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Journal articles on the topic 'Osteocyte autophagy'

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Published: 1 March 2025

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1

Toscani, Denise, Carla Palumbo, Benedetta Dalla Palma, Marina Bolzoni, Marzia Ferretti, Paola Sena, Daniela Guasco, Eugenia Martella, Franco Aversa, and Nicola Giuliani. "Myeloma-Induced Osteocyte Death Was Blunted By Proteasome Inhibitors Through The Modulation Of Autophagy." Blood 122, no. 21 (November 15, 2013): 3096. http://dx.doi.org/10.1182/blood.v122.21.3096.3096.

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Abstract Osteocytes are critical in the maintenance of bone integrity regulating bone remodeling through the cell death and autophagy, a cellular process stress-induced to prolong cell survival but when induced excessively can cause cell death. Recently we have demonstrated that an increased osteocyte death is involved in multiple myeloma (MM)-induced osteolysis. However the mechanisms involved in this process as well as the effect of the proteasome inhibitors able to stimulate bone formation are not known and have been investigated in this study. Firstly the effect of the proteasome inhibitors BOR and MG262 on osteocyte viability was evaluated in vitro in murine osteocytic cell line MLO-Y4 and in the human pre-osteocytic one HOB-01. Both cell lines were co-coltured for 48 hours in the presence or absence of the human myeloma cell lines (HMCLs) RPMI8226 and JJN3, placed in a traswell insert. The treatment for 12-24 hours with (BOR) (2nM) and MG262 (10nM) significantly blunted MLO-Y4 and HOB-01 cell death. In addition, dexamethasone (DEX)-induced MLO-Y4 apoptosis, obtained at high doses (10-5-10-6 M), was reduced by the treatment with proteasome inhibitors. Interestingly, we found that PTH short-term treatment potentiated the in vitro effects of proteasome inhibitors on DEX-induced osteocyte death. To evaluate the presence of autophagy in osteocytes, we checked the expression of the autophagic marker LC3 both by confocal microscopy and western blot analysis in the co-colture system with MLO-Y4 and RPMI-8226. Prevalence of autophagic cell death and in a lesser extent apoptosis was observed in this system. BOR increased the basal level of LC3 indicating a pro-survival and protective function of autophagy against the BOR-induce stress. On the contrary, when cells undergo to a stronger stress such as in the presence of HMCLs or by treatment with high dose of DEX we found that both proteasome inhibitors BOR and MG262 blocked autophagic cell death in osteocytes. To translate our in vitro evidence in a clinical perspective, thereafter we performed a histological evaluation on bone biopsies of a cohort of 37 newly diagnosis MM patients 31 of them with symptomatic MM and 6 with smoldering MM (SMM). The 55% of patients with MM have evidence of osteolytic lesions at the X-rays survey. Bone biopsies were obtained at the diagnosis and after an average time of 12 months of treatment or observation. Osteocyte viability was evaluated in a total of 500 lacunae per histological sections. A significant increase of the number of viable osteocytes was demonstrated in MM patients treated with BOR-based regimen as compared to those treated without BOR (% median increase: +6% vs. +1.30%; p=0.017). Patients treated with BOR alone showed the highest increase of osteocyte viability, as compared to those either treated without BOR (+11.6% vs. +1.3%, p=0.0019) or treated with BOR plus DEX (+11.6% vs. +4.4%, p=0.01). A reduction of both osteocyte apoptosis and autophagy was demonstrated by TUNEL assays and confocal microscopy. On the other hand, any significant difference was not observed in patients treated with Thalidomide (THAL) or Immunomodulatory drugs (IMiDs) than in those untreated with these drugs (p= 0.7). A multiple regression non-parametric analysis showed that BOR had a significant positive impact on osteocyte viability (p=0.042) whereas THAL/IMiDs as well as Zoledronic acid (ZOL) treatments have not (p=0.2). BOR also counterbalanced the negative effect of DEX treatment (p=0.035). Our data suggest that proteasome inhibitors blunted osteocyte cell death induced by MM cells and DEX through the modulation of the autophagy supporting their use to improve bone integrity in MM patients. Disclosures: Giuliani: Celgene Italy: Research Funding.
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2

Yao, Wei, Weiwei Dai, Jean X. Jiang, and Nancy E. Lane. "Glucocorticoids and osteocyte autophagy." Bone 54, no. 2 (June 2013): 279–84. http://dx.doi.org/10.1016/j.bone.2013.01.034.

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3

Mannino, Federica, and Post Doc. "ODP599 Modulation of Wnt/b-catenin and Autophagy in an in vitro Model of Glucocorticoid-induced Osteoporosis." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A186. http://dx.doi.org/10.1210/jendso/bvac150.384.

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Abstract Background During bone aging and osteoporosis, formation and resorption are not tightly coupled; the main cells involved in bone remodeling are osteoblasts and osteoclast but also osteocytes play a pivotal role in this process. Osteocytes are the most abundant cell type in bone and are mainly responsible for sensing mechanical signals on the bones, controlling osteoblast and osteoclast activities through cell-to-cell communication and via secreted factors. In particular, osteocytes regulate bone resorption, thanks to the production of RANKL, reducing osteoclast activity. Ellagic acid, a natural polyphenolic compound derived from pomegranate, could modulate cell function via specific estrogen receptor b; activation of ERb plays a critical role in bone remodeling suppressing osteoclast differentiation and function, promoting osteoblast proliferation through the Wnt/b-catenin pathway, increasing osteoprotegerin levels. In addition, stimulation of ERb plays an anti-inflammatory effect, increasing the expression of IL-10 and reducing the expression of proinflammatory cytokines, such as IL-1β and TNF-α, and can regulate the expression of autophagy inhibiting the PI3K/Akt/mTOR pathway. The hypothesis here tested is that ellagic acid, through ERb modulation, could induce Wnt/b-catenin and autophagy pathways in osteocytes challenged with dexamethasone to mimic glucocorticoid-induced osteoporosis. Materials and methods The osteocyte cells MLO-A5 were differentiated into osteocytes under appropriate culturing conditions. Cells were treated with Ellagic acid (1µM) following dexamethasone (1µM) challenge for 24h to induce an in vitro model of osteoporosis. At the end of the treatment period, cell viability was evaluated by MTT assay; qPCR was performed to evaluate the expression of the genes involved in osteocyte function (SOST, RANKL, Destrin and Dmp1) and Wnt/B-catenin signaling pathway (Wnt5a, Wnt10b, B-Catenin and DKK1); Western Blot was performed to evaluate the expression of proteins involved in apoptosis (cleaved-Caspase3) and autophagy (Beclin-1, LC3 and p62). In addition, the expression of Sclerostin and nuclear translocation of B-Catenin was evaluated by immunofluorescence. Results Ellagic acid reduced the gene expression of SOST, RANKL, Dmp1 and increased the expression of Destrin compared to untreated cells stimulated with dexamethasone; caused a significant increase of Wnt5a, Wnt10b and B-Catenin expression and reduced significantly the expression of DKK1. CGS21680 inhibited dexamethasone-induced apoptosis, reducing the expression of Caspase3, and increased the expression of Beclin-1 and LC3 compared to cell treated with dexamethasone. Finally, treatment with Ellagic acid stimulated the nuclear translocation of B-Catenin, promoting the transcription of genes involved in osteogenesis. Conclusion These preliminary data suggest that stimulation of ERb through Ellagic acid could modulate bone remodelling through activation of Wnt/b-catenin pathway and autophagy, providing evidence on the possible use of this natural compound as a new therapeutic approach for osteoporosis. Presentation: No date and time listed
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4

Chou, Hsin-Chiao, Sung-Yen Lin, Liang-Yin Chou, Mei-Ling Ho, Shu-Chun Chuang, Tsung-Lin Cheng, Lin Kang, et al. "Ablation of Discoidin Domain Receptor 1 Provokes an Osteopenic Phenotype by Regulating Osteoblast/Osteocyte Autophagy and Apoptosis." Biomedicines 10, no. 9 (September 2, 2022): 2173. http://dx.doi.org/10.3390/biomedicines10092173.

