Effects of Zinc Transporter on Differentiation of Bone Marrow Mesenchymal Stem Cells to Osteoblasts

Liu, Yang; Feng, Yan; Yang, Wenjing; Lu, Xiaofeng; Wang, Wenbo

doi:10.1007/s12011-013-9683-y

Cited by 24 publications

(14 citation statements)

References 34 publications

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“…Subsequently, MAPK transduces signals inducing phosphorylation of ALP and Runx2, leading to their up‐regulation. Furthermore, to maintain zinc homeostasis, cells exposed to abundant zinc could up‐regulate the expression of zinc transporters such as the ZIP (Zrt‐ or Irt‐like protein, SLC39) and ZnT (cation diffusion facilitator, SLC30) families, among which ZnT7 has been demonstrated to inhibit the Wnt/β‐catenin pathway by down‐regulating the level of p‐β‐catenin . The Wnt/β‐catenin pathway can result in the up‐regulation of BMP‐2 but the repression of Runx2 .…”

Section: Discussionmentioning

confidence: 99%

Osteogenic activity and antibacterial effect of porous titanium modified with metal‐organic framework films

Chen

Zhang

Huang

et al. 2016

J Biomedical Materials Res

110

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As a new class of crystalline nanoporous materials, metal-organic frameworks (MOFs) have recently been used for biomedical applications due to their large surface area, high porosity, and theoretically infinite structures. To improve the biological performance of titanium, MOF films were applied to surface modification of titanium. Zn-based MOF films composed of zeolitic imidazolate framework-8 (ZIF-8) crystals with nanoscale and microscale sizes (nanoZIF-8 and microZIF-8) were prepared on porous titanium surfaces by hydrothermal and solvothermal methods, respectively. The ZIF-8 films were characterized by powder X-ray diffraction (PXRD), Fourier transform infrared spectroscopy (FTIR), and scanning electron microscopy (SEM). The nanoZIF-8 film exhibited good biocompatibility, whereas the microZIF-8 film showed obvious cytotoxicity to MG63 cells. Compared to pure titanium and alkali- and heat-treated porous titanium, the nanoZIF-8 film not only enhanced alkaline phosphatase (ALP) activity, extracellular matrix mineralization, and expression of osteogenic genes (ALP, Runx2) in MG63 cells but also inhibited the growth of Streptococcus mutans. These results indicate that MOF films or coatings may be promising candidates for bone tissue engineering. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 834-846, 2017.

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Section: Discussionmentioning

confidence: 99%

Osteogenic activity and antibacterial effect of porous titanium modified with metal‐organic framework films

Chen

Zhang

Huang

et al. 2016

J Biomedical Materials Res

110

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“…Downregulation of ZnT7 expression by small interfering RNA (siRNA) increased the levels of osteogenesis-associated markers such as alkaline phosphatase (ALP), collagen I and osteocalcin, whereas overexpression of ZnT7 exerted the opposite effects. Further study demonstrated that ZnT7 could interfere with Wnt/β-catenin signaling, a key pathway involved in osteogenesis [56]. ZnT5 and ZnT7 might play opposite roles in osteogenesis; however, the underlying mechanism still needs to be explored.…”

Section: Role Of Znt Transporters In Bonementioning

confidence: 99%

“…induction of osteogenesis of MSCs [39][40][41] knockout no obvious bone phenotype [42][43][44] ZIP2 knockout no obvious bone phenotype [43][44][45] ZIP3 knockout no obvious bone phenotype [42][43][44] ZIP8 cartilage destruction and osteoarthritis [46][47][48][49] ZIP13 mutation spondylocheiro dysplastic form of Ehlers-Danlos syndrome [50] knockout connective tissue dysplasia [51] ZIP14 knockout growth retardation [52,53] mutation hyperostosis cranialis interna [54] ZnT5 knockout poor growth, osteopenia and heart failure [55] ZnT7 impaired osteogenesis of MSCs [56] protection of osteoblasts from apoptosis [57]…”

Section: Zip1mentioning

confidence: 99%

“…However, the roles of ZnT5 in bone and the related mechanisms are largely elusive. The ZnT7 protein is abundantly expressed in mouse osteoblast MC3T3-E1 cells [57] and is a crucial component of the functional activities of MSCs [56]. ZnT7 prevented MC3T3-E1 cells from undergoing apoptosis induced by oxidative stress by reducing the accumulation of intracellular cationic zinc [57].…”

Section: Role Of Znt Transporters In Bonementioning

confidence: 99%

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Zinc Homeostasis in Bone: Zinc Transporters and Bone Diseases

