研究者詳細 - WANG ZIYI

論文 - WANG ZIYI

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Neuropilin 1 (NRP1) Positively Regulates Adipogenic Differentiation in C3H10T1/2 Cells 査読

Yaqiong Yu, Yoko Uchida-Fukuhara, Yao Weng, Yuhan He, Mika Ikegame, Ziyi Wang, Kaya Yoshida, Hirohiko Okamura, Lihong Qiu

International Journal of Molecular Sciences 24 ( 8 ) 7394 2023年4月

Bulk RNA‐seq analyses of mandibular condylar cartilage in a post‐traumatic TMJ osteoarthritis rabbit model 査読国際共著国際誌

Ikue Tosa, Angela Ruscitto, Ziyi Wang, Kira Z. Chen, Mitsuaki Ono, Mildred C. Embree

Orthodontics & Craniofacial Research 26 ( S1 ) 131 - 141 2023年3月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Wiley

Abstract

Objective

The temporomandibular joint (TMJ) is anatomically comprised of the mandibular condylar cartilage (CC) lined with fibrocartilaginous superficial zone and is crucial for eating and dental occlusion. TMJ osteoarthritis (OA) leads to pain, joint dysfunction and permanent loss of cartilage tissue. However, there are no drugs clinically available that ameliorate OA and little is known about global profiles of genes that contribute to TMJ OA. Furthermore, animal models that recapitulate the complexity of signalling pathways contributing to OA pathogenesis are crucial for designing novel biologics that thwart OA progression. We have previously developed a New Zealand white rabbit TMJ injury model that demonstrates CC degeneration. Here, we performed genome‐wide profiling to identify new signalling pathways critical for cellular functions during OA pathology.

Materials and Methods

Temporomandibular joint OA was surgically induced in New Zealand white rabbits. Three months following injury, we performed global gene expression profiling of the TMJ condyle. RNA samples from TMJ condyles were subjected to sequencing. After raw RNA‐seq data were mapped to relevant genomes, differential expression was analysed with DESeq2. Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis were conducted.

Results/Conclusions

Our study revealed multiple pathways altered during TMJ OA induction including the Wnt, Notch and PI3K‐Akt signalling pathways. We demonstrate an animal model that recapitulates the complexity of the cues and signals underlying TMJ OA pathogenesis, which is essential for developing and testing novel pharmacologic agents to treat OA.

DOI： 10.1111/ocr.12649

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SOD3 Expression in Tumor Stroma Provides the Tumor Vessel Maturity in Oral Squamous Cell Carcinoma 査読国際誌

May Wathone Oo, Hotaka Kawai, Htoo Shwe Eain, Yamin Soe, Kiyofumi Takabatake, Sho Sanou, Qiusheng Shan, Yasunori Inada, Masae Fujii, Yoko Fukuhara, Ziyi Wang, Shintaro Sukegawa, Mitsuaki Ono, Keisuke Nakano, Hitoshi Nagatsuka

Biomedicines 10 ( 11 ) 2729 - 2729 2022年10月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：MDPI AG

Tumor angiogenesis is one of the hallmarks of solid tumor development. The progressive tumor cells produce the angiogenic factors and promote tumor angiogenesis. However, how the tumor stromal cells influence tumor vascularization is still unclear. In the present study, we evaluated the effects of oral squamous cell carcinoma (OSCC) stromal cells on tumor vascularization. The tumor stromal cells were isolated from two OSCC patients with different subtypes: low invasive verrucous squamous carcinoma (VSCC) and highly invasive squamous cell carcinoma (SCC) and co-xenografted with the human OSCC cell line (HSC-2) on nude mice. In comparison, the CD34+ vessels in HSC-2+VSCC were larger than in HSC-2+SCC. Interestingly, the vessels in the HSC-2+VSCC expressed vascular endothelial cadherin (VE-cadherin), indicating well-formed vascularization. Our microarray data revealed that the expression of extracellular superoxide dismutase, SOD3 mRNA is higher in VSCC stromal cells than in SCC stromal cells. Moreover, we observed that SOD3 colocalized with VE-cadherin on endothelial cells of low invasive stroma xenograft. These data suggested that SOD3 expression in stromal cells may potentially regulate tumor vascularization in OSCC. Thus, our study suggests the potential interest in SOD3-related vascular integrity for a better OSCC therapeutic strategy.