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Discoidin domain receptor 1 (DDR1) is a collagen receptor that belongs to the receptor tyrosine kinase family. We have previously shown that DDR1 plays a crucial role during bone development, resulting in dwarfism and a short stature in osteoblast-specific knockout mice (OKO mice). However, the detailed pathophysiological effects of DDR1 on bone development throughout adulthood have remained unclear. This study aims to identify how DDR1 regulates osteoblast and osteocyte functions in vivo and in vitro during bone development in adulthood. The metabolic changes in bone tissues were analyzed using Micro-CT and immunohistochemistry staining (IHC) in vivo; the role of DDR1 in regulating osteoblasts was examined in MC3T3-E1 cells in vitro. The Micro-CT analysis results demonstrated that OKO mice showed a 10% reduction in bone-related parameters from 10 to 14 weeks old and a significant reduction in cortical thickness and diameter compared with flox/flox control mice (FF) mice. These results indicated that DDR1 knockout in OKO mice exhibiting significant bone loss provokes an osteopenic phenotype. The IHC staining revealed a significant decrease in osteogenesis-related genes, including RUNX2, osteocalcin, and osterix. We noted that DDR1 knockout significantly induced osteoblast/osteocyte apoptosis and markedly decreased autophagy activity in vivo. Additionally, the results of the gain- and loss-of-function of the DDR1 assay in MC3T3-E1 cells indicated that DDR1 can regulate the osteoblast differentiation through activating autophagy by regulating the phosphorylation of the mechanistic target of rapamycin (p-mTOR), light chain 3 (LC3), and beclin-1. In conclusion, our study highlights that the ablation of DDR1 results in cancellous bone loss by regulating osteoblast/osteocyte autophagy. These results suggest that DDR1 can act as a potential therapeutic target for managing cancellous bone loss.
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5

Luo, D., H. Ren, T. Li, K. Lian, and D. Lin. "Rapamycin reduces severity of senile osteoporosis by activating osteocyte autophagy." Osteoporosis International 27, no. 3 (September 22, 2015): 1093–101. http://dx.doi.org/10.1007/s00198-015-3325-5.

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6

Florencio-Silva, Rinaldo, Gisela R. S. Sasso, Estela Sasso-Cerri, Manuel J. Simões, and Paulo S. Cerri. "Effects of estrogen status in osteocyte autophagy and its relation to osteocyte viability in alveolar process of ovariectomized rats." Biomedicine & Pharmacotherapy 98 (February 2018): 406–15. http://dx.doi.org/10.1016/j.biopha.2017.12.089.

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7

Zhu, Liang, Jifei Chen, Jing Zhang, Changan Guo, Wenshuai Fan, Yi-ming Wang, and Zuoqin Yan. "Parathyroid Hormone (PTH) Induces Autophagy to Protect Osteocyte Cell Survival from Dexamethasone Damage." Medical Science Monitor 23 (August 21, 2017): 4034–40. http://dx.doi.org/10.12659/msm.903432.

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8

Chen, Ke, Yue-Hua Yang, Sheng-Dan Jiang, and Lei-Sheng Jiang. "Decreased activity of osteocyte autophagy with aging may contribute to the bone loss in senile population." Histochemistry and Cell Biology 142, no. 3 (February 20, 2014): 285–95. http://dx.doi.org/10.1007/s00418-014-1194-1.

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9

Wang, Peige, Jie Ding, Guangyue Yang, Wen Sun, Hailing Guo, and Yongfang Zhao. "Study on the Mechanism of Qigu Capsule in Upregulating NF-κB/HIF-1α Pathway to Improve the Quality of Bone Callus in Mice at Different Stages of Osteoporotic Fracture Healing." Evidence-Based Complementary and Alternative Medicine 2021 (September 13, 2021): 1–10. http://dx.doi.org/10.1155/2021/9943692.

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Objective. The present study intends to investigate the effects and underlying molecular mechanism of Qigu Capsule (QG) on fracture healing in mice with osteoporosis. Methods. Ten-week-old female C57BL/6 mice were ovariectomized and three weeks later were evaluated for successful modeling. Then, all mice were prepared into models of transverse fracture in the right middle femoral shaft. Mice were treated daily using a gavage with normal saline (the NS group), Qigu Capsule (the QG group), or alendronate (the ALN group) postoperatively. Fracture callus tissues were collected and analyzed by X-ray, micro-CT, western blot (WB), and transmission electron microscope (TEM) on postoperation Day 14 (POD14), POD28, and POD42. Results. (1) X-ray results showed that on POD14, the QG group had the fracture healing score significantly higher than the NS and ALN groups, and on POD28, it had the fracture healing score higher than the NS group, suggesting that QG could promote fracture healing. (2) Micro-CT results showed that on POD14, the QG group had tissue bone density (TMD) significantly higher than the NS and ALN groups, and on POD28 and POD42, it had bone volume fraction, trabecular number, and TMD significantly higher than the NS group. (3) WB results showed that, compared with the NS group, the QG group had significantly increased expression of nuclear factor kappa-B (NF-κB), hypoxia-inducible factor-1α (HIF-1α), bone alkaline phosphatase (BALP), runt-related transcription factor 2 (Runx2), bone Gla protein (BGP) and collagen Iα1 (COLIα1) on POD14, significantly increased expression of NF-κB, HIF-1α, BALP and COLIα1 on POD28, and significantly increased expression of NF-κB, HIF-1α, and Runx2 on POD42. (4) TEM scanning results showed that, compared with the NS and ALN groups, the QG group had significantly increased numbers of autophagic vacuoles (AVs) in osteocytes on POD14, POD28, and POD42. Conclusion. QG could accelerate osteoporotic fracture healing by promoting bone formation and osteocyte autophagy, possibly through upregulating the NF-κB/HIF-1α signaling pathway.
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Yang, Yuehua, Xinfeng Zheng, Bo Li, Shengdan Jiang, and Leisheng Jiang. "Increased activity of osteocyte autophagy in ovariectomized rats and its correlation with oxidative stress status and bone loss." Biochemical and Biophysical Research Communications 451, no. 1 (August 2014): 86–92. http://dx.doi.org/10.1016/j.bbrc.2014.07.069.

