Matches in SemOpenAlex for { <https://semopenalex.org/work/W2164866483> ?p ?o ?g. }
- W2164866483 endingPage "1089" @default.
- W2164866483 startingPage "1080" @default.
- W2164866483 abstract "Excessive glucocorticoid administration accelerates osteoblast apoptosis and skeletal deterioration. Heat shock proteins (HSPs) regulate metabolic activities in osteoblastic cells. This study characterized the biological significance of HSP60 in glucocorticoid-induced bone loss. Rats were treated with glucocorticoid, HSP60 antisense oligonucleotides, or adenovirus-mediated HSP60 gene transfer. Bone mineral density, metaphyseal trabecular micro-architecture, and fragility were analyzed by dual X-ray absorptiometry, micro-computed tomography, and material testing, respectively. Differential proteomic profiles of bone tissue extracts were detected by bi-dimensional electrophoresis and mass spectrometry. Survival and proapoptotic signal transduction were quantified by immunoblotting. Glucocorticoid-treated rats had low bone mineral density and metaphyseal trabecular microstructure in association with downregulation of collagen 1α1 and HSP60 expressions in bone tissue. Gain of HSP60 function by adenovirus-mediated HSP60 gene transfer abrogated the deleterious effects of glucocorticoid treatment on bone mass, trabecular microstructure, and mechanical strength. Enhancement of HSP60 signaling attenuated the glucocorticoid-induced loss of trabecular bone volume, mineral acquisition reactions and osteoblast surface. HSP60 gene transfer activated ERK and Akt and reduced Bax and cytochrome c release, as well as caspase-3 cleavage, which attenuated the inhibitory effects of glucocorticoid treatment on osteoblast survival. Loss of HSP60 function by HSP60 antisense oligonucleotides accelerated mitochondrial apoptotic programs and osteoblast apoptosis. Knockdown of HSP60 induced loss of bone mass, micro-architecture integrity, and mechanical property. Taken together, loss of HSP60 signaling contributes to the glucocorticoid-induced enhancement of pro-apoptotic reactions, thereby accelerating osteoblast apoptosis and bone mass loss. Enhancement of HSP60 function is beneficial for protecting bone tissue against the glucocorticoid-induced inhibition of bone cell viability and bone formation." @default.
- W2164866483 created "2016-06-24" @default.
- W2164866483 creator A5004157315 @default.
- W2164866483 creator A5009825460 @default.
- W2164866483 creator A5019228211 @default.
- W2164866483 creator A5028006170 @default.
- W2164866483 creator A5030148493 @default.
- W2164866483 creator A5041407021 @default.
- W2164866483 creator A5051642293 @default.
- W2164866483 creator A5064795712 @default.
- W2164866483 date "2011-11-01" @default.
- W2164866483 modified "2023-09-25" @default.
- W2164866483 title "Heat shock protein 60 protects skeletal tissue against glucocorticoid-induced bone mass loss by regulating osteoblast survival" @default.
- W2164866483 cites W1907029095 @default.
- W2164866483 cites W1968064845 @default.
- W2164866483 cites W1968121880 @default.
- W2164866483 cites W1971494641 @default.
- W2164866483 cites W1974706978 @default.
- W2164866483 cites W1984368973 @default.
- W2164866483 cites W1984732690 @default.
- W2164866483 cites W1992310701 @default.
- W2164866483 cites W1992916574 @default.
- W2164866483 cites W1998466116 @default.
- W2164866483 cites W2000485424 @default.
- W2164866483 cites W2007187226 @default.
- W2164866483 cites W2007317632 @default.
- W2164866483 cites W2011203192 @default.
- W2164866483 cites W2012112276 @default.
- W2164866483 cites W2014537095 @default.
- W2164866483 cites W2018671017 @default.
- W2164866483 cites W2021115829 @default.
- W2164866483 cites W2029391324 @default.
- W2164866483 cites W2029690888 @default.
- W2164866483 cites W2041863225 @default.
- W2164866483 cites W2052437470 @default.
- W2164866483 cites W2054866872 @default.
- W2164866483 cites W2055288416 @default.
- W2164866483 cites W2062447638 @default.
- W2164866483 cites W2063531792 @default.
- W2164866483 cites W2066571367 @default.
- W2164866483 cites W2074760000 @default.
- W2164866483 cites W2074901733 @default.
- W2164866483 cites W2076830904 @default.
- W2164866483 cites W2079591191 @default.
- W2164866483 cites W2087378917 @default.
- W2164866483 cites W2089590765 @default.
- W2164866483 cites W2092485963 @default.
- W2164866483 cites W2093196075 @default.
- W2164866483 cites W2102392020 @default.
- W2164866483 cites W2102680446 @default.
- W2164866483 cites W2112877326 @default.
- W2164866483 cites W2138546242 @default.
- W2164866483 cites W2145937040 @default.
- W2164866483 cites W2147822482 @default.
- W2164866483 cites W2150637442 @default.
- W2164866483 cites W2157773408 @default.
- W2164866483 cites W2159176408 @default.
- W2164866483 cites W2161225255 @default.
- W2164866483 doi "https://doi.org/10.1016/j.bone.2011.08.006" @default.
- W2164866483 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21854881" @default.
- W2164866483 hasPublicationYear "2011" @default.
- W2164866483 type Work @default.
- W2164866483 sameAs 2164866483 @default.
- W2164866483 citedByCount "21" @default.
- W2164866483 countsByYear W21648664832013 @default.
- W2164866483 countsByYear W21648664832014 @default.
- W2164866483 countsByYear W21648664832016 @default.
- W2164866483 countsByYear W21648664832018 @default.
- W2164866483 countsByYear W21648664832019 @default.
- W2164866483 countsByYear W21648664832020 @default.
- W2164866483 countsByYear W21648664832021 @default.
- W2164866483 countsByYear W21648664832022 @default.
- W2164866483 crossrefType "journal-article" @default.
- W2164866483 hasAuthorship W2164866483A5004157315 @default.
- W2164866483 hasAuthorship W2164866483A5009825460 @default.
- W2164866483 hasAuthorship W2164866483A5019228211 @default.
- W2164866483 hasAuthorship W2164866483A5028006170 @default.
- W2164866483 hasAuthorship W2164866483A5030148493 @default.
- W2164866483 hasAuthorship W2164866483A5041407021 @default.
- W2164866483 hasAuthorship W2164866483A5051642293 @default.
- W2164866483 hasAuthorship W2164866483A5064795712 @default.
- W2164866483 hasConcept C104317684 @default.
- W2164866483 hasConcept C126322002 @default.
- W2164866483 hasConcept C134018914 @default.
- W2164866483 hasConcept C146621620 @default.
- W2164866483 hasConcept C185592680 @default.
- W2164866483 hasConcept C202751555 @default.
- W2164866483 hasConcept C205260736 @default.
- W2164866483 hasConcept C2778260815 @default.
- W2164866483 hasConcept C2780841215 @default.
- W2164866483 hasConcept C55493867 @default.
- W2164866483 hasConcept C68991219 @default.
- W2164866483 hasConcept C71924100 @default.
- W2164866483 hasConcept C86803240 @default.
- W2164866483 hasConcept C95444343 @default.
- W2164866483 hasConceptScore W2164866483C104317684 @default.
- W2164866483 hasConceptScore W2164866483C126322002 @default.
- W2164866483 hasConceptScore W2164866483C134018914 @default.