DOI： 10.3390/biomedicines10112729

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Treatment of Marmoset Intracerebral Hemorrhage with Humanized Anti-HMGB1 mAb 査読

Dengli Wang, Daiki Ousaka, Handong Qiao, Ziyi Wang, Kun Zhao, Shangze Gao, Keyue Liu, Kiyoshi Teshigawara, Kenzo Takada, Masahiro Nishibori

Cells 11 ( 19 ) 2970 2022年9月

A morphometric analysis of the osteocyte canaliculus using applied automatic semantic segmentation by machine learning 査読

Tabata, K., Hashimoto, M., Takahashi, H., Wang, Z., Nagaoka, N., Hara, T., Kamioka, H.

Journal of Bone and Mineral Metabolism 40 ( 4 ) 2022年

Endonuclease increases efficiency of osteoblast isolation from murine calvariae 査読国際共著国際誌

Yosuke Asano, Yoshinori Matsumoto, Jose La Rose, Fang He, Takayuki Katsuyama, Wang Ziyi, Shigetomo Tsuji, Hiroshi Kamioka, Robert Rottapel, Jun Wada

Scientific Reports 11 ( 1 ) 2021年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Springer Science and Business Media {LLC}

Abstract:
Bone is a highly dynamic organ that undergoes remodeling equally regulated by osteoblast-mediated bone formation and osteoclast-mediated bone resorption. To clarify the regulation of osteoblastogenesis, primary murine osteoblasts are required for an in vitro study. Primary osteoblasts are isolated from neonatal calvariae through digestion with collagenase. However, the number of cells collected from one pup is not sufficient for further in vitro experiments, leading to an increase in the use of euthanized pups. We hypothesized that the viscosity of digested calvariae and digestion solution supplemented with collagenase results in cell clumping and reduction of isolated cells from bones. We simply added Benzonase, a genetically engineered endonuclease that shears all forms of DNAs/RNAs, in order to reduce nucleic acid-mediated viscosity. We found that addition of Benzonase increased the number of collected osteoblasts by three fold compared to that without Benzonase through reduction of viscosity. Additionally, Benzonase has no effect on cellular identity and function. The new osteoblast isolation protocol with Benzonase minimizes the number of neonatal pups required for an in vitro study and expands the concept that isolation of other populations of cells including osteocytes that are difficult to be purified could be modified by Benzonase.

DOI： 10.1038/s41598-021-87716-8

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Roles for B[a]P and FICZ in subchondral bone metabolism and experimental temporomandibular joint osteoarthritis via the AhR/Cyp1a1 signaling axis 査読

Yuri Yoshikawa, Takashi Izawa, Yusaku Hamada, Hiroko Takenaga, Ziyi Wang, Naozumi Ishimaru, Hiroshi Kamioka

Scientific Reports 11 ( 1 ) 2021年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Springer Science and Business Media {LLC}