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11

Fu, Jiayao, Lingyu Hao, Yawen Tian, Yang Liu, Yijing Gu, and Junhua Wu. "miR-199a-3p is involved in estrogen-mediated autophagy through the IGF-1/mTOR pathway in osteocyte-like MLO-Y4 cells." Journal of Cellular Physiology 233, no. 3 (August 25, 2017): 2292–303. http://dx.doi.org/10.1002/jcp.26101.

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12

Toscani, Denise, Carla Palumbo, Benedetta Dalla Palma, Marzia Ferretti, Marina Bolzoni, Valentina Marchica, Paola Sena, et al. "The Proteasome Inhibitor Bortezomib Maintains Osteocyte Viability in Multiple Myeloma Patients by Reducing Both Apoptosis and Autophagy: A New Function for Proteasome Inhibitors." Journal of Bone and Mineral Research 31, no. 4 (December 14, 2015): 815–27. http://dx.doi.org/10.1002/jbmr.2741.

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Inaba, Nao, Shinichiro Kuroshima, Yusuke Uto, Muneteru Sasaki, and Takashi Sawase. "Cyclic mechanical stretch contributes to network development of osteocyte-like cells with morphological change and autophagy promotion but without preferential cell alignment in rat." Biochemistry and Biophysics Reports 11 (September 2017): 191–97. http://dx.doi.org/10.1016/j.bbrep.2017.04.018.

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14

Schteingart, D. E. "Glucocorticoid-Induced Autophagy in Osteocytes." Yearbook of Endocrinology 2011 (January 2011): 262–63. http://dx.doi.org/10.1016/j.yend.2011.05.007.

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15

Xia, Xuechun, Rekha Kar, Jelica Gluhak-Heinrich, Wei Yao, Nancy E. Lane, Lynda F. Bonewald, Sondip K. Biswas, Woo-Kuen Lo, and Jean X. Jiang. "Glucocorticoid-induced autophagy in osteocytes." Journal of Bone and Mineral Research 25, no. 11 (June 18, 2010): 2479–88. http://dx.doi.org/10.1002/jbmr.160.

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16

McCarty, Mark F., Lidianys Lewis Lujan, and Simon Iloki Assanga. "Targeting Sirt1, AMPK, Nrf2, CK2, and Soluble Guanylate Cyclase with Nutraceuticals: A Practical Strategy for Preserving Bone Mass." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4776. http://dx.doi.org/10.3390/ijms23094776.

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There is a vast pre-clinical literature suggesting that certain nutraceuticals have the potential to aid the preservation of bone mass in the context of estrogen withdrawal, glucocorticoid treatment, chronic inflammation, or aging. In an effort to bring some logical clarity to these findings, the signaling pathways regulating osteoblast, osteocyte, and osteoclast induction, activity, and survival are briefly reviewed in the present study. The focus is placed on the following factors: the mechanisms that induce and activate the RUNX2 transcription factor, a key driver of osteoblast differentiation and function; the promotion of autophagy and prevention of apoptosis in osteoblasts/osteoclasts; and the induction and activation of NFATc1, which promotes the expression of many proteins required for osteoclast-mediated osteolysis. This analysis suggests that the activation of sirtuin 1 (Sirt1), AMP-activated protein kinase (AMPK), the Nrf2 transcription factor, and soluble guanylate cyclase (sGC) can be expected to aid the maintenance of bone mass, whereas the inhibition of the serine kinase CK2 should also be protective in this regard. Fortuitously, nutraceuticals are available to address each of these targets. Sirt1 activation can be promoted with ferulic acid, N1-methylnicotinamide, melatonin, nicotinamide riboside, glucosamine, and thymoquinone. Berberine, such as the drug metformin, is a clinically useful activator of AMPK. Many agents, including lipoic acid, melatonin, thymoquinone, astaxanthin, and crucifera-derived sulforaphane, can promote Nrf2 activity. Pharmacological doses of biotin can directly stimulate sGC. Additionally, certain flavonols, notably quercetin, can inhibit CK2 in high nanomolar concentrations that may be clinically relevant. Many, though not all, of these agents have shown favorable effects on bone density and structure in rodent models of bone loss. Complex nutraceutical regimens providing a selection of these nutraceuticals in clinically meaningful doses may have an important potential for preserving bone health. Concurrent supplementation with taurine, N-acetylcysteine, vitamins D and K2, and minerals, including magnesium, zinc, and manganese, plus a diet naturally high in potassium, may also be helpful in this regard.
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McCarty, Mark F., Lidianys Lewis Lujan, and Simon Iloki Assanga. "Targeting Sirt1, AMPK, Nrf2, CK2, and Soluble Guanylate Cyclase with Nutraceuticals: A Practical Strategy for Preserving Bone Mass." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4776. http://dx.doi.org/10.3390/ijms23094776.

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There is a vast pre-clinical literature suggesting that certain nutraceuticals have the potential to aid the preservation of bone mass in the context of estrogen withdrawal, glucocorticoid treatment, chronic inflammation, or aging. In an effort to bring some logical clarity to these findings, the signaling pathways regulating osteoblast, osteocyte, and osteoclast induction, activity, and survival are briefly reviewed in the present study. The focus is placed on the following factors: the mechanisms that induce and activate the RUNX2 transcription factor, a key driver of osteoblast differentiation and function; the promotion of autophagy and prevention of apoptosis in osteoblasts/osteoclasts; and the induction and activation of NFATc1, which promotes the expression of many proteins required for osteoclast-mediated osteolysis. This analysis suggests that the activation of sirtuin 1 (Sirt1), AMP-activated protein kinase (AMPK), the Nrf2 transcription factor, and soluble guanylate cyclase (sGC) can be expected to aid the maintenance of bone mass, whereas the inhibition of the serine kinase CK2 should also be protective in this regard. Fortuitously, nutraceuticals are available to address each of these targets. Sirt1 activation can be promoted with ferulic acid, N1-methylnicotinamide, melatonin, nicotinamide riboside, glucosamine, and thymoquinone. Berberine, such as the drug metformin, is a clinically useful activator of AMPK. Many agents, including lipoic acid, melatonin, thymoquinone, astaxanthin, and crucifera-derived sulforaphane, can promote Nrf2 activity. Pharmacological doses of biotin can directly stimulate sGC. Additionally, certain flavonols, notably quercetin, can inhibit CK2 in high nanomolar concentrations that may be clinically relevant. Many, though not all, of these agents have shown favorable effects on bone density and structure in rodent models of bone loss. Complex nutraceutical regimens providing a selection of these nutraceuticals in clinically meaningful doses may have an important potential for preserving bone health. Concurrent supplementation with taurine, N-acetylcysteine, vitamins D and K2, and minerals, including magnesium, zinc, and manganese, plus a diet naturally high in potassium, may also be helpful in this regard.
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18

Onal, Melda, Marilina Piemontese, Jinhu Xiong, Yiying Wang, Li Han, Shiqiao Ye, Masaaki Komatsu, et al. "Suppression of Autophagy in Osteocytes Mimics Skeletal Aging." Journal of Biological Chemistry 288, no. 24 (May 3, 2013): 17432–40. http://dx.doi.org/10.1074/jbc.m112.444190.

