Role of ANTXR1 in the regulation of RANKL-induced osteoclast differentiation and function

Baek, Jong Min; Kwak, Sung Chul; Yoon, Kwon‐Ha; Kim, Ju‐Young; Lee, Myeung Su

doi:10.1016/j.bbrc.2019.01.094

Cited by 9 publications

(6 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…18 F–choline uptake has instead shown a positive significant association with the expression of all in situ biomarkers of mature osteoblasts (RANKL, VDR, and PTX3) that in our model underline the molecular profile of POLCs [9]. In fact, these molecules are expressed by osteoblasts during their physiological activities, i.e., bone matrix formation [37,38,39]. From the biological point of view, the uptake of 18 F–choline in lesions characterized by a high number of POLCs (RANKL, VDR, and PTX3 expression) can be explained by the uptake of choline in cells rich in mitochondria.…”

Section: Discussionmentioning

confidence: 85%

18F–Choline PET/CT Identifies High-Grade Prostate Cancer Lesions Expressing Bone Biomarkers

Urbano

Scimeca

Crocco

et al. 2019

JCM

View full text Add to dashboard Cite

The main aim of this study was to investigate the possible association between 18F–choline uptake and histopathological features of prostate biopsies such as the Gleason Group and the expression of both epithelial to mesenchymal transition (vimentin) and bone mineralization (bone morphogenetics protein (BMP)-2, runt-related transcription factor 2 (RUNX2), receptor activator of nuclear factor-κB ligand (RANKL), vitamin D receptor (VDR), and pentraxin 3 (PTX3) in situ biomarkers. To this end, we enrolled 79 consecutive prostate cancer patients that underwent both the 18F–choline PET/CT analysis and the prostate bioptic procedure. The standardized uptake value (SUV) average values were collected from 18F–choline PET/CT analysis whereas Gleason Group and immunostaining data were collected from paraffin-embedded sections. Histological classification showed a heterogenous population including both low/intermediate and high-grade prostate cancers. A significant increase of 18F–choline uptake in high-grade prostate lesions (Gleason Score ≥8) was found. Also, linear regression analysis showed a significant correlation between 18F–choline uptake and the number of vimentin, RANKL, VDR, or PTX3 positive prostate cancer cells. Conversely, we observed no significant association between 18F–choline uptake and the expression of bone biomarkers involved in the early phases of osteoblast differentiation (BMP-2, RUNX2). In conclusion, results here reported can lay the foundation for the use of 18F–choline positron emission tomography (PET)/computed tomography (CT) as a diagnostic tool capable of identifying high-grade prostate cancer lesions expressing bone biomarkers.

show abstract

Section: Discussionmentioning

confidence: 85%

18F–Choline PET/CT Identifies High-Grade Prostate Cancer Lesions Expressing Bone Biomarkers

Urbano

Scimeca

Crocco

et al. 2019

JCM

View full text Add to dashboard Cite

show abstract

“…Moreover, previous studies have shown that Hyal1 expression is upregulated via osteoclast formation and that Serpine1 is enriched in osteoporosis patients (44,45). In addition, Antxr1 is also involved in RANKL-induced osteoclastogenesis (46).…”

Section: Discussionmentioning

confidence: 94%

miR-134-5p inhibits osteoclastogenesis through a novel miR-134-5p/Itgb1/MAPK pathway

Huang¹,

Wang²,

Wang³

et al. 2022

Journal of Biological Chemistry

View full text Add to dashboard Cite

“…Several animal studies ( 26 , 27 ) showed that severe osteoporosis occurs in mice with OPG knockout, and the BMD of these mice increased after the injection of OPG-Fc. The expression of RANKL is regulated by many signaling molecules and hormones, including 1,25(OH) 2 D and Wnt signaling ligand ( 28 – 30 ). Another report showed that osteoblasts can respond to bone formation by expressing RANKL, and 1,25(OH) 2 D plays a crucial role in inducing the expression of RANKL in osteoblasts ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Vitamin D inhibits bone loss in mice with thyrotoxicosis by activating the OPG/RANKL and Wnt/β-catenin signaling pathways

Gao

et al. 2022

Front. Endocrinol.

View full text Add to dashboard Cite

ObjectiveVitamin D and thyroid hormones have crucial roles in bone metabolism. This study aims to explore the effects of vitamin D on bone metabolism in mice with thyrotoxicosis and its mechanisms.Methods12-week-old mice were randomly divided into 6 groups (6 mice/group), the control (CON) group, vitamin D (VD) group, low-dose LT4 (Low LT4) group, low-dose LT4+VD (Low LT4+VD) group, high-dose LT4 (High LT4) group, high-dose LT4+VD (High LT4+VD) group, LT4 was provided every day and vitamin D3 every other day for 12 weeks. Thyroid function, 25-hydroxy vitamin D, type I collagen carboxy-terminal peptide (CTX), and type I procollagen amino-terminal peptide were determined. In addition, microcomputed tomography, bone histology and histomorphometry, a three-point bending test, and the mRNA expression of osteoprotegerin (OPG), receptor activator of nuclear factor-κB ligand (RANKL) and β-catenin in bone were conducted.ResultsThe BMD of lumbar vertebrae and femur decreased and the bone microstructure was destroyed significantly in thyrotoxicosis mice. Addition of vitamin D improved the BMD and bone microstructure only in the low LT4+VD group. Mice with thyrotoxicosis had a significantly higher level of CTX (P<0.05), which was decreased by treatment with vitamin D (P<0.05). The eroded surface per bone surface (Er. S/BS) of the cancellous bone and elongated surface/endocortical perimeter (Er. S/E Pm) of the cortical bone significantly increased in the Low LT4 and High LT4 groups (P<0.05). Treatment with vitamin D significantly decreased the Er. S/BS and Er. S/E Pm. But, treatment with vitamin D did not significantly improve the toughness and rigidity of bones. The ratio of OPG to RANKL and mRNA expression of β-catenin in the Low LT4+VD group were higher than that in the Low LT4 group (P<0.05).ConclusionIn mice with thyrotoxicosis, treatment with vitamin D can inhibit bone resorption and improve the BMD and trabecular bone architecture by increasing the ratio of OPG to RANKL and upregulating the expression of Wnt/β-catenin.

show abstract

Role of ANTXR1 in the regulation of RANKL-induced osteoclast differentiation and function

Cited by 9 publications

References 27 publications

18F–Choline PET/CT Identifies High-Grade Prostate Cancer Lesions Expressing Bone Biomarkers

18F–Choline PET/CT Identifies High-Grade Prostate Cancer Lesions Expressing Bone Biomarkers

miR-134-5p inhibits osteoclastogenesis through a novel miR-134-5p/Itgb1/MAPK pathway

Vitamin D inhibits bone loss in mice with thyrotoxicosis by activating the OPG/RANKL and Wnt/β-catenin signaling pathways

Contact Info

Product

Resources

About