<jats:title>Abstract</jats:title><jats:p>Bone loss due to smoking represents a major risk factor for fractures and bone osteoporosis. Signaling through the aryl hydrocarbon receptor (AhR) and its ligands contributes to both bone homeostasis and inflammatory diseases. It remains unclear whether the same AhR signaling axis affects the temporomandibular joint (TMJ). The aim of this study was to investigate possible mechanisms which mediate bone loss in the TMJ due to smoking. In particular, whether benzo[<jats:italic>a</jats:italic>]pyrene (B[<jats:italic>a</jats:italic>]P), a carcinogen of tobacco smoke, induces expression of the AhR target gene, Cyp1a1, in mandibular condyles. Possible functions of an endogenous ligand of FICZ, were also investigated in a TMJ-osteoarthritis (OA) mouse model. B[<jats:italic>a</jats:italic>]P was administered orally to wild-type and <jats:italic>AhR</jats:italic><jats:sup>−/−</jats:sup> mice and bone metabolism was subsequently examined. TMJ-OA was induced in wild-type mice with forceful opening of the mouth. Therapeutic functions of FICZ were detected with μCT and histology. Exposure to B[<jats:italic>a</jats:italic>]P accelerated bone loss in the mandibular subchondral bone. This bone loss manifested with osteoclastic bone resorption and upregulated expression of Cyp1a1 in an <jats:italic>AhR</jats:italic>-dependent manner. In a mouse model of TMJ-OA, FICZ exhibited a dose-dependent rescue of mandibular subchondral bone loss by repressing osteoclast activity. Meanwhile, in vitro, pre-treatment with FICZ reduced RANKL-mediated osteoclastogenesis. B[<jats:italic>a</jats:italic>]P regulates mandibular subchondral bone metabolism via the Cyp1a1. The AhR ligand, FICZ, can prevent TMJ-OA by regulating osteoclast differentiation.</jats:p>

DOI： 10.1038/s41598-021-94470-4

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Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury 査読

Kayo Yoshida, Kaya Yoshida, Natsumi Fujiwara, Mariko Seyama, Kisho Ono, Hotaka Kawai, Jiajie Guo, Ziyi Wang, Yao Weng, Yaqiong Yu, Yoko Uchida-Fukuhara, Mika Ikegame, Akira Sasaki, Hitoshi Nagatsuka, Hiroshi Kamioka, Hirohiko Okamura, Kazumi Ozaki

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1867 ( 11 ) 166236 - 166236 2021年11月

Investigation of the molecular causes underlying physical abnormalities in Diamond‐Blackfan anemia patients with RPL5 haploinsufficiency 査読国際誌

Yuko Fukui, Satoru Hayano, Noriaki Kawanabe, Ziyi Wang, Akira Shimada, Megumu K. Saito, Isao Asaka, Hiroshi Kamioka

Pathology International 71 ( 12 ) 803 - 813 2021年9月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Wiley

Abstract

Diamond‐Blackfan anemia (DBA) is a genetic disorder caused by mutations in genes encoding ribosomal proteins and characterized by erythroid aplasia and various physical abnormalities. Although accumulating evidence suggests that defective ribosome biogenesis leads to p53‐mediated apoptosis in erythroid progenitor cells, little is known regarding the underlying causes of the physical abnormalities. In this study, we established induced pluripotent stem cells from a DBA patient with RPL5 haploinsufficiency. These cells retained the ability to differentiate into osteoblasts and chondrocytes. However, RPL5 haploinsufficiency impaired the production of mucins and increased apoptosis in differentiated chondrocytes. Increased expression of the pro‐apoptotic genes BAX and CASP9 further indicated that RPL5 haploinsufficiency triggered p53‐mediated apoptosis in chondrocytes. Murine double minute 2 (MDM2), the primary negative regulator of p53, plays a crucial role in erythroid aplasia in DBA patient. We found the phosphorylation level of MDM2 was significantly decreased in RPL5 haploinsufficient chondrocytes. In stark contrast, we found no evidence that RPL5 haploinsufficiency impaired osteogenesis. Collectively, our data support a model in which RPL5 haploinsufficiency specifically induces p53‐mediated apoptosis in chondrocytes through MDM2 inhibition, which leads to physical abnormalities in DBA patients.