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Lin, Yanjun, Min Zhang, Lin Zhou, Xuxi Chen, Jiang Chen, and Dong Wu. "Promoting effect of rapamycin on osteogenic differentiation of maxillary sinus membrane stem cells." PeerJ 9 (June 1, 2021): e11513. http://dx.doi.org/10.7717/peerj.11513.

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Background Stem cells located in the maxillary sinus membrane can differentiate into osteocytes. Our study aimed to evaluate the effect of rapamycin (RAPA) on the osteogenic differentiation of maxillary sinus membrane stem cells (MSMSCs). Methods Colony-forming unit assay, immunophenotype identification assay, and multi-differentiation assay confirmed characteristics of MSMSCs obtained from SD rats. Transmission electron microscopy (TEM) and flow cytometry (FCM) identified the initial autophagic level of MSMSCs induced by RAPA. Real-time quantitative PCR (qPCR) evaluated subsequent autophagic levels and osteogenic differentiation. Alkaline phosphatase (ALP) activity assay and alizarin red staining (ARS) evaluated subsequent osteogenic differentiation. We performed a histological examination to clarify in vivo osteogenesis with ectopic bone mass from BALB/c nude mice. Results MSMSCs possessed an active proliferation and multi-differentiation capacity, showing a phenotype of mesenchymal stem cells. The autophagic level increased with increasing RAPA (0, 10, 100, 1,000 nM) and decreased over time. ALP activity and calcium nodules forming in four RAPA-treated groups on three-time points (7, 14, 21 d) showed significant differences. Col1a1, Runx2, and Spp1 expressed most in 100 nM RAPA group on 7 and 14 d. Osteogenesis-related genes except for Ibsp expression between four groups tended to be consistent on 21 d. 100 nM and 10 nM RAPA-treated groups showed more bone formation in vivo. Conclusion RAPA can promote osteogenic differentiation of MSMSCs, indicating a possible relationship between osteogenic differentiation and autophagy.
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Li, Wenlei, Jing Zhao, Wen Sun, Hua Wang, Yongchu Pan, Lin Wang, and Wei-Bing Zhang. "Osteocytes promote osteoclastogenesis via autophagy-mediated RANKL secretion under mechanical compressive force." Archives of Biochemistry and Biophysics 694 (November 2020): 108594. http://dx.doi.org/10.1016/j.abb.2020.108594.

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21

Trojani, M. C., C. Arnaud, B. Isabelle, R. Bernard De Dompsure, J. F. Gonzalez, C. Trojani, S. Santucci, G. F. Carle, V. Pierrefite-Carle, and V. Breuil. "AB0042 AUTOPHAGY IS DECREASED IN BONE FROM OSTEOPOROTIC PATIENTS." Annals of the Rheumatic Diseases 82, Suppl 1 (May 30, 2023): 1200.2–1200. http://dx.doi.org/10.1136/annrheumdis-2023-eular.286.

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BackgroundOsteoporosis (OP) is a diffuse skeletal pathology characterized by major bone fragility that affects one out of 3 women after menopause. In addition to estrogen loss, an increase in oxidative stress is now recognized as a central mechanism in this pathology. Autophagy is an intracellular process allowing the removal and recycling of damaged proteins and organelles. Thanks to the elimination of damaged mitochondria, which are the main sources of reactive oxygen species, autophagy plays a major role in reducing oxidative stress. An age-related autophagy decline, associated with various experimental arguments in animal models, suggests autophagy implication in OP. However, a definitive proof in humans remains to be obtained.ObjectivesOur objective was to show for the first time that there is a defect in autophagy in the bone of osteoporotic patients.MethodsWe have analyzed autophagy by Western Blot in bone samples from 14 postmenopausal women with OP fracture compared to 30 controls undergoing total hip replacement for osteoarthritis.ResultsOur results indicate that the expression level of the autophagosome marker LC3-II is significantly decreased in OP patients compared to the age-matched controls. We also observed a tendency for the accumulation of the SQSTM1/p62 protein, which is an autophagy substrate, thus supporting the previous results. Finally, we also demonstrate a significant decrease in the hormonally up-regulated neu-associated kinase (HUNK) in bone samples from OP patients compared to the control group. This kinase, whose expression is upregulated by female hormones, promotes autophagy by inhibiting the autophagy inhibitor Rubicon through phosphorylation.ConclusionTaken together, these data demonstrate for the first time that OP patients have a deficit in osteocytes autophagy and suggest the involvement of the HUNK kinase in OP pathogenesis. This study should contribute to better understand the role of autophagy in OP pathophysiology and could lead to the design of new therapeutics targeting autophagy for the management of pathological aging.AcknowledgementsWe thank the French Society of Rheumatology for their funding.Disclosure of InterestsNone Declared.
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Gao, Junjie, Tak Sum Cheng, An Qin, Nathan J. Pavlos, Tao Wang, Kai Song, Yan Wang, et al. "Glucocorticoid impairs cell-cell communication by autophagy-mediated degradation of connexin 43 in osteocytes." Oncotarget 7, no. 19 (April 27, 2016): 26966–78. http://dx.doi.org/10.18632/oncotarget.9034.

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23

Kar, Rekha, Manuel A. Riquelme, Rui Hua, and Jean X. Jiang. "Glucocorticoid-Induced Autophagy Protects Osteocytes Against Oxidative Stress Through Activation of MAPK/ERK Signaling." JBMR Plus 3, no. 4 (December 11, 2018): e10077. http://dx.doi.org/10.1002/jbm4.10077.

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Gao, Junjie, Tak Sum Cheng, An Qin, Nathan J. Pavlos, Tao Wang, Kai Song, Yan Wang, et al. "Correction: Glucocorticoid impairs cell-cell communication by autophagy-mediated degradation of connexin 43 in osteocytes." Oncotarget 10, no. 40 (June 18, 2019): 4079. http://dx.doi.org/10.18632/oncotarget.27035.

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Zhang, Bingbing, Rutao Hou, Zhen Zou, Tiantian Luo, Yang Zhang, Liyun Wang, and Bin Wang. "Mechanically induced autophagy is associated with ATP metabolism and cellular viability in osteocytes in vitro." Redox Biology 14 (April 2018): 492–98. http://dx.doi.org/10.1016/j.redox.2017.10.021.

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Gao, Li, Gen Liu, Xiangnan Wu, Chuanzi Liu, Yiqiao Wang, Meirui Ma, Yuanyuan Ma, and Zhichao Hao. "Osteocytes autophagy mediated by mTORC2 activation controls osteoblasts differentiation and osteoclasts activities under mechanical loading." Archives of Biochemistry and Biophysics 742 (July 2023): 109634. http://dx.doi.org/10.1016/j.abb.2023.109634.

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Piemontese, Marilina, Melda Onal, Jinhu Xiong, Yiying Wang, Maria Almeida, Jeff D. Thostenson, Robert S. Weinstein, Stavros C. Manolagas, and Charles A. O'Brien. "Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone." Bone 75 (June 2015): 18–26. http://dx.doi.org/10.1016/j.bone.2015.02.005.

