Linked Life Data

9231654

Source:http://linkedlifedata.com/resource/pubmed/id/9231654

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-8-13
pubmed:abstractText
We have previously reported that in the well-differentiated beta-cell line MIN6 cells, the beta-cell-specific differentiated characteristics, such as insulin content, expression of prohormone convertases PC2 and PC3, and glucose-regulated insulin secretion, diminished when the proprotein-processing endoprotease furin was highly expressed. Since furin converts many growth-related protein precursors to their bioactive forms, we compared the four pancreatic islet cell lines RINm5F, betaTC3, betaHC9, and MIN6 with respect to cell growth rate, furin expression, endoprotease activity, and insulin content. RINm5F cells exhibited the strongest furin expression, higher furin-type endoprotease activity, and the fastest cell growth, but had the least insulin content. In contrast, MIN6 cells exhibited only a weak furin expression, little furin-type endoprotease activity, and the slowest cell growth, but had the highest insulin content. To test whether furin-expressing cells secrete growth-promoting factors cleaved by furin, we prepared conditioned media from RINm5F and furin cDNA-introduced MIN6 (MIN6-F) cells. The conditioned media from RINm5F and MIN6-F induced increased DNA synthesis and promoted the growth of normal MIN6 cells, compared with the medium from the empty vector-introduced MIN6-0 cells. We then examined the effect of the protease inhibitors alpha1-antitrypsin and its variants by infecting their vaccinia recombinants to the four cell lines. All conditioned media from each cell line expressing the furin-specific alpha1-antitrypsin variant exhibited the least DNA synthetic capacity on normal MIN6 cells. Furthermore, all three sublines of MIN6-F grew faster than MIN6-0 and MIN6. Thus, we suggest that the islet cells with higher furin expression may induce increased production of growth factors, which result in an increase in cell growth, through an autocrine/paracrine mechanism.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1296-304
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:9231654-Animals, pubmed-meshheading:9231654-Cell Count, pubmed-meshheading:9231654-Cell Division, pubmed-meshheading:9231654-Cell Line, pubmed-meshheading:9231654-Culture Media, Conditioned, pubmed-meshheading:9231654-Cytoplasmic Granules, pubmed-meshheading:9231654-DNA, pubmed-meshheading:9231654-Furin, pubmed-meshheading:9231654-Guinea Pigs, pubmed-meshheading:9231654-Hydrogen-Ion Concentration, pubmed-meshheading:9231654-Immune Sera, pubmed-meshheading:9231654-Immunohistochemistry, pubmed-meshheading:9231654-Insulin, pubmed-meshheading:9231654-Islets of Langerhans, pubmed-meshheading:9231654-Oligopeptides, pubmed-meshheading:9231654-Radioimmunoassay, pubmed-meshheading:9231654-Serine Proteinase Inhibitors, pubmed-meshheading:9231654-Subtilisins, pubmed-meshheading:9231654-Time Factors, pubmed-meshheading:9231654-alpha 1-Antitrypsin
pubmed:year
1997
pubmed:articleTitle
Proprotein-processing endoprotease furin controls growth of pancreatic beta-cells.
pubmed:affiliation
Department of Molecular Medicine, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't