DOI： 10.1111/pin.13168

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その他リンク： https://onlinelibrary.wiley.com/doi/full-xml/10.1111/pin.13168

O-GlcNAcylation drives calcium signaling toward osteoblast differentiation: A bioinformatics-oriented study 査読

Weng, Y., Wang, Z., Fukuhara, Y., Tanai, A., Ikegame, M., Yamada, D., Takarada, T., Izawa, T., Hayano, S., Yoshida, K., Kamioka, H., Okamura, H.

BioFactors 47 ( 6 ) 992 - 1015 2021年

The expression and regulation of Wnt1 in tooth movement–initiated mechanotransduction 査読国際誌

Ei Ei Hsu Hlaing, Yoshihito Ishihara, Naoya Odagaki, Ziyi Wang, Mika Ikegame, Hiroshi Kamioka

American Journal of Orthodontics and Dentofacial Orthopedics 158 ( 6 ) e151 - e160 2020年12月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Elsevier BV

Abstract
Introduction: The Wnt signaling pathway acts as a key regulator of skeletal development and its homeostasis. However, the potential role of Wnt1 in the mechanotransduction machinery of orthodontic tooth movement-initiated bone remodeling is still unclear. Hence, this study focused on the regulatory dynamics of the Wnt1 expression in both the periodontal ligament (PDL) and osteocytes in vivo and in vitro.

Methods: The Wnt1 expression in the orthodontically moved maxillary first molar in mice was assessed at 0, 1, and 5 days, on both the compression and tension sides. Primary isolated human PDL (hPDL) fibroblasts, as well as murine long-bone osteocyte-Y4 (MLO-Y4) cells, were exposed to continuous compressive force and static tensile force.

Results: The relative quantification of immunodetection showed that orthodontic tooth movement significantly stimulated the Wnt1 expression in both the PDL and alveolar osteocytes on the tension side on day 5, whereas the expression on the compression side did not change. This increase in the Wnt1 expression, shown in vivo, was also noted after the application of 12% static tensile force in isolated hPDL fibroblasts and 20% in MLO-Y4 cells. In contrast, a compressive force led to the attenuation of the Wnt1 gene expression in both hPDL fibroblasts and MLO-Y4 cells in a force-dependent manner. In the osteocyte-PDL coculture system, recombinant sclerostin attenuated Wnt1 in PDL, whereas the antisclerostin antibody upregulated its gene expression, indicating that mechanically-driven Wnt1 signaling in PDL might be regulated by osteocytic sclerostin.

Conclusions: Our findings provide that Wnt1 signaling plays a vital role in tooth movement-initiated bone remodeling via innovative mechanotransduction approaches.

DOI： 10.1016/j.ajodo.2020.08.006

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N-(3-oxododecanoyl)-homoserine lactone regulates osteoblast apoptosis and differentiation by mediating intracellular calcium 査読国際共著国際誌

Jiajie Guo, Ziyi Wang, Yao Weng, Haoze Yuan, Kaya Yoshida, Mika Ikegame, Kenta Uchibe, Hiroshi Kamioka, Kazuhiko Ochiai, Hirohiko Okamura, Lihong Qiu

Cellular Signalling 75 109740 - 109740 2020年11月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Elsevier BV

