemin pretreatment in caerulein-induced pancreatitis reduces serum amylase and lipase, decreases pancreatic trypsin generation, and protects from lung injury. Therefore, hemin-like compounds or hemin-activated macrophages may offer novel therapeutic approaches for preventing acute pancreatitis and its pulmonary complication via upregulation of HO-1.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-10228193,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-10506590,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-10737372,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-11823983,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-11875494,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-11923691,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/16239966-9884342
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
115
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3007-14
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16239966-Acute Disease,
pubmed-meshheading:16239966-Animals,
pubmed-meshheading:16239966-Cell Movement,
pubmed-meshheading:16239966-Disease Models, Animal,
pubmed-meshheading:16239966-Enzyme Induction,
pubmed-meshheading:16239966-Female,
pubmed-meshheading:16239966-Heme Oxygenase-1,
pubmed-meshheading:16239966-Hemin,
pubmed-meshheading:16239966-Macrophages,
pubmed-meshheading:16239966-Macrophages, Peritoneal,
pubmed-meshheading:16239966-Mice,
pubmed-meshheading:16239966-Mice, Inbred BALB C,
pubmed-meshheading:16239966-Mice, Transgenic,
pubmed-meshheading:16239966-Pancreas,
pubmed-meshheading:16239966-Pancreatitis
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pubmed:year |
2005
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pubmed:articleTitle |
Hemin-activated macrophages home to the pancreas and protect from acute pancreatitis via heme oxygenase-1 induction.
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pubmed:affiliation |
Department of Medicine, VA Palo Alto Health Care System, Palo Alto, California, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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