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Plekhova, Natalya G., Polina A. Krivolutskaya, and Ivan N. Chernenko. "Cellular mechanisms of age-dependent bone remodeling." Kazan medical journal 105, no. 4 (July 25, 2024): 648–60. http://dx.doi.org/10.17816/kmj632264.

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The structural integrity of the skeleton is ensured by the constant remodeling of bone tissue, which is based on the functioning and interaction of osteolytic cells (osteoclasts) and bone tissue forming cells (osteoblasts/osteocytes). Despite the general understanding that the degree of mineralization of the bone matrix determines the fragility of the skeleton, there is currently insufficient information about its age-related changes associated with the functioning of these cells. The purpose of the review is to evaluate existing data on age-related bone changes associated with the functional state of mesenchymal stem cells, osteoblasts/osteocytes and osteoclasts. Inclusion criteria: randomized or non-randomized controlled studies examining age-related bone change. A search for studies in the field of bone tissue condition was carried out in electronic scientific databases Google Scholar, Medline, PubMed, Scopus, Web of Science and Cochrane Library by keywords and their combinations using the AMSTAR 2 program. The selection of publications (59 out of 680 included) was carried out randomly, after which three authors independently assessed their methodological quality. The main pathogenetic mechanism involved in bone loss with age is a decrease in the formation of osteoblasts with impairment of their ability to osteogenic differentiation. Osteocytes in old age are subject to excessive and prolonged stress, which causes unbalanced autophagy and apoptosis, which leads to changes in their ability to deposit and mineralize extracellular organic matrix. With age, accelerated osteoclastogenesis occurs, mediated by osteoblasts, which leads to increased expression of certain receptors at the level of bone stromal cells and osteoblasts. The presented literature data demonstrate convincing evidence that an increase in bone resorption due to complex metabolic processes with age occurs against the background of an increase in the number and activity of osteoclasts, apoptosis of osteoblasts with a decrease in their metabolic activity, as well as a redistribution of osteogenic differentiation of mesenchymal stem cells towards adipocytes. The results presented in the review can be used as a basis for developing diagnostic criteria for identifying senile osteoporosis and the risk of fractures.
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Wang, Xin-Yuan, Lin-Jing Gong, Jun-Ming Huang, Chang Jiang, and Zuo-Qin Yan. "Pinocembrin alleviates glucocorticoid-induced apoptosis by activating autophagy via suppressing the PI3K/Akt/mTOR pathway in osteocytes." European Journal of Pharmacology 880 (August 2020): 173212. http://dx.doi.org/10.1016/j.ejphar.2020.173212.

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Wang, Zhenheng, Zhantao Deng, Jingjing Gan, Gang Zhou, Tongguo Shi, Zhenzhen Wang, Zhen Huang, et al. "TiAl 6 V 4 particles promote osteoclast formation via autophagy-mediated downregulation of interferon-beta in osteocytes." Acta Biomaterialia 48 (January 2017): 489–98. http://dx.doi.org/10.1016/j.actbio.2016.11.020.

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Zeng, Zhipeng, Xuchang Zhou, Yan Wang, Hong Cao, Jianmin Guo, Ping Wang, Yajing Yang, and Yan Wang. "Mitophagy—A New Target of Bone Disease." Biomolecules 12, no. 10 (October 4, 2022): 1420. http://dx.doi.org/10.3390/biom12101420.

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Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.
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Herrmann, Markus. "Marrow Fat-Secreted Factors as Biomarkers for Osteoporosis." Current Osteoporosis Reports 17, no. 6 (November 16, 2019): 429–37. http://dx.doi.org/10.1007/s11914-019-00550-w.

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Abstract Purpose of Review The age-related accumulation of bone marrow adipose tissue (BMAT) negatively impacts bone metabolism and hematopoiesis. This review provides an overview about BMAT-secreted factors as biomarkers for BMAT accumulation and osteoporosis risk. Recent Findings The adipokines leptin and adiponectin are regulators of BMAT. It remains to be clarified if locally produced adipokines substantially contribute to their peripheral serum levels and if they influence bone metabolism beyond that of extraosseous adipokine production. Existing data also suggests that BMAT disturbs bone metabolism primarily through palmitate-mediated toxic effects on osteoblasts and osteocytes, including dysregulated autophagy and apoptosis. Summary BMAT-secreted factors are important modulators of bone metabolism. However, the majority of our understanding about MAT-secreted factors and their paracrine and endocrine effects is derived from in vitro studies and animal experiments. Therefore, more research is needed before BMAT-secreted biomarkers can be applied in medical practice.
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Zhang, Yun, Ming Yan, Shumeng Kuang, Yiqiang Lou, Shouqian Wu, Yurong Li, Zihan Wang, and Hongjiao Mao. "Bisphenol A induces apoptosis and autophagy in murine osteocytes MLO-Y4: Involvement of ROS-mediated mTOR/ULK1 pathway." Ecotoxicology and Environmental Safety 230 (January 2022): 113119. http://dx.doi.org/10.1016/j.ecoenv.2021.113119.

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Wu, Xinhui, Xiaoxin Fang, Feng Lu, Qiong Chen, Junjian Liu, and Longpo Zheng. "An update on the role of ferroptosis in the pathogenesis of osteoporosis." EFORT Open Reviews 9, no. 8 (August 1, 2024): 712–22. http://dx.doi.org/10.1530/eor-23-0148.

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Ferroptosis is a novel form of programmed cell death, distinguished from apoptosis, autophagy, and programmed necrosis and has received much attention since it was defined in 2012. Ferroptotic cells physiologically exhibit iron metabolism dysregulation, oxidative stress, and lipid peroxidation. Morphologically, they show plasma membrane disruption, cytoplasmic swelling, and mitochondrial condensation. Osteoporosis is taken more and more seriously as the proportion of the aging population continues to increase globally. Interestingly, ferroptosis has been demonstrated to be involved in the development and progression of osteoporosis in many extant studies. The review summarizes iron metabolism, lipid peroxidation, and the different regulatory signals in ferroptosis. Changes in signaling mechanisms within osteoblasts, osteoclasts, and osteocytes after ferroptosis occur are explained here. Studies showed ferroptosis play an important role in different osteoporosis models (diabetes osteoporosis, postmenopausal osteoporosis, glucocorticoid-induced osteoporosis). Inhibitors and EC (Exos) targeting ferroptosis could ameliorate bone loss in osteoporotic mice by protecting cells against lipid peroxidation. Shortly, we hope that more effective and appropriate clinical therapy means will be utilized in the treatment of osteoporosis.
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Wang, Yonghui, Chao Xia, Yang Chen, Tianyuan Jiang, Yan Hu, and Yanhong Gao. "Resveratrol Synergistically Promotes BMP9-Induced Osteogenic Differentiation of Mesenchymal Stem Cells." Stem Cells International 2022 (July 25, 2022): 1–13. http://dx.doi.org/10.1155/2022/8124085.

