High magnesium prevents matrix vesicle‐mediated mineralization in human bone marrow‐derived mesenchymal stem cells via mitochondrial pathway and autophagy

Li, Yaqiang; Wang, Jing; Yue, Jiaji; Wang, Yu; Yang, Chunxi; Cui, Quanjun

doi:10.1002/cbin.10888

Cited by 29 publications

(31 citation statements)

References 34 publications

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“…The downregulating effect of high magnesium on mitophagy has been previously reported 31 , but the specific mechanism is still unclear. Magnesium ion stimulation may enhance the osteogenic activity of bone marrow stromal cells by upregulating the expression of PGC-1α according to a previous study 32 .…”

Section: Discussionmentioning

confidence: 93%

NIPA2 regulates osteoblast function by modulating mitophagy in type 2 diabetes osteoporosis

Zhao

Zhang

et al. 2020

Sci Rep

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The highly selective magnesium transporter non-imprinted in Prader-Willi/Angelman syndrome region protein 2 (NIPA2) has recently been associated with the development and progression of type 2 diabetes osteoporosis, but the mechanisms involved are still poorly understood. Because mitophagy is involved in the pathology of type 2 diabetes osteoporosis, the present study aimed to explore the relationship among NIPA2, mitophagy and osteoblast osteogenic capacity. NIPA2 expression was reduced in C57BKS background db/db mice and in vitro models of type 2 diabetes osteoporosis, and the activation of mitophagy in primary culture osteoblast-derived from db/db mice and in high glucose-treated human fetal osteoblastic cells (hFOB1.19) was observed. Knockdown, overexpression of NIPA2 and pharmacological inhibition of peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) showed that NIPA2 increased osteoblast function, which was likely regulated by PTEN induced kinase 1 (PINK1)/E3 ubiquitin ligase PARK2 (Parkin)-mediated mitophagy via the PGC-1α/ forkhead box O3a(FoxO3a)/mitochondrial membrane potential (MMP) pathway. Furthermore, the negative effect of mitophagy on osteoblast function was confirmed by pharmacological regulation of mitophagy and knockdown of Parkin. Taken together, these results suggest that NIPA2 positively regulates the osteogenic capacity of osteoblasts via the mitophagy pathway in type 2 diabetes. Plasma measurements. Blood samples were collected from the animals' tail veins. The samples were used for measuring the fasting blood glucose (FBG) levels (Roche blood glucose instrument, Roche, Basel, Switzerland). Radioimmunoassay (3v-diagnostic Bioengineer, Shandong, China) was used for the fasting plasma insulin (FINS) analysis, while ELISA (Rat Estrogen/E ELISA Kit, 3v-diagnostic Bioengineer) was used for the plasma estrogen analysis. The insulin sensitivity index (ISI) was calculated as the -ln(FINS•FPG) 42 . Scientific RepoRtS |(2020) 10:3078 | https://doi.

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Section: Discussionmentioning

confidence: 93%

NIPA2 regulates osteoblast function by modulating mitophagy in type 2 diabetes osteoporosis

Zhao

Zhang

et al. 2020

Sci Rep

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“…Senescence and cellular metabolism of ECM are implicated in mitochondrial dysfunction . Exposure of cells to TNF‐α induces more generation of ROS, and overproduction of ROS can result in mitochondrial dysfunction .…”

Section: Discussionmentioning

confidence: 99%

Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats

Wang

Huang

Lin

et al. 2018

J Cellular Molecular Medi

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Intervertebral disc degeneration (IVDD) is one of the major causes of low back pain. Polydatin (PD) has been shown to exert multiple pharmacological effects on different diseases; here, we test the therapeutic potential of PD for IVDD. In in‐vitro experiments, we confirmed PD is nontoxic to nucleus pulposus cells (NPCs) under the concentration of 400 μmol/L. Furthermore, PD was able to decrease the level of senescence in TNF‐α‐treated NPCs, as indicated by β‐gal staining as well as senescence markers p53 and p16 expression. In the aspect of extracellular matrix (ECM), PD not only reduced metalloproteinase 3 (MMP‐3), metalloproteinase 13 (MMP‐13) and a disintegrin‐like and metalloproteinase thrombospondin type 1 motif 4 (ADAMTS‐4) expression, but also increased aggrecan and collagen II levels. Mitochondrion is closely related to cellular senescence and ECM homeostasis; mechanistically, we found PD may rescue TNF‐α‐induced mitochondrial dysfunction, and it may also promote Nrf2 expression and activity. Silencing Nrf2 partly abolished the protective effects of PD on mitochondrial homeostasis, senescence and ECM homeostasis in TNF‐α‐treated NPCs. Correspondingly, PD ameliorated IVDD in rat model by promoting Nrf2 activity, preserving ECM and inhibiting senescence in nucleus pulposus cells. To sum up, our study suggests that PD exerts protective effects in NPCs against IVDD and reveals the underlying mechanism of PD on Nrf2 activation in NPCs.

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“…However, phenomenologically significant calcification was reduced, indicating that other interdependent or independent mechanisms might be consequential [197,199]. In addition, recently, processes reported to associate with VC include mitochondrial dynamics, mitophagy, ROS, matrix vesicle release, apoptosis, and degradation of matrix [146,[200][201][202]. Considering the results of animal experiments, further studies are needed, to determine whether these phenomena are related to PDK4.…”

Section: Pyruvate Dehydrogenase Kinase (Pdk)4mentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

254

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Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

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High magnesium prevents matrix vesicle‐mediated mineralization in human bone marrow‐derived mesenchymal stem cells via mitochondrial pathway and autophagy

Cited by 29 publications

References 34 publications

NIPA2 regulates osteoblast function by modulating mitophagy in type 2 diabetes osteoporosis

NIPA2 regulates osteoblast function by modulating mitophagy in type 2 diabetes osteoporosis

Polydatin suppresses nucleus pulposus cell senescence, promotes matrix homeostasis and attenuates intervertebral disc degeneration in rats

Vascular Calcification—New Insights into Its Mechanism

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