Linked Life Data

20814988

Source:http://linkedlifedata.com/resource/pubmed/id/20814988

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-2-21
pubmed:abstractText
Evidence demonstrates that sympathetic nervous system (SNS) activation causes osteopenia via ?(2)-adrenoceptor (?2-AR) signaling. Here we show that female mice with chronic sympathetic hyperactivity owing to double knockout of adrenoceptors that negatively regulate norepinephrine release, ?(2A)-AR and ?(2C)-AR (?(2A) /?(2C)-ARKO), present an unexpected and generalized phenotype of high bone mass with decreased bone resorption and increased formation. In ?(2A) /?(2C)-ARKO versus wild-type (WT) mice, micro-computed tomographic (µCT) analysis showed increased, better connected, and more plate-shaped trabeculae in the femur and vertebra and increased cortical thickness in the vertebra, whereas biomechanical analysis showed increased tibial and femoral strength. Tibial mRNA expression of tartrate-resistant acid phosphatase (TRACP) and receptor activator of NF-?B (RANK), which are osteoclast-related factors, was lower in knockout (KO) mice. Plasma leptin and brain mRNA levels of cocaine amphetamine-regulated transcript (CART), which are factors that centrally affect bone turnover, and serum levels of estradiol were similar between mice strains. Tibial ?(2)-AR mRNA expression also was similar in KO and WT littermates, whereas ?(2A)-, ?(2B)- and ?(2C)-AR mRNAs were detected in the tibia of WT mice and in osteoblast-like MC3T3-E1 cells. By immunohistochemistry, we detected ?(2A)-, ?(2B)-, ?(2C)- and ?(2)-ARs in osteoblasts, osteoclasts, and chondrocytes of 18.5-day-old mouse fetuses and 35-day-old mice. Finally, we showed that isolated osteoclasts in culture are responsive to the selective ?(2)-AR agonist clonidine and to the nonspecific ?-AR antagonist phentolamine. These findings suggest that ?(2)-AR is not the single adrenoceptor involved in bone turnover regulation and show that ?(2)-AR signaling also may mediate the SNS actions in the skeleton.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1523-4681
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 American Society for Bone and Mineral Research.
pubmed:issnType
Electronic
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
591-603
pubmed:meshHeading
pubmed-meshheading:20814988-Adrenergic alpha-2 Receptor Agonists, pubmed-meshheading:20814988-Animals, pubmed-meshheading:20814988-Bone Resorption, pubmed-meshheading:20814988-Bone and Bones, pubmed-meshheading:20814988-Brain, pubmed-meshheading:20814988-Estradiol, pubmed-meshheading:20814988-Female, pubmed-meshheading:20814988-Gene Deletion, pubmed-meshheading:20814988-Gene Expression Regulation, pubmed-meshheading:20814988-Hyperkinesis, pubmed-meshheading:20814988-Leptin, pubmed-meshheading:20814988-Mice, pubmed-meshheading:20814988-Mice, Knockout, pubmed-meshheading:20814988-Myocardium, pubmed-meshheading:20814988-Nerve Tissue Proteins, pubmed-meshheading:20814988-Norepinephrine, pubmed-meshheading:20814988-Organ Size, pubmed-meshheading:20814988-Osteoclasts, pubmed-meshheading:20814988-Osteogenesis, pubmed-meshheading:20814988-Phenotype, pubmed-meshheading:20814988-Receptors, Adrenergic, alpha-2, pubmed-meshheading:20814988-Sympathetic Nervous System
pubmed:year
2011
pubmed:articleTitle
Double disruption of ?2A- and ?2C-adrenoceptors results in sympathetic hyperactivity and high-bone-mass phenotype.
pubmed:affiliation
Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't