Source:http://linkedlifedata.com/resource/pubmed/id/16449294
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
2006-6-8
|
| pubmed:abstractText |
We have recently reported that Pdx1-Cre-mediated whole pancreas inactivation of IGF-I gene [in pancreatic-specific IGF-I gene-deficient (PID) mice] results in increased beta-cell mass and significant protection against both type 1 and type 2 diabetes. Because the phenotype is unlikely a direct consequence of IGF-I deficiency, the present study was designed to explore possible activation of proislet factors in PID mice by using a whole genome DNA microarray. As a result, multiple members of the Reg family genes (Reg2, -3alpha, and -3beta, previously not known to promote islet cell growth) were significantly upregulated in the pancreas. This finding was subsequently confirmed by Northern blot and/or real-time PCR, which exhibited 2- to 8-fold increases in the levels of these mRNAs. Interestingly, these Reg family genes were also activated after streptozotocin-induced beta-cell damage and diabetes (wild-type T1D mice) when islet cells were undergoing regeneration. Immunohistochemistry revealed increased Reg proteins in exocrine as well as endocrine pancreas and suggested their potential role in beta-cell neogenesis in PID or T1D mice. Previously, other Reg proteins (Reg1 and islet neogenesis-associated protein) have been shown to promote islet cell replication and neogenesis. These uncharacterized Reg proteins may play a similar but more potent role, not only in normal islet cell growth in PID mice, but also in islet cell regeneration after T1D.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0193-1849
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
291
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
E50-8
|
| pubmed:dateRevised |
2010-12-3
|
| pubmed:meshHeading |
pubmed-meshheading:16449294-Animals,
pubmed-meshheading:16449294-Blotting, Northern,
pubmed-meshheading:16449294-Crosses, Genetic,
pubmed-meshheading:16449294-Diabetes Mellitus, Experimental,
pubmed-meshheading:16449294-Diabetes Mellitus, Type 1,
pubmed-meshheading:16449294-Female,
pubmed-meshheading:16449294-Gene Expression Regulation,
pubmed-meshheading:16449294-Immunohistochemistry,
pubmed-meshheading:16449294-Insulin-Like Growth Factor I,
pubmed-meshheading:16449294-Islets of Langerhans,
pubmed-meshheading:16449294-Lithostathine,
pubmed-meshheading:16449294-Male,
pubmed-meshheading:16449294-Mice,
pubmed-meshheading:16449294-Mice, Inbred C57BL,
pubmed-meshheading:16449294-Mice, Inbred DBA,
pubmed-meshheading:16449294-Mice, Transgenic,
pubmed-meshheading:16449294-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:16449294-RNA, Messenger,
pubmed-meshheading:16449294-Reverse Transcriptase Polymerase Chain Reaction
|
| pubmed:year |
2006
|
| pubmed:articleTitle |
Activation of the Reg family genes by pancreatic-specific IGF-I gene deficiency and after streptozotocin-induced diabetes in mouse pancreas.
|
| pubmed:affiliation |
Fraser Laboratories, Rm. M3-15, Royal Victoria Hospital, 687 Pine Ave. West, Montreal, QC H3A 1A1, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|