2014
DOI: 10.1016/j.bone.2014.08.016
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Disruption of glucocorticoid signaling in chondrocytes delays metaphyseal fracture healing but does not affect normal cartilage and bone development

Abstract: States of glucocorticoid excess are associated with defects in chondrocyte function. Most prominently there is a reduction in linear growth but delayed healing of fractures that require endochondral ossification to also occur. In contrast, little is known about the role of endogenous glucocorticoids in chondrocyte function. As glucocorticoids exert their cellular actions through the glucocorticoid receptor (GR), we aimed to elucidate the role of endogenous glucocorticoids in chondrocyte function in vivo throug… Show more

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Cited by 29 publications
(31 citation statements)
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“…Yet, the molecular mechanisms may differ between the cell types, being direct in osteoblasts (Spencer et al, 2006) and potentially indirect in chondrocytes via interference with a glucocorticoid receptor (GR)-dependent mechanism (Wang et al, 2014). However, the latter is questioned by the fact that the cartilage-specific GR ( Nr3c1 ) knockout has no apparent growth plate or bone phenotype (Tu et al, 2014). Wang and colleagues used Col2a1 -CreER in their study to inactivate β-catenin.…”
Section: Discussionmentioning
confidence: 99%
“…Yet, the molecular mechanisms may differ between the cell types, being direct in osteoblasts (Spencer et al, 2006) and potentially indirect in chondrocytes via interference with a glucocorticoid receptor (GR)-dependent mechanism (Wang et al, 2014). However, the latter is questioned by the fact that the cartilage-specific GR ( Nr3c1 ) knockout has no apparent growth plate or bone phenotype (Tu et al, 2014). Wang and colleagues used Col2a1 -CreER in their study to inactivate β-catenin.…”
Section: Discussionmentioning
confidence: 99%
“…It is dispensable in GPCs and ACCs in mice under physiological conditions [83, 84], but its over-activation in children treated with glucocorticoids likely underlies the deleterious effects observed on GPs [85]. In contrast, the thyroid hormone receptors α and β ( NR1A1 and A2 ) are critical for normal skeletal growth [86].…”
Section: Zinc-coordinating Transcription Factorsmentioning
confidence: 99%
“…The GR is highly expressed in chondrocytes, cells that are closely related to osteoblasts developmentally (9) and directly involved in the process of cartilage degradation during joint inflammation (6,7). This, as well as the observations previously described, makes it conceivable that glucocorticoid signaling in chondrocytes plays a role in the regulation of inflammatory arthritis.…”
mentioning
confidence: 71%
“…This, as well as the observations previously described, makes it conceivable that glucocorticoid signaling in chondrocytes plays a role in the regulation of inflammatory arthritis. To test this hypothesis, we examined both the AIA and STIA models of arthritis in tamoxifen-inducible, chondrocyte-specific GR-knockout (GRKO) mice [collagen 2a1 Cre (Col2a1-CreER T2 ); GR flox/flox , referred to as chondrocyte-specific GRKO (chGRKO)] (9). The impact of cartilage-specific GRKO was investigated in regard to joint inflammation, cartilage damage, and bone metabolism.…”
mentioning
confidence: 99%