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Background. Mesenchymal stem cells (MSCs) differentiate into osteocytes, adipocytes, and chondrocytes. Resveratrol and bone morphogenetic protein 9 (BMP9) are known osteogenic induction factors of MSCs, but the effect of both resveratrol and BMP9 on osteogenesis is unknown. Herein, we explored whether resveratrol cooperates with BMP9 to improve osteogenic induction. Methods. The osteogenic induction of resveratrol and BMP9 on C3H10T1/2 cells was evaluated by detecting the staining and activity of the early osteogenic marker alkaline phosphatase (ALP). In addition, the late osteogenic effect was measured by the mRNA and protein levels of osteogenic markers, such as osteopontin (OPN) and osteocalcin (OCN). To assess the bone formation function of resveratrol plus BMP9 in vivo, we transplanted BMP9-infected C3H10T1/2 cells into nude mice followed by intragastric injection of resveratrol. Western blot (WB) analysis was utilized to elucidate the mechanism of resveratrol plus BMP9. Results. Resveratrol not only enhanced osteogenic induction alone but also improved BMP9-induced ALP at 3, 5, and 7 d postinduction. Both the early osteogenic markers (ALP, Runx2, and SP7) and the late osteogenic markers (OPN and OCN) were significantly increased when resveratrol was combined with BMP9. The fetal limb explant culture further verified these results. The in vivo bone formation experiment, which involved transplanting BMP9-overexpressing C3H10T1/2 cells into nude mice, also confirmed that resveratrol synergistically enhanced the BMP9-induced bone formation function. Resveratrol phosphorylated adenosine monophosphate- (AMP-) activated protein kinase (AMPK) and stimulated autophagy, but these effects were abolished by inhibiting AMPK and Beclin1 using an inhibitor or siRNA. Conclusions. Resveratrol combined with BMP9 significantly improves the osteogenic induction of C3H10T1/2 cells by activating AMPK and autophagy.
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Hou, Yi-Chou, Cai-Mei Zheng, Hui-Wen Chiu, Wen-Chih Liu, Kuo-Cheng Lu, and Chien-Lin Lu. "Role of Calcimimetics in Treating Bone and Mineral Disorders Related to Chronic Kidney Disease." Pharmaceuticals 15, no. 8 (July 31, 2022): 952. http://dx.doi.org/10.3390/ph15080952.

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Renal osteodystrophy is common in patients with chronic kidney disease and end-stage renal disease and leads to the risks of fracture and extraosseous vascular calcification. Secondary hyperparathyroidism (SHPT) is characterized by a compensatory increase in parathyroid hormone (PTH) secretion in response to decreased renal phosphate excretion, resulting in potentiating bone resorption and decreased bone quantity and quality. Calcium-sensing receptors (CaSRs) are group C G-proteins and negatively regulate the parathyroid glands through (1) increasing CaSR insertion within the plasma membrane, (2) increasing 1,25-dihydroxy vitamin D3 within the kidney and parathyroid glands, (3) inhibiting fibroblast growth factor 23 (FGF23) in osteocytes, and (4) attenuating intestinal calcium absorption through Transient Receptor Potential Vanilloid subfamily member 6 (TRPV6). Calcimimetics (CaMs) decrease PTH concentrations without elevating the serum calcium levels or extraosseous calcification through direct interaction with cell membrane CaSRs. CaMs reduce osteoclast activity by reducing stress-induced oxidative autophagy and improving Wnt-10b release, which promotes the growth of osteoblasts and subsequent mineralization. CaMs also directly promote osteoblast proliferation and survival. Consequently, bone quality may improve due to decreased bone resorption and improved bone formation. CaMs modulate cardiovascular fibrosis, calcification, and renal fibrosis through different mechanisms. Therefore, CaMs assist in treating SHPT. This narrative review focuses on the role of CaMs in renal osteodystrophy, including their mechanisms and clinical efficacy.
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Xu, Huiyue, Meng Xia, Lian Sun, Hua Wang, and Wei-Bing Zhang. "Osteocytes Enhance Osteogenesis by Autophagy-Mediated FGF23 Secretion Under Mechanical Tension." Frontiers in Cell and Developmental Biology 9 (January 31, 2022). http://dx.doi.org/10.3389/fcell.2021.782736.

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Mechanical stimuli control cell behaviors that are crucial for bone tissue repair. Osteocytes sense extracellular mechanical stimuli then convert them into biochemical signals to harmonize bone remodeling. However, the mechanisms underlying this process remain unclear. Autophagy, which is an evolutionarily preserved process, that occurs at a basal level when stimulated by multiple environmental stresses. We postulated that mechanical stimulation upregulates osteocyte autophagy via AMPK-associated signaling, driving osteocyte-mediated osteogenesis. Using a murine model of orthodontic tooth movement, we show that osteocyte autophagy is triggered by mechanical tension, increasing the quantity of LC3B-positive osteocytes by 4-fold in the tension side. Both in vitro mechanical tension as well as the chemical autophagy agonist enhanced osteocyte Fibroblast growth factor 23 (FGF23) secretion, which is an osteogenenic related cytokine, by 2-and 3-fold, respectively. Conditioned media collected from tensioned osteocytes enhanced osteoblast viability. These results indicate that mechanical tension drives autophagy-mediated FGF23 secretion from osteocytes and promotes osteogenesis. Our findings highlight a potential strategy for accelerating osteogenesis in orthodontic clinical settings.
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Wei, Liwei, Shuang Chai, Chen Yue, Hong Zhang, Jitian Li, and Na Qin. "Resveratrol protects osteocytes against oxidative stress in ovariectomized rats through AMPK/JNK1-dependent pathway leading to promotion of autophagy and inhibition of apoptosis." Cell Death Discovery 9, no. 1 (January 21, 2023). http://dx.doi.org/10.1038/s41420-023-01331-2.

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AbstractA large number of studies in recent years indicate that osteocytes are the orchestrators of bone remodeling by regulating both osteoblast and osteoclast activities. Oxidative stress-induced osteocyte apoptosis plays critical roles in the pathological processes of postmenopausal osteoporosis. Resveratrol is a natural polyphenolic compound that ameliorates postmenopausal osteoporosis. However, whether resveratrol regulates osteocyte apoptosis via autophagy remains largely unknown. The effects of resveratrol on regulating osteocyte apoptosis and autophagy were analyzed both in vivo and in vitro. In vitro, cultured MLO-Y4 cells were exposed to H2O2 with or without resveratrol. In vivo, an ovariectomy-induced osteoporosis model was constructed in rats with or without daily intraperitoneal injection of 10 mg/kg body weight resveratrol. It was found that resveratrol attenuated H2O2-induced apoptosis through activating autophagy in cultured MLO-Y4 cells, which was mediated by the dissociation of Beclin-1/Bcl-2 complex in AMPK/JNK1-dependent pathway, ultimately regulating osteocytes function. Furthermore, it was shown that resveratrol treatment reduced osteocytes oxidative stress, inhibited osteocytes apoptosis and promoted autophagy in ovariectomized rats. Our study suggests that resveratrol protects against oxidative stress by restoring osteocytes autophagy and alleviating apoptosis via AMPK/JNK1 activation, therefore dissociating Bcl-2 from Beclin-1.
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Jia, Yewei, Rui Li, Yixuan Li, Katerina Kachler, Xianyi Meng, Andreas Gießl, Yi Qin, et al. "Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis." Bone Research 13, no. 1 (January 16, 2025). https://doi.org/10.1038/s41413-024-00384-y.