Abstract
Pseudomonas aeruginosa (P. aeruginosa) is associated with periapical periodontitis. The lesions are characterized by a disorder in osteoblast metabolism. Quorum sensing molecular N-(3-oxododecanoyl)-homoserine lactone (AHL) is secreted by P. aeruginosa and governs the expression of numerous virulence factors. AHL can trigger intracellular calcium ([Ca2+]i) fluctuations in many host cells. However, it is unclear whether AHL can regulate osteoblast metabolism by affecting [Ca2+]i changes or its spatial correlation. We explored AHL-induced apoptosis and differentiation in pre-osteoblastic MC3T3-E1 cells and evaluated [Ca2+]i mobilization using several extraction methods. The spatial distribution pattern of [Ca2+]i among cells was investigated by Moran's I, an index of spatial autocorrelation. We found that 30 μM and 50 μM AHL triggered opposing osteoblast fates. At 50 μM, AHL inhibited osteoblast differentiation by promoting mitochondrial-dependent apoptosis and negatively regulating osteogenic marker genes, including Runx2, Osterix, bone sialoprotein (Bsp), and osteocalcin (OCN). In contrast, prolonged treatment with 30 μM AHL promoted osteoblast differentiation concomitantly with cell apoptosis. The elevation of [Ca2+]i levels in osteoblasts treated with 50 μM AHL was spatially autocorrelated, while no such phenomenon was observed in 30 μM AHL-treated osteoblasts. The blocking of cell-to-cell spatial autocorrelation in the osteoblasts provoked by 50 μM AHL significantly inhibited apoptosis and partially restored differentiation. Our observations suggest that AHL affects the fate of osteoblasts (apoptosis and differentiation) by affecting the spatial correlation of [Ca2+]i changes. Thus, AHL acts as a double-edged sword for osteoblast function.

Keywords: Apoptosis; Calcium; Differentiation; N-(3-oxododecanoyl)-homoserine lactone; Osteoblast metabolism; Spatial autocorrelation.

DOI： 10.1016/j.cellsig.2020.109740

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Outer membrane vesicles derived from Porphyromonas gingivalis induced cell death with disruption of tight junctions in human lung epithelial cells 査読国際誌

Yuhan He, Noriko Shiotsu, Yoko Uchida-Fukuhara, Jiajie Guo, Yao Weng, Mika Ikegame, Ziyi Wang, Kisho Ono, Hiroshi Kamioka, Yasuhiro Torii, Akira Sasaki, Kaya Yoshida, Hirohiko Okamura

Archives of Oral Biology 118 104841 - 104841 2020年10月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Elsevier BV

Abstract
Objective
Porphyromonas gingivalis (P. gingivalis) is a major bacterium responsible for the progression of periodontitis. P. gingivalis produces small vesicles called outer membrane vesicles (OMVs) containing virulence factors. Increasing evidence suggests a close relationship between periodontitis and respiratory system diseases, such as aspiration pneumonia. However, little is known about whether P. gingivalis OMVs give rise to the impediment of lung epithelial cells. We investigated the effect of the OMVs on cell viability and tight junctions of lung epithelial cells.

Design
Human lung epithelial A549 cells were treated with P. gingivalis OMVs. Cell viability was evaluated, and cell morphology was examined using scanning electron and phase contrast microscopies. To detect apoptosis induced by P. gingivalis OMVs, activation of caspase-3 and poly ADP-ribose polymerase (PARP) cleavage was examined by using Western blotting. Immunocytochemistry was performed to stain tight junction proteins.

Results
P. gingivalis OMVs decreased cell viability in A549 cells in a dose- and time-dependent manner. Microscopic analysis revealed that the OMVs induced morphological changes leading to irregular cell membrane structures. The OMVs caused cell shrinkage, membrane blebbing, and cytoplasmic expulsion in a dose-dependent manner. Western blot analysis showed the OMVs induced caspase-3 activation and PARP cleavage. Treatment with the OMVs disrupted the intact distributions of tight junction proteins.

Conclusions
These results indicate that P. gingivalis OMVs induced cell death by destroying the barrier system in lung epithelial cells. Our present study raises the possibility that P. gingivalis OMVs is an important factor in the engagement of periodontitis with respiratory system diseases.

