The effect of melatonin on bone tissue metabolism

Ih, Litovka; Yo, Mazepa-Kryzhanivs'ka; VIa, Berezovs'kyĭ

doi:10.15407/fz60.02.102

Cited by 3 publications

(1 citation statement)

References 38 publications

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“…Since the time course of the reduction of melatonin production and the progression of bone deterioration run in parallel shows possible role of melatonin in bone metabolism. It can prevent the premature destruction of bone and promote its recovery through mechanisms of melatoninrelated receptors and receptors of independent action [142]. One study reported the role of melatonin and RANKL/RANK/ OPG system (receptor activator of nuclear factor-kappa B ligand/receptor activator of nuclear factor-kappa B/osteoprotegerin) on the regulation of bone turnover [143].…”

Section: Melatonin In Bone Diseasementioning

confidence: 99%

An insight into the scientific background and future perspectives for the potential uses of melatonin

Anwar

Muhammad²,

Bader³

et al. 2015

Egyptian Journal of Basic and Applied Sciences

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Antiepileptic Antiosteoporotic Antioxidant Cardiovascular disease Circardian rhythm Hypnotic Immunodulatory Melatonin a b s t r a c t Melatonin is one of the most versatile and ubiquitous molecule widely distributed in nature has been reported to play a role in a wide variety of physiological responses including reproduction, circadian homeostasis, sleep, retinal neuromodulation, and vasomotor responses. In most vertebrates, including humans, melatonin is synthesized primarily in the pineal gland and is regulated by the environmental light ⁄ dark cycle via the suprachiasmatic nucleus. Melatonin is synthesized in all areas of the body such as gastrointestinal tract, skin, bone marrow, retina and in lymphocytes, from which it may influence other physiological functions through paracrine signalling. In addition to regulation of circadian rhythm of melatonin a variety of other physiological effects such as hypnotic, antidepressant, antiepileptic, oncostatic, immunomodulatory, antiosteoporotic, in cardiovascular disease, neuromodulatory and cerebral ischaemic condition have been reported.Moreover there is scarcity of literature that reviewed the scientific evidence for its use in these conditions. Therefore in this article we review recent advances in this research field, which is preceded by a concise account of general information about melatonin, melatonin receptors and intracellular signalling pathways for melatonin actions.

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Section: Melatonin In Bone Diseasementioning

confidence: 99%

An insight into the scientific background and future perspectives for the potential uses of melatonin

Anwar

Muhammad²,

Bader³

et al. 2015

Egyptian Journal of Basic and Applied Sciences

View full text Add to dashboard Cite

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Melatonin Inhibits Osteoclastogenesis and Bone Loss in Ovariectomized Mice by Regulating PRMT1-Mediated Signaling

et al. 2021

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Melatonin, a pineal gland hormone, has been suggested to treat postmenopausal osteoporosis due to its inhibitory effect on osteoclast differentiation. We previously reported that protein arginine methyltransferase 1 (PRMT1) was an important mediator of receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. However, the relationship between melatonin and PRMT1 in osteoclast differentiation and estrogen deficiency-induced osteoporosis is unclear. In this study, we investigated the inhibitory mechanisms of melatonin in vitro and in vivo by focusing on PRMT1. Melatonin treatment effectively blocked RANKL-induced osteoclastogenesis by inhibiting PRMT1 and asymmetric dimethylarginine (ADMA) expression. RANKL-induced tumor necrosis factor receptor-associated factor 6 (TRAF6) and the phosphorylation of JNK were also suppressed by melatonin, and TRAF6 siRNA attenuated RANKL-induced p-JNK and PRMT1 production. Melatonin inhibited the transcriptional activity of NF-κB by interfering with the binding of PRMT1 and NF-κB subunit p65 in RANKL-treated BMDMs. Our results also revealed that melatonin inhibits RANKL-induced PRMT1 expression through receptors-independent pathway. Thus, the anti-osteoclastogenic effect of melatonin was mediated by a cascade of inhibition of RANKL-induced TRAF6, JNK, PRMT1, and NF-κB signaling in melatonin receptors-independent pathway. In vivo, ovariectomy caused significant decreases in bone mineral density, but melatonin treatment alleviated the ovariectomized (OVX)-induced bone loss by inhibiting bone resorption. Furthermore, the expression PRMT1 and TRAP mRNA was upregulated in OVX-femurs, but effectively suppressed by melatonin injection. These findings suggest that melatonin inhibited osteoclast differentiation and estrogen deficiency-induced osteoporosis by suppressing RANKL-induced TRAF6, JNK, PRMT1, and NF-κB signaling cascades in melatonin receptors-independent pathway.

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Inhibition of iron overload-induced apoptosis and necrosis of bone marrow mesenchymal stem cells by melatonin

Yang

Yan

et al. 2017

Oncotarget

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Iron overload induces severe damage to several vital organs such as the liver, heart and bone, and thus contributes to the dysfunction of these organs. The aim of this study is to investigate whether iron overload causes the apoptosis and necrosis of bone marrow mesenchymal stem cells (BMSCs) and melatonin may prevent its toxicity. Perls’ Prussion blue staining showed that exposure to increased concentrations of ferric ammonium citrate (FAC) induced a gradual increase of intracellular iron level in BMSCs. Trypan blue staining demonstrated that FAC decreased the viability of BMSCs in a concentration-dependent manner. Notably, melatonin protected BMSCs against apoptosis and necrosis induced by FAC and it was vertified by Live/Dead, TUNEL and PI/Hoechst stainings. Furthermore, melatonin pretreatment suppressed FAC-induced reactive oxygen species accumulation. Western blot showed that exposure to FAC resulted in the decrease of anti-apoptotic protein Bcl-2 and the increase of pro-apoptotic protein Bax and Cleaved Caspase-3, and necrosis-related proteins RIP1 and RIP3, which were significantly inhibited by melatonin treatment. At last, melatonin receptor blocker luzindole failed to block the protection of BMSCs apoptosis and necrosis by melatonin. Taken together, melatonin protected BMSCs from iron overload induced apoptosis and necrosis by regulating Bcl-2, Bax, Cleaved Caspase-3, RIP1 and RIP3 pathways.

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The effect of melatonin on bone tissue metabolism

Cited by 3 publications

References 38 publications

An insight into the scientific background and future perspectives for the potential uses of melatonin

An insight into the scientific background and future perspectives for the potential uses of melatonin

Melatonin Inhibits Osteoclastogenesis and Bone Loss in Ovariectomized Mice by Regulating PRMT1-Mediated Signaling

Inhibition of iron overload-induced apoptosis and necrosis of bone marrow mesenchymal stem cells by melatonin

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