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Abstract Osteocytes are the main cells in mineralized bone tissue. Elevated osteocyte apoptosis has been observed in lytic bone lesions of patients with multiple myeloma. However, their precise contribution to bone metastasis remains unclear. Here, we investigated the pathogenic mechanisms driving melanoma-induced osteocyte death. Both in vivo models and in vitro assays were combined with untargeted RNA sequencing approaches to explore the pathways governing melanoma-induced osteocyte death. We could show that ferroptosis is the primary mechanism behind osteocyte death in the context of melanoma bone metastasis. HMOX1 was identified as a crucial regulatory factor in this process, directly involved in inducing ferroptosis and affecting osteocyte viability. We uncover a non-canonical pathway that involves excessive autophagy-mediated ferritin degradation, highlighting the complex relationship between autophagy and ferroptosis in melanoma-induced osteocyte death. In addition, HIF1α pathway was shown as an upstream regulator, providing a potential target for modulating HMOX1 expression and influencing autophagy-dependent ferroptosis. In conclusion, our study provides insight into the pathogenic mechanisms of osteocyte death induced by melanoma bone metastasis, with a specific focus on ferroptosis and its regulation. This would enhance our comprehension of melanoma-induced osteocyte death.
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Gunn, Nicholas J., Stephen P. Kidd, Lucian B. Solomon, Dongqing Yang, Eugene Roscioli, and Gerald J. Atkins. "Staphylococcus aureus persistence in osteocytes: weathering the storm of antibiotics and autophagy/xenophagy." Frontiers in Cellular and Infection Microbiology 14 (June 10, 2024). http://dx.doi.org/10.3389/fcimb.2024.1403289.

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Staphylococcus aureus is a major causative pathogen of osteomyelitis. Intracellular infections of resident bone cells including osteocytes can persist despite gold-standard clinical intervention. The mechanisms by which intracellular S. aureus evades antibiotic therapy are unknown. In this study, we utilised an in vitro S. aureus infection model of human osteocytes to investigate whether antibiotic-mediated dysregulation of autophagy contributes to this phenomenon. Infected or non-infected osteocyte-like cells were exposed to combinations of rifampicin, vancomycin, and modulators of autophagy. Intracellular bacterial growth characteristics were assessed using colony-forming unit (CFU) analysis, viable bacterial DNA abundance, and the rate of escape into antibiotic-free medium, together with measures of autophagic flux. Rifampicin, alone or in combination with vancomycin, caused a rapid decrease in the culturability of intracellular bacteria, concomitant with stable or increased absolute bacterial DNA levels. Both antibiotics significantly inhibited autophagic flux. However, modulation of autophagic flux did not affect viable bacterial DNA levels. In summary, autophagy was shown to be a factor in the host–pathogen relationship in this model, as its modulation affected the growth state of intracellular S. aureus with respect to both their culturability and propensity to escape the intracellular niche. While rifampicin and vancomycin treatments moderately suppressed autophagic flux acutely, this did not explain the paradoxical response of antibiotic treatment in decreasing S. aureus culturability whilst failing to clear bacterial DNA and hence intracellular bacterial load. Thus, off-target effects of rifampicin and vancomycin on autophagic flux in osteocyte-like cells could not explain the persistent S. aureus infection in these cells.
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Kurihara, Mai, Yoshiki Mukudai, Hitoshi Watanabe, Mariko Asakura, Yuzo Abe, Asami Houri, Junichiro Chikuda, Toshikazu Shimane, and Tatsuo Shirota. "Autophagy prevents osteocyte cell death under hypoxic conditions." Cells Tissues Organs, August 19, 2021. http://dx.doi.org/10.1159/000519086.

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42

Devi, Kadirvel, and Thukani Sathanantham Shanmugarajan. "Therapeutic Potential of Plant Metabolites in Bone Apoptosis: A Review." Current Drug Targets 24 (August 1, 2023). http://dx.doi.org/10.2174/1389450124666230801094525.

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Abstract: Osteoporosis is one of the skeletal diseases of major health concern worldwide. Homeostasis of bone occurs with the help of cells, namely, osteoblasts and osteoclasts. Physiological and pathological conditions involve the death of the cells by apoptosis, autophagy, and necrosis. Apoptosis is a key factor in the growth, development, and maintenance of the skeleton. Apoptosis is generated by two pathways: the intrinsic (mitochondria) and extrinsic (death receptor) pathways. Osteoblast apoptosis is governed by the factors like B cell lymphoma 2 (Bcl-2) family proteins, extracellular signal-regulated kinase (ERK), mitogen-activated protein kinases (MAPK), phosphoinositide-3-kinase/ protein kinase B (PI3-K/Akt), Janus kinase 2 (JAK2), bone morphogenetic protein (BMP), and bone matrix protein. Cytokines interact with osteocytes and induce apoptosis. A pro-inflammatory signal stimulates osteocyte apoptosis and increases osteocyte cytokines production. Current therapies have adverse effects which limit their applications. Various plant metabolites have shown beneficial effects on bone. The present review converses about normal bone metabolism and the mechanism of apoptosis leading to bone deterioration. Furthermore, it discusses the role of plant metabolites on bone apoptosis with related indications of efficacy in various experimental models.
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Zhang, Shenyao, Kefang Dong, Xiangjing Zeng, Fan Wang, and Min Lu. "Astragalus polysaccharide ameliorates steroid-induced osteonecrosis of the femoral head by regulating miR-200b-3p-mediated Wnt/β-catenin signaling pathway via inhibiting SP1 expression." BMC Musculoskeletal Disorders 24, no. 1 (May 10, 2023). http://dx.doi.org/10.1186/s12891-023-06447-1.

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Abstract Background Steroid-induced osteonecrosis of the femoral head (SONFH) is the necrosis of the femur bone caused by prolonged and massive use of corticosteroids. The present study probed into the significance of Astragalus polysaccharide (APS) in SONFH progression. Methods SONFH cell model was constructed using murine long bone osteocyte Y4 (MLO-Y4) cells and then treated with APS. mRNA microarray analysis selected differentially expressed genes between control group and SONFH group. RT-qPCR determined SP1 and miR-200b-3p expression. Levels of SP1, β-catenin, autophagy-related proteins (LC3II/LC3I, Beclin1, p62) and apoptosis-related proteins (Bax, C-caspase3, C-caspase9, Bcl-2) were tested by Western blot. ChIP and luciferase reporter assays confirmed relationship between SP1 and miR-200b-3p. Fluorescence intensity of LC3 in cells was detected by immunofluorescence. Flow cytometry assessed cell apoptosis. Osteonecrosis tissues from SONFH mice were examined by HE and TRAP staining. Results APS induced autophagy and suppressed apoptosis in SONFH cell model. APS inhibited SP1 expression and SP1 overexpression reversed effects of APS on SONFH cell model. Mechanistically, SP1 targeted miR-200b-3p to inhibit Wnt/β-catenin pathway. MiR-200b-3p depletion rescued the promoting effect of SP1 on SONFH cell model by activating Wnt/β-catenin pathway. HE staining showed that APS treatment reduced the empty lacunae and alleviated inflammation in trabecular bone of SONFH mice. TRAP staining revealed decreased osteoclasts number in SONFH mice after APS treatment. Conclusion APS regulated osteocyte autophagy and apoptosis via SP1/miR-200b-3p axis and activated Wnt/β-catenin signaling, thereby alleviating SONFH, shedding new insights for therapy of SONFH.
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Piemontese, Marilina, Melda Onal, Jinhu Xiong, Li Han, Jeff D. Thostenson, Maria Almeida, and Charles A. O’Brien. "Low bone mass and changes in the osteocyte network in mice lacking autophagy in the osteoblast lineage." Scientific Reports 6, no. 1 (April 2016). http://dx.doi.org/10.1038/srep24262.

