Linked Life Data

20118412

Source:http://linkedlifedata.com/resource/pubmed/id/20118412

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-2-25
pubmed:abstractText
Many members of the TGF-beta superfamily are indicated to play important roles in ovarian follicular development, such as affecting granulosa cell function and oocyte maturation. Abnormalities associated with TGF-beta1 signaling transduction could result in female infertility. MicroRNAs (miRNAs), as small noncoding RNAs, were recently found to regulate gene expression at posttranscriptional levels. However, little is known about the role of miRNAs in TGF-beta-mediated granulosa cell proliferation and granulosa cell function. In this study, the miRNA expression profiling was identified from TGF-beta1-treated mouse preantral granulosa cells (GCs), and three miRNAs were found to be significantly up-regulated and 13 miRNAs were down-regulated. Among up-regulated miRNAs, miR-224 was the second most significantly elevated miRNA. This up-regulation was attenuated by treatment of GCs with SB431542 (an inhibitor of TGFbeta superfamily type I receptors, thus blocking phosphorylation of the downstream effectors Smad2/3), indicating that miR-224 expression was regulated by TGF-beta1/Smads pathway. The ectopic expression of miR-224 can enhance TGF-beta1-induced GC proliferation through targeting Smad4. Inhibition of endogenous miR-224 partially suppressed GC proliferation induced by TGF-beta1. In addition, both miR-224 and TGF-beta1 can promote estradiol release from GC, at least in part, through increasing CYP19A1 mRNA levels. This is the first demonstration that miRNAs can control reproductive functions resulting in promoting TGF-beta1-induced GC proliferation and ovarian estrogen release. Such miRNA-mediated effects could be potentially used for regulation of reproductive processes or for treatment of reproductive disorders.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1944-9917
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
540-51
pubmed:meshHeading
pubmed-meshheading:20118412-Animals, pubmed-meshheading:20118412-Benzamides, pubmed-meshheading:20118412-Cell Line, pubmed-meshheading:20118412-Cell Proliferation, pubmed-meshheading:20118412-Computational Biology, pubmed-meshheading:20118412-Dioxoles, pubmed-meshheading:20118412-Female, pubmed-meshheading:20118412-Granulosa Cells, pubmed-meshheading:20118412-Humans, pubmed-meshheading:20118412-Immunohistochemistry, pubmed-meshheading:20118412-In Situ Hybridization, pubmed-meshheading:20118412-Mice, pubmed-meshheading:20118412-Mice, Inbred ICR, pubmed-meshheading:20118412-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:20118412-Phosphorylation, pubmed-meshheading:20118412-Polymerase Chain Reaction, pubmed-meshheading:20118412-Receptors, Transforming Growth Factor beta, pubmed-meshheading:20118412-Signal Transduction, pubmed-meshheading:20118412-Smad4 Protein, pubmed-meshheading:20118412-Transforming Growth Factor beta
pubmed:year
2010
pubmed:articleTitle
MicroRNA-224 is involved in transforming growth factor-beta-mediated mouse granulosa cell proliferation and granulosa cell function by targeting Smad4.
pubmed:affiliation
School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230026, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't