Linked Life Data

1713586

Source:http://linkedlifedata.com/resource/pubmed/id/1713586

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
1991-9-4
pubmed:abstractText
The reverse transcription-polymerase chain reaction was used to examine alternative splicing at each of the three fibronectin exons known to undergo alternative splicing, i.e. extra domain A (ED-A), extra domain B (ED-B), and type III connecting sequence (IIICS). Ratios of fibronectin mRNAs with or without a given exon were determined in several rat tissues and human cell lines during aging in vivo and cellular senescence in vitro. We demonstrate that statistically significant shifts in the alternative splicing of fibronectin occur during aging in vivo and in vitro. Since all three alternatively spliced exons are spliced out at a higher frequency in aging tissues and cells, the fibronectin protein produced by old cells should be slightly smaller than that obtained from young cells. The reverse transcription-polymerase chain reaction demonstrates tissue-specific patterns of alternative splicing in several tissues. Whereas fibronectin mRNAs from adult rat tissues were found to range from 0 to 25% ED-A+ and from 0 to 10% ED-B+, fibronectin mRNAs from cultured cell lines were found to be approximately 50-60% ED-A+ and 15-25% ED-B+. We observed similarity in splicing of fibronectin RNA by the different cultured cell lines obtained from many tissues and attribute this observation to the effect of growth factors. We demonstrate that serum deprivation; placement of cells into primary culture; and growth factors such as transforming growth factor beta 1, retinoic acid, and 1,25-dihydroxyvitamin D3 can all change the alternative splicing of fibronectin pre-mRNA in the ED-A, ED-B, and type III connecting sequence exons. Possible mechanisms for the regulation of the alternative splicing of fibronectin RNA by growth factors are discussed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
14654-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1713586-Aging, pubmed-meshheading:1713586-Animals, pubmed-meshheading:1713586-Base Sequence, pubmed-meshheading:1713586-Cholecalciferol, pubmed-meshheading:1713586-DNA, pubmed-meshheading:1713586-Electrophoresis, Agar Gel, pubmed-meshheading:1713586-Exons, pubmed-meshheading:1713586-Fibronectins, pubmed-meshheading:1713586-Growth Substances, pubmed-meshheading:1713586-Humans, pubmed-meshheading:1713586-Male, pubmed-meshheading:1713586-Molecular Sequence Data, pubmed-meshheading:1713586-Polymerase Chain Reaction, pubmed-meshheading:1713586-RNA, Messenger, pubmed-meshheading:1713586-RNA Precursors, pubmed-meshheading:1713586-RNA Splicing, pubmed-meshheading:1713586-RNA-Directed DNA Polymerase, pubmed-meshheading:1713586-Rats, pubmed-meshheading:1713586-Rats, Inbred F344, pubmed-meshheading:1713586-Tretinoin
pubmed:year
1991
pubmed:articleTitle
The alternative splicing of fibronectin pre-mRNA is altered during aging and in response to growth factors.
pubmed:affiliation
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio 78284-7762.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.