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Che, Jingmin, Xin Chen, Weihao Ren, and Peng Shang. "PTH 1–34 reduced apoptosis of MLO-Y4 osteocyte-like cells by activating autophagy and inhibiting ER stress under RPM conditions." European Journal of Pharmacology, February 2024, 176364. http://dx.doi.org/10.1016/j.ejphar.2024.176364.

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46

Yin, Xing, Chenchen Zhou, Jingtao Li, Renkai Liu, Bing Shi, Quan Yuan, and Shujuan Zou. "Autophagy in bone homeostasis and the onset of osteoporosis." Bone Research 7, no. 1 (October 3, 2019). http://dx.doi.org/10.1038/s41413-019-0058-7.

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Abstract Autophagy is an evolutionarily conserved intracellular process, in which domestic cellular components are selectively digested for the recycling of nutrients and energy. This process is indispensable for cell homeostasis maintenance and stress responses. Both genetic and functional studies have demonstrated that multiple proteins involved in autophagic activities are critical to the survival, differentiation, and functioning of bone cells, including osteoblasts, osteocytes, and osteoclasts. Dysregulation at the level of autophagic activity consequently disturbs the balance between bone formation and bone resorption and mediates the onset and progression of multiple bone diseases, including osteoporosis. This review aims to introduce the topic of autophagy, summarize the understanding of its relevance in bone physiology, and discuss its role in the onset of osteoporosis and therapeutic potential.
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Zhu, Chenyu, Shiwei Shen, Shihua Zhang, Mei Huang, Lan Zhang, and Xi Chen. "Autophagy in Bone Remodeling: A Regulator of Oxidative Stress." Frontiers in Endocrinology 13 (June 30, 2022). http://dx.doi.org/10.3389/fendo.2022.898634.

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Bone homeostasis involves bone formation and bone resorption, which are processes that maintain skeletal health. Oxidative stress is an independent risk factor, causing the dysfunction of bone homeostasis including osteoblast-induced osteogenesis and osteoclast-induced osteoclastogenesis, thereby leading to bone-related diseases, especially osteoporosis. Autophagy is the main cellular stress response system for the limination of damaged organelles and proteins, and it plays a critical role in the differentiation, apoptosis, and survival of bone cells, including bone marrow stem cells (BMSCs), osteoblasts, osteoclasts, and osteocytes. High evels of reactive oxygen species (ROS) induced by oxidative stress induce autophagy to protect against cell damage or even apoptosis. Additionally, pathways such as ROS/FOXO3, ROS/AMPK, ROS/Akt/mTOR, and ROS/JNK/c-Jun are involved in the regulation of oxidative stress-induced autophagy in bone cells, including osteoblasts, osteocytes and osteoclasts. This review discusses how autophagy regulates bone formation and bone resorption following oxidative stress and summarizes the potential protective mechanisms exerted by autophagy, thereby providing new insights regarding bone remodeling and potential therapeutic targets for osteoporosis.
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Yin, Zhaoyang, Ge Gong, Xiang Wang, Wei Liu, Bin Wang, and Jian Yin. "The dual role of autophagy in periprosthetic osteolysis." Frontiers in Cell and Developmental Biology 11 (March 24, 2023). http://dx.doi.org/10.3389/fcell.2023.1123753.

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Periprosthetic osteolysis (PPO) induced by wear particles is an important cause of aseptic loosening after artificial joint replacement, among which the imbalance of osteogenesis and osteoclastic processes occupies a central position. The cells involved in PPO mainly include osteoclasts (macrophages), osteoblasts, osteocytes, and fibroblasts. RANKL/RANK/OGP axis is a typical way for osteolysis. Autophagy, a mode of regulatory cell death and maintenance of cellular homeostasis, has a dual role in PPO. Although autophagy is activated in various periprosthetic cells and regulates the release of inflammatory cytokines, osteoclast activation, and osteoblast differentiation, its beneficial or detrimental role remains controversy. In particular, differences in the temporal control and intensity of autophagy may have different effects. This article focuses on the role of autophagy in PPO, and expects the regulation of autophagy to become a powerful target for clinical treatment of PPO.
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Li, Zhichao, Dandan Li, Hui Su, Haipeng Xue, Guoqing Tan, and Zhanwang Xu. "Autophagy: An important target for natural products in the treatment of bone metabolic diseases." Frontiers in Pharmacology 13 (November 18, 2022). http://dx.doi.org/10.3389/fphar.2022.999017.

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Bone homeostasis depends on a precise dynamic balance between bone resorption and bone formation, involving a series of complex and highly regulated steps. Any imbalance in this process can cause disturbances in bone metabolism and lead to the development of many associated bone diseases. Autophagy, one of the fundamental pathways for the degradation and recycling of proteins and organelles, is a fundamental process that regulates cellular and organismal homeostasis. Importantly, basic levels of autophagy are present in all types of bone-associated cells. Due to the cyclic nature of autophagy and the ongoing bone metabolism processes, autophagy is considered a new participant in bone maintenance. Novel therapeutic targets have emerged as a result of new mechanisms, and bone metabolism can be controlled by interfering with autophagy by focusing on certain regulatory molecules in autophagy. In parallel, several studies have reported that various natural products exhibit a good potential to mediate autophagy for the treatment of metabolic bone diseases. Therefore, we briefly described the process of autophagy, emphasizing its function in different cell types involved in bone development and metabolism (including bone marrow mesenchymal stem cells, osteoblasts, osteocytes, chondrocytes, and osteoclasts), and also summarized research advances in natural product-mediated autophagy for the treatment of metabolic bone disease caused by dysfunction of these cells (including osteoporosis, rheumatoid joints, osteoarthritis, fracture nonunion/delayed union). The objective of the study was to identify the function that autophagy serves in metabolic bone disease and the effects, potential, and challenges of natural products for the treatment of these diseases by targeting autophagy.
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Song, Ruilong, Shuangjiang He, Ying Cao, Yicheng Lu, Yunwen Peng, Hui Zou, Xishuai Tong, Di Ran, Yonggang Ma, and Zongping Liu. "Cadmium accelerates autophagy of osteocytes by inhibiting the PI3K / AKT / mTOR signaling pathway." Environmental Toxicology, May 6, 2023. http://dx.doi.org/10.1002/tox.23823.

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