What question did this study set out to answer?

To determine whether human microvascular endothelial cells express RANKL and osteoprotegerin under inflammatory conditions and examine their functional capacity to drive osteoclast development and bone resorption.

January 1, 2001Journal of Biological ChemistryOpen Access

Receptor Activator of NF-κB and Osteoprotegerin Expression by Human Microvascular Endothelial Cells, Regulation by Inflammatory Cytokines, and Role in Human Osteoclastogenesis

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Authors

PCPatricia Collin‐OsdobyWashington University in St. Louis LRLinda RotheWashington University in St. Louis FAFred AndersonPittsburgh Theological Seminary

Discussion

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Implication

Laboratory study demonstrates that cytokine-activated endothelial cells express RANKL and osteoprotegerin to regulate osteoclasts, suggesting a direct vascular driver of inflammatory bone loss.

Key Points

To determine whether human microvascular endothelial cells express RANKL and osteoprotegerin under inflammatory conditions and examine their functional capacity to drive osteoclast development and bone resorption.
Treated human microvascular endothelial cells (HMVEC) with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha (IL-1alpha) to quantify RANKL and osteoprotegerin (OPG) transcript and protein expression.
Assessed osteoclast formation, fusion, and bone resorption in co-cultures of cytokine-stimulated HMVEC and human monocytic precursors in the presence or absence of exogenous OPG.
Conducted immunohistochemical analysis of RANKL expression in paraffin-embedded tissue sections of fractured human osteoporotic bone.
Stimulation with TNF-alpha and IL-1alpha induced a 5- to 40-fold increase in RANKL and OPG transcript expression in HMVEC and elevated cell-surface RANKL protein levels.
Cytokine-activated HMVEC promoted the formation, fusion, and bone resorption of osteoclasts from monocytic precursors via a RANKL-mediated mechanism fully neutralized by exogenous OPG.
Vascular endothelial cells in human osteoporotic fracture sections displayed increased RANKL immunostaining adjacent to actively resorbing osteoclasts at bone turnover sites.

Cite This Study

Collin‐Osdoby et al. (2001) studied this question.

synapsesocial.com/papers/6a71e345e5469ee92be22e0b https://doi.org/10.1074/jbc.m010153200

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January 1, 2001Journal of Biological ChemistryOpen Access

Receptor Activator of NF-κB and Osteoprotegerin Expression by Human Microvascular Endothelial Cells, Regulation by Inflammatory Cytokines, and Role in Human Osteoclastogenesis

View Full Paper

Ask AI

Bookmark

Authors

PCPatricia Collin‐OsdobyWashington University in St. Louis LRLinda RotheWashington University in St. Louis FAFred AndersonPittsburgh Theological Seminary

Discussion

Member takes

Implication

Laboratory study demonstrates that cytokine-activated endothelial cells express RANKL and osteoprotegerin to regulate osteoclasts, suggesting a direct vascular driver of inflammatory bone loss.

Key Points

To determine whether human microvascular endothelial cells express RANKL and osteoprotegerin under inflammatory conditions and examine their functional capacity to drive osteoclast development and bone resorption.
Treated human microvascular endothelial cells (HMVEC) with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1alpha (IL-1alpha) to quantify RANKL and osteoprotegerin (OPG) transcript and protein expression.
Assessed osteoclast formation, fusion, and bone resorption in co-cultures of cytokine-stimulated HMVEC and human monocytic precursors in the presence or absence of exogenous OPG.
Conducted immunohistochemical analysis of RANKL expression in paraffin-embedded tissue sections of fractured human osteoporotic bone.
Stimulation with TNF-alpha and IL-1alpha induced a 5- to 40-fold increase in RANKL and OPG transcript expression in HMVEC and elevated cell-surface RANKL protein levels.
Cytokine-activated HMVEC promoted the formation, fusion, and bone resorption of osteoclasts from monocytic precursors via a RANKL-mediated mechanism fully neutralized by exogenous OPG.
Vascular endothelial cells in human osteoporotic fracture sections displayed increased RANKL immunostaining adjacent to actively resorbing osteoclasts at bone turnover sites.

Cite This Study

Collin‐Osdoby et al. (2001) studied this question.

synapsesocial.com/papers/6a71e345e5469ee92be22e0b https://doi.org/10.1074/jbc.m010153200

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