Faculty Profiles - AOYAMA Eriko

Papers - AOYAMA Eriko

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Necrotic and apoptotic cells serve as nuclei for calcification on osteoblastic differentiation of human mesenchymal stem cells in vitro Reviewed

Hirofumi Fujita, Masanao Yamamoto, Tetsuya Ogino, Hirotsugu Kobuchi, Naoko Ohmoto, Eriko Aoyama, Takashi Oka, Tohru Nakanishi, Keiji Inoue, Junzo Sasaki

CELL BIOCHEMISTRY AND FUNCTION 32 ( 1 ) 77 - 86 2014.1

Language：English Publishing type：Research paper (scientific journal) Publisher：WILEY-BLACKWELL

A close relationship between cell death and pathological calcification has recently been reported, such as vascular calcification in atherosclerosis. However, the roles of cell death in calcification by osteoblast lineage have not been elucidated in detail. In this study, we investigated whether cell death is involved in the calcification on osteoblastic differentiation of human bone marrow mesenchymal stem cells (hMSC) under osteogenic culture in vitro. Apoptosis and necrosis occurred in an osteogenic culture of hMSC, and cell death preceded calcification. The generation of intracellular reactive oxygen species, chromatin condensation and fragmentation, and caspase-3 activation increased in this culture. A pan-caspase inhibitor (Z-VAD-FMK) and anti-oxidants (Tiron and n-acetylcysteine) inhibited osteogenic culture-induced cell death and calcification. Furthermore, calcification was significantly promoted by the addition of necrotic dead cells or its membrane fraction. Spontaneously dead cells by osteogenic culture and exogenously added necrotic cells were surrounded by calcium deposits. Induction of localized cell death by photodynamic treatment in the osteogenic culture resulted in co-localized calcification. These findings show that necrotic and apoptotic cell deaths were induced in an osteogenic culture of hMSC and indicated that both necrotic and apoptotic cells of osteoblast lineage served as nuclei for calcification on osteoblastic differentiation of hMSC in vitro. Copyright (c) 2013 John Wiley & Sons, Ltd.

DOI： 10.1002/cbf.2974

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The regenerative effects of CCN2 independent modules on chondrocytes in vitro and osteoarthritis models in vivo Reviewed

El Kader, Tarek Abd, Kubota Satoshi, Nishida Takashi, Hattori Takako, Aoyama Eriko, Janune Danilo, Hara Emilio S, Ono Mitsuaki, Tabata Yasuhiko, Kuboki Takuo, Takigawa Masaharu

Bone 59 180 - 188 2014

CCN3の抗線維化効果に伴うCCNファミリー遺伝子発現プロファイルの変化

アブド・エル・ケーダー・タレック, 久保田聡, ジャヌネ・ダニーロ, 西田崇, 服部高子, 青山絵理子, 窪木拓男, 滝川正春

岡山歯学会雑誌 32 ( 2 ) 83 - 83 2013.12

CCNファミリー遺伝子の発現プロフィールの操作を介したCCN3の線維化抑制作用の理解(Understanding the anti-fibrotic role of CCN3 through manipulation of CCN family gene expression profile)

El Kader Tarek Abd, Kubota Satoshi, Janune Danilo, Nishida Takashi, Hattori Takako, Aoyama Eriko, Perbal Bernard, Kuboki Takuo, Takigawa Masaharu

日本生化学会大会プログラム・講演要旨集 86回 1T11a - 15 2013.9

Cartilage-Specific Over-Expression of CCN Family Member 2/Connective Tissue Growth Factor (CCN2/CTGF) Stimulates Insulin-Like Growth Factor Expression and Bone Growth Reviewed

Tomita Nao, Hattori Takako, Itoh Shinsuke, Aoyama Eriko, Yao Mayumi, Yamashiro Takashi, Takigawa Masaharu

PLOS ONE 8 ( 3 ) e59226 2013.3

Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family Reviewed

El Kader, Tarek Abd, Kubota Satoshi, Janune Danilo, Nishida Takashi, Hattori Takako, Aoyama Eriko, Perbal Bernard, Kuboki Takuo, Takigawa Masaharu

JOURNAL OF CELL COMMUNICATION AND SIGNALING 7 ( 1 ) 11 - 18 2013.3

Language：English Publishing type：Research paper (scientific journal) Publisher：SPRINGER

CCN family proteins 2 and 3 (CCN2 and CCN3) belong to the CCN family of proteins, all having a high level of structural similarity. It is widely known that CCN2 is a profibrotic molecule that mediates the development of fibrotic disorders in many different tissues and organs. In contrast, CCN3 has been recently suggested to act as an anti-fibrotic factor in several tissues. This CCN3 action was shown earlier to be exerted by the repression of the CCN2 gene expression in kidney tissue, whereas different findings were obtained for liver cells. Thus, the molecular action of CCN3 yielding its anti-fibrotic effect is still controversial. Here, using a general model of fibrosis, we evaluated the effect of CCN3 overexpression on the gene expression of all of the CCN family members, as well as on that of fibrotic marker genes. As a result, repression of CCN2 gene expression was modest, while type I collagen and a-smooth muscle actin gene expression was prominently repressed. Interestingly, not only CCN2, but also CCN4 gene expression showed a decrease upon CCN3 overexpression. These findings indicate that fibrotic gene induction is under the control of a complex molecular network conducted by CCN family members functioning together.

