Linked Life Data

11730986

Source:http://linkedlifedata.com/resource/pubmed/id/11730986

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
2001-12-3
pubmed:abstractText
Organisms respond to infection in a complex manner involving bidirectional interactions between the neuroendocrine and immune systems. Many of the bioactive endocrine/immune factors are synthesized in a precursor form and are expected to be activated by prohormone convertases (PCs). Since patients with both type 1 and type 2 diabetes have an increased incidence and severity of infections, we hypothesized that in a condition of hyperglycemia, these processing enzymes would be activated in an immune tissue, the spleen. To test this hypothesis, we treated rats with intraperitoneal streptozotocin (STZ) (50 mg/kg/day) daily for 5 days and measured splenic PC1 and PC2 mRNA by ribonuclease protection assay. We found that PC1 mRNA was increased 6.0+/-0.02-fold (P<0.05) and PC2 mRNA was increased 1.80+/-0.01-fold (P<0.005) in the spleen of rats that received STZ compared to rats that received vehicle. Western blot indicated that the 75-kDa form of PC1 was the only form of PC1 present in the spleen and that this form increased with STZ treatment. Immunohistochemistry revealed that PC1 was found in both the white pulp (T-lymphocytes) and red pulp (monocytes and macrophages) and that its increase in immunoreactivity occurred primarily in the white pulp. PC2 and pro-opiomelanocortin (POMC, a possible splenic substrate for PC1/PC2) immunoreactivity was found predominantly in the red pulp. STZ induced an increase in splenic PC1 and POMC, but not PC2 protein levels. We conclude that in the STZ model of diabetes, splenic PCs are induced, which could lead to an increased activation of many immune-derived hormones. We speculate that this up-regulation of prohormone converting enzymes may be related to the increased infections seen in patients with both type 1 and type 2 diabetes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0167-0115
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-45
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11730986-Animals, pubmed-meshheading:11730986-Anti-Bacterial Agents, pubmed-meshheading:11730986-Aspartic Acid Endopeptidases, pubmed-meshheading:11730986-Blotting, Western, pubmed-meshheading:11730986-Diabetes Mellitus, Experimental, pubmed-meshheading:11730986-Disease Models, Animal, pubmed-meshheading:11730986-Hypothalamus, pubmed-meshheading:11730986-Immunohistochemistry, pubmed-meshheading:11730986-Pituitary Gland, pubmed-meshheading:11730986-Pro-Opiomelanocortin, pubmed-meshheading:11730986-Proprotein Convertase 2, pubmed-meshheading:11730986-Proprotein Convertases, pubmed-meshheading:11730986-RNA, Messenger, pubmed-meshheading:11730986-Rats, pubmed-meshheading:11730986-Ribonucleases, pubmed-meshheading:11730986-Spleen, pubmed-meshheading:11730986-Streptozocin, pubmed-meshheading:11730986-Subtilisins, pubmed-meshheading:11730986-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Up-regulation of splenic prohormone convertases PC1 and PC2 in diabetic rats.
pubmed:affiliation
Division of Endocrinology, Department of Medicine, Cedars-Sinai Research Institute-UCLA School of Medicine, Los Angeles, CA 90048, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't