Heme oxygenase 1 (HO‐1) regulates osteoclastogenesis and bone resorption

@article{Zwerina2005HemeO1,
  title={Heme oxygenase 1 (HO‐1) regulates osteoclastogenesis and bone resorption},
  author={Jochen Zwerina and Sotiria Tzima and Silvia Hayer and Kurt Redlich and Oskar Hoffmann and Beatrice Hanslik-Schnabel and Josef S. Smolen and George Kollias and Georg Schett},
  journal={The FASEB Journal},
  year={2005},
  volume={19}
}
Heme oxygenase 1 (HO‐1) plays an important role in vascular disease, transplantation, and inflammation. In animal models of acute and chronic inflammation, induction of HO‐1 has anti‐inflammatory and cytoprotective properties. Since inflammation is an important trigger of osteoclastogenesis, we hypothesized that HO‐1 might influence osteoclastogenesis. We investigated the effects of induction of HO‐1 on osteoclast formation in vitro and in vivo. Furthermore, we addressed the role of HO‐1 in… 
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Upregulation of heme oxygenase‐1 inhibits the maturation and mineralization of osteoblasts
TLDR
The results showed that induction of HO‐1 inhibited the maturation of osteoblasts including mineralized bone nodule formation, alkaline phosphatase activity and decreased mRNA expression of several differentiation markers such as alkaline phosphate, osteocalcin, and RUNX2.
Bach1 regulates osteoclastogenesis in a mouse model via both heme oxygenase 1-dependent and heme oxygenase 1-independent pathways.
TLDR
The present findings demonstrate that Bach1 regulates osteoclastogenesis under inflammatory conditions, via both HO-1-dependent and HO- 1-independent mechanisms.
Hemeoxygenase-1 maintains bone mass via attenuating a redox imbalance in osteoclast
Suppression of RANKL‐dependent heme oxygenase‐1 is required for high mobility group box 1 release and osteoclastogenesis
TLDR
It is reported that RANKL‐induced suppression of heme oxygenase‐1 (HO‐1), a heme‐degrading enzyme, promotes HMGB1 release during osteoclastogenesis and suggests that RankL‐dependent HO‐1 suppression leads to caspase‐3 activation and HMGB 1 release during bone marrow‐derived macrophages and RAW‐D precursor cells.
Heme oxygenase-1 mediates protective effects on inflammatory, catabolic and senescence responses induced by interleukin-1β in osteoarthritic osteoblasts.
Heme oxygenase-1 mediates protective effects on inflammatory , catabolic and senescence responses induced by interleukin-1 b in osteoarthritic osteoblasts
TLDR
The results have shown that HO-1 decreases the production of relevant inflammatory and catabolic mediators that participate in OA pathophysiology thus eliciting protective effects in O a osteoblasts.
Various roles of heme oxygenase-1 in response of bone marrow macrophages to RANKL and in the early stage of osteoclastogenesis
TLDR
The data indicate that HO-1 is involved in the response of bone marrow macrophages to RANKL and the induction of OCLs markers, but it is dispensable in early-stage O CLs.
Heme Oxygenase-1 (HO-1) Expression in Prostate Cancer Cells Modulates the Oxidative Response in Bone Cells
TLDR
It is demonstrated that HO-1 pharmacological induction (hemin treatment) abrogated the diminution of PMOs proliferation induced by PCa cells and decreased the expression of osteoclast-modulating factors in osteoblasts.
Trolox Prevents Osteoclastogenesis by Suppressing RANKL Expression and Signaling*
TLDR
The findings indicate that Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteOClast precursors.
Dual role of VEGF-induced heme-oxygenase-1 in angiogenesis.
TLDR
It is proposed that during chronic inflammation, HO-1 has two roles, first an antiinflammatory action inhibiting leukocyte infiltration, and second, promotion of VEGF-driven noninflammatory angiogenesis, which facilitates tissue repair.
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References

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TLDR
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TLDR
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