Melatonin Rescues the Ti Particle-Impaired Osteogenic Potential of Bone Marrow Mesenchymal Stem Cells via the SIRT1/SOD2 Signaling Pathway

Zhang, Yazhong; Zhu, Xu; Wang, Genlin; Chen, Liang; Yang, Huilin; He, Fan; Lin, Jun

doi:10.1007/s00223-020-00741-z

Cited by 35 publications

(25 citation statements)

References 47 publications

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“…Tremendous amounts of studies have confirmed that melatonin has a protective effect on the prevention and treatment of osteoporosis, arthritis, and other orthopedic diseases [ 42 – 45 ]. The beneficial effects of melatonin in Ti-particles induced aseptic inflammatory osteolysis has also been confirmed by our previous studies [ 25 , 26 ]. In this study, we demonstrated that oral melatonin supplementation could alleviate osteolysis with a lower level of bone erosion parameters (BV/TV, BMD, total porosity), fewer osteoclasts activation and accompany with changes in gut microbiota.…”

Section: Discussionsupporting

confidence: 79%

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Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway

Zhang

et al. 2021

J Nanobiotechnol

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Background Inflammatory osteolysis after total joint replacement (TJR) may cause implant failure, periprosthetic fractures, and be a severe threat to global public health. Our previous studies demonstrated that melatonin had a therapeutic effect on wear-particles induced osteolysis. Gut microbiota is closely related to bone homeostasis, and has been proven to be affected by melatonin. However, whether melatonin could play its anti-osteolysis effects through reprogramming gut microbiota remains elusive. Results Here, we demonstrated that melatonin could alleviate Ti-particles induced osteolysis, while this therapeutic effect was blocked by antibiotic cocktail treatment. Interestingly, transplantation of fecal microbiota from mice treated with melatonin reappeared the same beneficial effect. Analysis of the 16S rRNA revealed that melatonin could reverse dysbacteriosis triggered by osteolysis, and elevate the relative abundance of some short chain fatty acid (SCFA) producing bacteria. Moreover, butyrate was enriched by exogenous melatonin administration, while acetate and propionate did not show an evident difference. This was consistent with the results of the metagenomic approach (PICRUSt2) analysis, which revealed a general increase in the synthetic enzymes of butyrate. More importantly, direct supplementation of butyrate could also recapitulate the anti-osteolysis effect of melatonin. Further analysis identified that butyrate alleviated osteolysis via activating its receptor GPR109A, and thus to suppress the activation of NLRP3 inflammasome triggered by Ti-particles. Conclusions Taken together, our results suggested that the benefits of melatonin mainly depend on the ability of modulating gut microbiota and regulating butyrate production. Graphic Abstract

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Section: Discussionsupporting

confidence: 79%

“…Although our previous studies have demonstrated the benefits of melatonin on inflammatory osteolysis [ 25 , 26 ], whether melatonin plays the anti-osteolysis effects indirectly through gut microbiota reprogramming is still unknown. Gut microbiota is well known to be affected by antibiotics [ 32 – 35 ].…”

Section: Resultsmentioning

confidence: 99%

Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway

Zhang

et al. 2021

J Nanobiotechnol

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“…Through a number of pathways involving cellular metabolism, the coenzyme ßnicotinamide adenine dinucleotide (NAD + ) can play a critical role with circadian rhythm and clock genes that is tied to SIRT1 and mTOR [3,16,74,221,222]. SIRT1 control of circadian rhythm and melatonin may affect cellular glucose tolerance [107], stem cell function [223], and inflammation during obesity [96] and neurodegeneration [178]. In addition, cellular NAD + pools are known to fluctuate with circadian rhythmicity and with aging [74].…”

Section: Circadian Clock Genes and The Silent Mating Type Information Regulation 2 Homolog 1 (Saccharomyces Cerevisiae) (Sirt1)mentioning

confidence: 99%

Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways

Maiese

2021

Biomolecules

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Neurodegenerative disorders affect fifteen percent of the world’s population and pose a significant financial burden to all nations. Cognitive impairment is the seventh leading cause of death throughout the globe. Given the enormous challenges to treat cognitive disorders, such as Alzheimer’s disease, and the inability to markedly limit disease progression, circadian clock gene pathways offer an exciting strategy to address cognitive loss. Alterations in circadian clock genes can result in age-related motor deficits, affect treatment regimens with neurodegenerative disorders, and lead to the onset and progression of dementia. Interestingly, circadian pathways hold an intricate relationship with autophagy, the mechanistic target of rapamycin (mTOR), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), mammalian forkhead transcription factors (FoxOs), and the trophic factor erythropoietin. Autophagy induction is necessary to maintain circadian rhythm homeostasis and limit cortical neurodegenerative disease, but requires a fine balance in biological activity to foster proper circadian clock gene regulation that is intimately dependent upon mTOR, SIRT1, FoxOs, and growth factor expression. Circadian rhythm mechanisms offer innovative prospects for the development of new avenues to comprehend the underlying mechanisms of cognitive loss and forge ahead with new therapeutics for dementia that can offer effective clinical treatments.

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“…Melatonin also plays the role of a scavenger of free radicals to inhibit the oxidative stress in mitochondria. Recent studies demonstrated that melatonin can alleviate mitochondrial oxidative stress-induced via SIRT3/SOD2 pathway, though the experimental models were not aging-related [139,140]. Another therapeutic target for aging by melatonin application is inflammation.…”

Section: Agingmentioning

confidence: 99%

Potential Role of Melatonin as an Adjuvant for Atherosclerotic Carotid Arterial Stenosis

Zhang

et al. 2021

Molecules

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Carotid artery stenosis (CAS) is an atherosclerotic disease characterized by a narrowing of the artery lumen and a high risk of ischemic stroke. Risk factors of atherosclerosis, including smoking, hypertension, hyperglycemia, hyperlipidemia, aging, and disrupted circadian rhythm, may potentiate atherosclerosis in the carotid artery and further reduce the arterial lumen. Ischemic stroke due to severe CAS and cerebral ischemic/reperfusion (I/R) injury after the revascularization of CAS also adversely affect clinical outcomes. Melatonin is a pluripotent agent with potent anti-inflammatory, anti-oxidative, and neuroprotective properties. Although there is a shortage of direct clinical evidence demonstrating the benefits of melatonin in CAS patients, previous studies have shown that melatonin may be beneficial for patients with CAS in terms of reducing endothelial damage, stabilizing arterial plaque, mitigating the harm from CAS-related ischemic stroke and cerebral I/R injury, and alleviating the adverse effects of the related risk factors. Additional pre-clinical and clinical are required to confirm this speculation.

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Melatonin Rescues the Ti Particle-Impaired Osteogenic Potential of Bone Marrow Mesenchymal Stem Cells via the SIRT1/SOD2 Signaling Pathway

Cited by 35 publications

References 47 publications

Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway

Melatonin alleviates titanium nanoparticles induced osteolysis via activation of butyrate/GPR109A signaling pathway

Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways

Potential Role of Melatonin as an Adjuvant for Atherosclerotic Carotid Arterial Stenosis

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