Caveolin-1 Regulates Osteoclastogenesis and Bone Metabolism in a Sex-dependent Manner

Lee, Yong Deok; Yoon, Soo‐Hyun; Park, Cheol‐Kyu; Lee, Jiyeon; Lee, Zang Hee; Kim, Hong-Hee

doi:10.1074/jbc.m114.598581

Cited by 28 publications

(22 citation statements)

References 41 publications

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“…According to the results observed by X‐ray, the area of new bone formation at the bone‐tendon junction in the experimental group was larger than that in the control group. This result is consistent with other studies reporting that knockdown of caveolin‐1, due to the decrease in Receptor Activator of Nuclear Factor‐κ B Ligand (RNAKL), reduced osteoclastogenesis, which is one of the major producers for new bone resorption through reshaping bone and inhibiting pathological bone loss . On the other hand, the general findings from the experimental animals showed no fibrous proliferation in the experimental group but great fibrous proliferation was observed in the control group.…”

Section: Discussionsupporting

confidence: 92%

“…This result is consistent with other studies reporting that knockdown of caveolin-1, due to the decrease in Receptor Activator of Nuclear Factor-κ B Ligand (RNAKL), reduced osteoclastogenesis, which is one of the major producers for new bone resorption through reshaping bone and inhibiting pathological bone loss. 15,16 On the other hand, the general findings from the experimental animals showed no fibrous proliferation in the experimental group but great fibrous proliferation was observed in the control group. Similar result has been revealed that the loss of caveolae protein in alveolar epithelial cells may result in a serious injury to type I pneumocytes in the process of fibrogenesis.…”

Section: Discussionmentioning

confidence: 92%

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In vitro effect of caveolin‐1 as a slow‐release material on bone‐tendon junction healing: A comparative study

Liang

2019

The Kaohsiung J of Med Scie

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Bone tendon junction injury is hard to cure because of its special anatomical structure, and the treatment applied for bone‐tendon junction injury cannot result in the perfect vascular regeneration and restoration of the fibrocartilage zone. In this article, we aim to explore the effect of caveolin‐1 as a slow‐release material on bone‐tendon junction healing. Seventy‐two New Zealand rabbits were randomly selected and assigned into the experimental, sham‐operated and control groups (n = 24). Caveolin‐1 microspheres and microcapsule were developed as drug delivery system. At the 4th, 8th, and 12th weeks after surgery, quadriceps muscle patella‐patellar tendon (QMPPT) was obtained from each rabbit to observe the tendon‐to‐bone tunnel healing, and X‐ray examination, histological examination and biomechanical testing were applied for evaluating new bone formation. As the X‐ray showed, caveolin‐1 increased the new bone area at each time point. At the 4th and 8th weeks after surgery, the rabbit treated with caveolin‐1 slow release material showed repair of fibrocartilage. According to the biomechanical results, the cross‐sectional area, breaking load and ultimate tensile strength were increased along with time. At the same time point, caveolin‐1 increased the ultimate tensile strength. Our study demonstrates that caveolin‐1 as a slow‐release material could accelerate bone‐tendon junction healing by promoting the formation of the transition zone.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 92%

In vitro effect of caveolin‐1 as a slow‐release material on bone‐tendon junction healing: A comparative study

Liang

2019

The Kaohsiung J of Med Scie

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“…In concert with M-CSF, RANKL enables OCG in vitro from primary OC progenitors (Quinn et al, 1998). While OCG in vitro can be induced by trace amounts (∼1 ng/ml) of sRANKL (Lin et al, 2007), commonly used concentrations of sRANKL are 10-200 ng/ ml (Lee et al, 2015;Uchiyama and Yamaguchi, 2004). Here, we show that TNFα (but not IL1β) is a potent inducer of OCG and adseverin in the absence of sRANKL, which is consistent with earlier data that TNFα, but not IL1β, can promote the differentiation of OC progenitors into mature, TRAcP-positive multinucleated cells in the absence of RANKL (Azuma et al, 2000;Fuller et al, 2006;Kim et al, 2005;O'Brien et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

IL1β and TNFα promote RANKL-dependent adseverin expression and osteoclastogenesis