Huang

Yan

Guan

2020

IJMS

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Zinc is an essential micronutrient that plays critical roles in numerous physiological processes, including bone homeostasis. The majority of zinc in the human body is stored in bone. Zinc is not only a component of bone but also an essential cofactor of many proteins involved in microstructural stability and bone remodeling. There are two types of membrane zinc transporter proteins identified in mammals: the Zrt-and Irt-like protein (ZIP) family and the zinc transporter (ZnT) family. They regulate the influx and efflux of zinc, accounting for the transport of zinc through cellular and intracellular membranes to maintain zinc homeostasis in the cytoplasm and in intracellular compartments, respectively. Abnormal function of certain zinc transporters is associated with an imbalance of bone homeostasis, which may contribute to human bone diseases. Here, we summarize the regulatory roles of zinc transporters in different cell types and the mechanisms underlying related pathological changes involved in bone diseases. We also present perspectives for further studies on bone homeostasis-regulating zinc transporters.

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“…Possibly, low zinc levels may also contribute to the de-differentiation of cells, e.g. it was observed that zinc is crucial in the differentiation of certain cell types 191,192 . Beside zinc itself, this could include the transcription factor KLF4, which is known both as iPS stem cell factor in the induction of pluripotent stem cells 193 and as a regulator of the zinc transporter ZIP4 (SLC39A4) 194,195 .…”

Section: Trace Elements and The Hallmarks Of Cancermentioning

confidence: 99%

The disruption of trace element homeostasis due to aneuploidy as a unifying theme in the etiology of cancer

Engelken

Altmeyer

2014

Preprint

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Abstracts Abstract for ScientistsWhile decades of cancer research have firmly established multiple "hallmarks of cancer" 1,2 , cancer's genomic landscape remains to be fully understood. Particularly, the phenomenon of aneuploidy -gains and losses of large genomic regions, i.e. whole chromosomes or chromosome arms -and why most cancer cells are aneuploid remains enigmatic 3 . Another frequent observation in many different types of cancer is the deregulation of the homeostasis of the trace elements copper, zinc and iron. Concentrations of copper are markedly increased in cancer tissue and the blood plasma of cancer patients, while zinc levels are typically decreased [4][5][6][7][8][9] . Here we discuss the hypothesis that the disruption of trace element homeostasis and the phenomenon of aneuploidy might be linked. Our tentative analysis of genomic data from diverse tumor types mainly from The Cancer Genome Atlas (TCGA) project suggests that gains and losses of metal transporter genes occur frequently and correlate well with transporter gene expression levels. Hereby they may confer a cancer-driving selective growth advantage at early and possibly also later stages during cancer development. This idea is consistent with recent observations in yeast, which suggest that through chromosomal gains and losses cells can adapt quickly to new carbon sources 10 , nutrient starvation 11 as well as to copper toxicity 12 . In human cancer development, candidate driving events may include, among others, the gains of zinc transporter genes SLC39A1 and SLC39A4 on chromosome arms 1q and 8q, respectively, and the losses of zinc transporter genes SLC30A5, SLC39A14 and SLC39A6 on 5q, 8p and 18q. The recurrent gain of 3q might be associated with the iron transporter gene TFRC and the loss of 13q with the copper transporter gene ATP7B. By altering cellular trace element homeostasis such events might contribute to the initiation of the malignant transformation. Intriguingly, attenuation or overexpression of several of these metal transporter genes has been shown to lead to malignant cellular behavior in vitro. Consistently, it has been shown that zinc affects a number of the observed "hallmarks of cancer" characteristics including DNA repair, inflammation and apoptosis, e.g. through its effects on NF-kappa B signaling. We term this model the "aneuploidy metal transporter cancer" (AMTC) hypothesis and find it compatible with the cancer-promoting role of point mutations and focal copy number alterations in established tumor suppressor genes and oncogenes (e.g. MYC, MYCN, TP53, PIK3CA, BRCA1, ERBB2). We suggest a number of approaches for how this hypothesis could be tested experimentally and briefly touch on possible implications for cancer etiology, metastasis, drug resistance and therapy.. CC-BY-NC 4.0 International license not peer-reviewed) is the author/funder. It is made available under a The copyright holder for this preprint (which was . http://dx.doi.org/10.1101/002105 doi: bioRxiv preprint first posted online Jan. 29, 2014; [3...

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Effects of Zinc Transporter on Differentiation of Bone Marrow Mesenchymal Stem Cells to Osteoblasts

Cited by 24 publications

References 34 publications

Osteogenic activity and antibacterial effect of porous titanium modified with metal‐organic framework films

Osteogenic activity and antibacterial effect of porous titanium modified with metal‐organic framework films

Zinc Homeostasis in Bone: Zinc Transporters and Bone Diseases

The disruption of trace element homeostasis due to aneuploidy as a unifying theme in the etiology of cancer

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