Linked Life Data

21068162

Source:http://linkedlifedata.com/resource/pubmed/id/21068162

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-12-24
pubmed:abstractText
Estrogens cause growth plate closure in both males and females, by decreasing proliferation and inducing apoptosis of postproliferative growth plate chondrocytes. In vitro studies using 17?-estradiol (E(2)) conjugated to bovine serum albumin (E(2)-BSA) show that rat costochondral growth plate resting zone chondrocytes also respond to E(2). Moreover, they are regulated by E(2)-BSA via a protein kinase C and ERK MAPK signaling pathway that is functional only in female cells. To better understand how E(2) regulates apoptosis of growth plate chondrocytes, rat resting zone chondrocytes cells were treated with E(2) or E(2)-BSA. E(2) caused apoptosis in male and female resting zone and growth zone chondrocytes in a dose-dependent manner, based on elevated DNA fragmentation, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and caspase-3 activation. E(2) also up-regulated p53 and Bax protein (Bcl-2-associated X protein) levels and induced release of cytochrome C from the mitochondria, indicating a mitochondrial apoptotic pathway. The apoptotic effect of E(2) did not involve elevated nitric oxide production or MAPKs. It was reduced by ICI 182780, which is an estrogen receptor (ER) antagonist and blocked by antibodies to Er?36, a membrane-associated ER. E(2)-BSA reduced cell viability and increased caspase-3 activity; ICI 182780 had no effect, but anti-ER?36 antibodies blocked the effect. The results indicate that estrogen is able to directly affect the cell population kinetics of growth plate chondrocytes by regulating apoptosis, as well as proliferation and differentiation in both resting zone and growth zone cells. They also have provided further information about the physiological functions of estrogen on longitudinal bone growth.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1945-7170
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
82-92
pubmed:meshHeading
pubmed-meshheading:21068162-Animals, pubmed-meshheading:21068162-Apoptosis, pubmed-meshheading:21068162-Cell Membrane, pubmed-meshheading:21068162-Cell Nucleus, pubmed-meshheading:21068162-Cells, Cultured, pubmed-meshheading:21068162-Chondrocytes, pubmed-meshheading:21068162-DNA Fragmentation, pubmed-meshheading:21068162-Epiphyses, pubmed-meshheading:21068162-Estradiol, pubmed-meshheading:21068162-Female, pubmed-meshheading:21068162-Foscarnet, pubmed-meshheading:21068162-Gene Expression Regulation, Enzymologic, pubmed-meshheading:21068162-Male, pubmed-meshheading:21068162-Mitochondria, pubmed-meshheading:21068162-Mitogen-Activated Protein Kinases, pubmed-meshheading:21068162-Nitric Oxide, pubmed-meshheading:21068162-Peptide Fragments, pubmed-meshheading:21068162-Rats, pubmed-meshheading:21068162-Rats, Sprague-Dawley, pubmed-meshheading:21068162-Receptors, Estrogen, pubmed-meshheading:21068162-Sex Characteristics, pubmed-meshheading:21068162-Thrombin
pubmed:year
2011
pubmed:articleTitle
17?-Estradiol regulates rat growth plate chondrocyte apoptosis through a mitochondrial pathway not involving nitric oxide or MAPKs.
pubmed:affiliation
Department of Biomedical Engineering, Georgia Institute of Technology, 315 Ferst Drive NW, Atlanta, Georgia 30332-0363, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't