DOI： 10.1016/j.archoralbio.2020.104841

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The Analysis of Gap Junctional Intercellular Communication Among Osteocytes in Chick Calvariae by Fluorescence Recovery After Photobleaching 招待査読国際誌

Ziyi Wang, Yoshihito Ishihara, Hiroshi Kamioka

Methods in Molecular Biology 215 - 223 2020年9月

Benzonaseを用いた新規骨芽細胞分離法の開発

浅野洋介, 松本佳則, 王紫儀, 佐田憲映, 上岡寛, 和田淳

日本骨形態計測学会雑誌 30 ( 1 ) S99 - S99 2020年5月

Role of intracellular Ca2+–based mechanotransduction of human periodontal ligament fibroblasts 査読国際誌

Ei Ei Hsu Hlaing, Yoshihito Ishihara, Ziyi Wang, Naoya Odagaki, Hiroshi Kamioka

The FASEB Journal 33 ( 9 ) 10409 - 10424 2019年7月

記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Wiley

Abstract
Human periodontal ligament (hPDL) fibroblasts are thought to receive mechanical stress (MS) produced by orthodontic tooth movement, thereby regulating alveolar bone remodeling. However, the role of intracellular calcium ([Ca2+]i)-based mechanotransduction is not fully understood. We explored the MS-induced [Ca2+]i responses both in isolated hPDL fibroblasts and in intact hPDL tissue and investigated its possible role in alveolar bone remodeling. hPDL fibroblasts were obtained from healthy donors' premolars that had been extracted for orthodontic reasons. The oscillatory [Ca2+]i activity induced by static compressive force was measured by a live-cell Ca2+ imaging system and evaluated by several feature extraction method. The spatial pattern of cell-cell communication was investigated by Moran's I, an index of spatial autocorrelation and the gap junction (GJ) inhibitor. The Ca2+-transporting ionophore A23187 was used to further investigate the role of [Ca2+]i up-regulation in hPDL cell behavior. hPDL fibroblasts displayed autonomous [Ca2+]i responses. Compressive MS activated this autonomous responsive behavior with an increased percentage of responsive cells both in vitro and ex vivo. The integration, variance, maximum amplitude, waveform length, and index J in the [Ca2+]i responses were also significantly increased, whereas the mean power frequency was attenuated in response to MS. The increased Moran's I after MS indicated that MS might affect the pattern of cell-cell communication via GJs. Similar to the findings of MS-mediated regulation, the A23187-mediated [Ca2+]i uptake resulted in the up-regulation of receptor activator of NF-κB ligand (Rankl) and Sost along with increased sclerostin immunoreactivity, suggesting that [Ca2+]i signaling networks may be involved in bone remodeling. In addition, A23187-treated hPDL fibroblasts also showed the suppression of osteogenic differentiation and mineralization. Our findings suggest that augmented MS-mediated [Ca2+]i oscillations in hPDL fibroblasts enhance the production and release of bone regulatory signals via Rankl/Osteoprotegerin and the canonical Wnt/β-catenin pathway as an early process in tooth movement-initiated alveolar bone remodeling.

DOI： 10.1096/fj.201900484r

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その他リンク： https://onlinelibrary.wiley.com/doi/full-xml/10.1096/fj.201900484R

CBCT Analysis of Mesiodistal Angulation of Maxillary Molars for Female Patient with Skeletal Class II Malocclusion 査読

Jun Li, Ziyi Wang, Xiaodong Zhang

Journal of Oral Science Research 34 ( 8 ) 896 - 901 2018年8月

Role of Osteocyte-PDL Crosstalk in Tooth Movement via SOST/Sclerostin 査読

Odagaki, N., Ishihara, Y., Wang, Z., Ei Hsu Hlaing, E., Nakamura, M., Hoshijima, M., Hayano, S., Kawanabe, N., Kamioka, H.

Journal of Dental Research 97 ( 12 ) 1374 - 1382 2018年

Efficacy of Glucosamine Hydrochloride Tablets combined with Sodium Hyaluronate in the treatment of Temporomandibular Joint Osteoarthritis 査読

Jianlin Liu, Yansong Wang, Ziyi Wang, Yao Weng

Progress in Modern Biomedicine 17 ( 2 ) 331 - 333 2017年2月

ナトリウムヒアルロン酸注射と関節穿刺が顎関節症患者に与える影響査読

17 ( 7 ) 1304 - 1307 2017年1月

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