Wang

Galli

Silver

et al. 2018

Journal of Cell Science

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Adseverin is an actin-binding protein involved in osteoclastogenesis, but its role in inflammation-induced bone loss is not well-defined. Here, we examined whether IL1β and TNFα regulate adseverin expression to control osteoclastogenesis in mouse primary monocytes and RAW264.7 cells. Adseverin was colocalized with subcortical actin filaments and was enriched in the fusopods of fusing cells. In precursor cells, adseverin overexpression boosted the formation of RANKL-induced multinucleated cells. Both IL1β and TNFα enhanced RANKL-dependent TRAcP activity by 1.6-fold and multinucleated cell formation (cells with ≥3 nuclei) by 2.6- and 3.3-fold, respectively. However, IL1β and TNFα did not enhance osteoclast formation in adseverin-knockdown cells. RANKL-dependent adseverin expression in bone marrow cells was increased by both IL1β (5.4-fold) and TNFα (3.3-fold). Luciferase assays demonstrated that this expression involved transcriptional regulation of the adseverin promoter. Activation of the promoter was restricted to a 1118 bp sequence containing an NF-κB binding site, upstream of the transcription start site. TNFα also promoted RANKL-induced osteoclast precursor cell migration. We conclude that IL1β and TNFα enhance RANKL-dependent expression of adseverin, which contributes to fusion processes in osteoclastogenesis.

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“…Estrogen has a proapoptotic effect on osteoclasts. ERα deletion suppresses this effect in females, but not males, so that the Cav-1 effect might be due to a stronger dependency of estrogen signaling on Cav-1 in females ( 95 ). Sexually dimorphic effects of ER and Cav-1 and bone cancer metastasis are worthy of further mechanistic study.…”

Section: Literature Analysismentioning

confidence: 99%

Sex Differences and Bone Metastases of Breast, Lung, and Prostate Cancers: Do Bone Homing Cancers Favor Feminized Bone Marrow?

et al. 2017

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Sex-associated differences in bone metastasis formation from breast, lung, and prostate cancer exist in clinical studies, but have not been systematically reviewed. Differences in the bone marrow niche can be attributed to sexual dimorphism, to genetic variations that affect sex hormone levels, or to the direct effects of sex hormones, natural or exogenously delivered. This review describes the present understanding of sex-associated and sex hormone level differences in the marrow niche and in formation of bone metastasis during the transition of these three cancers from treatable disease to an often untreatable, lethal metastatic one. Our purpose is to provide insight into some underlying molecular mechanisms for hormonal influence in bone metastasis formation, and to the potential influence of sexual dimorphism, genetic differences affecting sex assignment, and sex hormone level differences on the bone niche and its favorability for metastasis formation. We reviewed publications in PubMed and EMBASE, including full length manuscripts, case reports, and clinical studies of relevance to our topic. We focused on bone metastasis formation in breast, lung, and prostate cancer because all three commonly present with bone metastases. Several clear observations emerged. For breast cancer bone metastasis formation, estrogen receptor (ER) signaling pathways indicate a role for ER beta (ERβ). Estrogen influences the bone microenvironment, creating and conditioning a favorable niche for colonization and breast cancer progression. For lung cancer, studies support the hypothesis that females have a more favorable bone microenvironment for metastasis formation. For prostate cancer, a decrease in the relative androgen to estrogen balance or a “feminization” of bone marrow favors bone metastasis formation, with a potentially important role for ERβ that may be similar to that in breast cancer. Long-term estrogen administration or androgen blockade in males may feminize the bone marrow niche to one more favorable for bone metastases in prostate cancer. Administration of androgens in females, especially combined with mastectomy, may reduce risk of developing bone metastatic breast cancer. We conclude that it should be considered that females, those with female-leaning genetic variations, or hormonal states that feminize the bone marrow, may offer favorable sites for bone metastases.

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Caveolin-1 Regulates Osteoclastogenesis and Bone Metabolism in a Sex-dependent Manner

Cited by 28 publications

References 41 publications

In vitro effect of caveolin‐1 as a slow‐release material on bone‐tendon junction healing: A comparative study

In vitro effect of caveolin‐1 as a slow‐release material on bone‐tendon junction healing: A comparative study

IL1β and TNFα promote RANKL-dependent adseverin expression and osteoclastogenesis

Sex Differences and Bone Metastases of Breast, Lung, and Prostate Cancers: Do Bone Homing Cancers Favor Feminized Bone Marrow?

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