Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-5-9
pubmed:abstractText
Previous studies have demonstrated that the mechanical compressive loading affects the biosynthesis of chondrocytes seeded in three dimensional scaffolds. In this study, the level of type II collagen mRNA expression was increased by a continuous dynamic compression at 10% compressive strain and 0.1 Hz in chondrocytes seeded in a biodegradable, elastomeric scaffold, poly(L-lactide-co-epsilon-caprolactone) (PLCL). To further examine this molecular mechanism, the promoter region of COL2A1 gene, which is encoding type II collagen, was analyzed using rabbit chondrocytes transfected with luciferase reporter vectors containing the 5'-flanking regions of human COL2A1 gene. A deletion mutant analysis revealed that the most active short promoter in response to continuous dynamic compression is in the region between -509 and -109 base pairs, where the transcription factor Sp1 is located. Additionally, an mRNA decay experiment using transcription inhibitor actinomycin D demonstrated that dynamic compression do not stabilize type II collagen mRNA. Our results indicate that mechanical compression increases the level of type II mRNA expression by transcriptional activation possibly through the Sp1 binding sites residing in the proximal region of the COL2A1 gene promoter.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
344
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1192-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Mechanical compressive loading stimulates the activity of proximal region of human COL2A1 gene promoter in transfected chondrocytes.
pubmed:affiliation
Division of Biomedical Engineering, Graduate School of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't