DOI： 10.1007/s12079-012-0180-4

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Dextran sulfate-induced degradation of spontaneously apoptotic B cells Reviewed

Kadota, Yusuke, Sakai, Nao, Fujikawa, Ryoma, Aoyama, Eriko, Zhong, Ming, Tanaka, Satoshi, Gohda, Eiichi

International Immunopharmacology 15 ( 3 ) 581 - 587 2013

Impaired glycolytic metabolism causes chondrocyte hypertrophy-like changes via promotion of phospho-Smad1/5/8 translocation into nucleus.

Nishida T, Kubota S, Aoyama E, Takigawa M

Osteoarthritis Cartilage 21 700 - 709 2013

CCN family member 2/connective tissue growth factor (CCN2/CTGF) has anti-aging effects that protect articular cartilage from age-related degenerative changes. Reviewed

Itoh S, Hattori T, Tomita N, Aoyama E, Yutani Y, Yamashiro T, Takigawa M

PloS one 8 ( 8 ) e71156 2013

CCN2/CTGF binds to fibroblast growth factor receptor 2 and modulates its signaling

Eriko Aoyama, Satoshi Kubota, Masaharu Takigawa

FEBS LETTERS 586 ( 24 ) 4270 - 4275 2012.12

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCIENCE BV

CCN2 plays a critical role in the development of mesenchymal tissues such as cartilage and bone, and the binding of CCN2 to various cytokines and receptors regulates their signaling. By screening a protein array, we found that CCN2 could bind to fibroblast growth factor receptors (FGFRs) 2 and 3, with a higher affinity toward FGFR2. We ascertained that FGFR2 bound to CCN2 and that the binding of FGFR2 to FGF2 and FGF4 was enhanced by CCN2. CCN2 and FGF2 had a collaborative effect on the phosphorylation of ERK and the differentiation of osteoblastic cells. The present results indicate the biological significance of the binding of CCN2 to FGFR2 in bone metabolism.
Structured summary of protein interactions:
FGFR2 binds to CCN2 by protein array (View interaction)
FGFR1OP binds to CCN2 by protein array (View interaction)
FGFR3 binds to CCN2 by protein array (View interaction) (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

DOI： 10.1016/j.febslet.2012.10.038

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CCN2非依存性モジュールの軟骨再生能力(Cartilage regeneration potential of CCN2 independent modules)

El Kader Tarek Abd, Kubota Satoshi, Nishida Takashi, Hattori Takako, Aoyama Eriko, Janune Danilo, Kuboki Takuo, Takigawa Masaharu

日本再生歯科医学会誌 10 ( 1 ) 50 - 50 2012.12

軟骨組織特異的低密度リポタンパク受容体欠損マウスにおける骨格形成(Deficiency of the low-density lipoprotein receptor related protein 1 (LRP1) in the cartilaginous tissue leads to skeletal dysmorphisms)

河田かずみ, 久保田聡, 服部高子, 青山絵理子, ダニーロ・ジャヌネ, 滝川正春

日本生化学会大会プログラム・講演要旨集 85回 3P - 668 2012.12

Roles of heterotypic CCN2/CTGF-CCN3/NOV and homotypic CCN2-CCN2 interactions in expression of the differentiated phenotype of chondrocytes Reviewed

Hoshijima Mitsuhiro, Hattori Takako, Aoyama Eriko, Nishida Takashi, Yamashiro Takashi, Takigawa Masaharu

FEBS JOURNAL 279 ( 19 ) 3584 - 3597 2012.10

軟骨細胞と骨芽細胞に対するCCN2独立モジュールの影響(Effects of CCN2 independent modules on chondrocytic and osteoblastic cells)

El Kader Tarek Abd, Kubota Satoshi, Nishida Takashi, Hattori Takako, Aoyama Eriko, Janune Danilo, Kuboki Takuo, Takigawa Masaharu

日本骨代謝学会学術集会プログラム抄録集 30回 232 - 232 2012.7

Role of LRP1 in transport of CCN2 protein in chondrocytes. Reviewed

Kawata K, Kubota S, Eguchi T, Aoyama E, Moritani NH, Kondo S, Nishida T, Takigawa M

Journal of cell science 125 ( Pt 12 ) 2965 - 2972 2012.6

Publishing type：Research paper (scientific journal) Publisher：The Company of Biologists

LRP1 is known to be a receptor for signal transmission and endocytosis. We formerly reported that LRP1 regulates WNT/β-catenin and protein kinase C signaling in chondrocytes and represses the hypertrophy of chondrocytes during endochondral ossification, and that LRP1 is co-localized with a ligand, CCN2, which conducts endochondral ossification, on chondrocytes. However, the role of LRP1 in endocytotic transport of CCN2 in chondrocytes is not yet understood. In the present study, we investigated the interaction between LRP1 and CCN2 during endocytotic trafficking.

RNAi-mediated knockdown of LRP1 in chondrocytic HCS-2/8 cells showed that the amount of exogenous CCN2 binding/incorporation was decreased in the LRP1 down-regulated cells. Importantly, we observed that CCN2 internalization in chondrocytes was dependent on clathrin and internalizated CCN2 was co-localized with an early or recycling endosome marker. Transcytosis of CCN2 through HCS-2/8 cells was confirmed by performing experiments with a trans-well apparatus, and the amount of transcytosed CCN2 was decreased by an LRP1 antagonist. These findings rule out possible leakage and confirm the critical involvement of LRP1 during experimental transcytosis. Moreover, under the hypoxic condition mimicking the cartilaginous microenvironment, the production level of LRP1 and the amount of transcytosed CCN2 were increased, which increases were neutralized by the LRP1 antagonist. The distribution of LRP1 and its antagonist in the growth plate in vivo was consistent with that of CCN2 therein, which was produced by and transported from the chondrocytes in the prehypertrophic layer.

These findings suggest that LRP1 mediates the transcytosis of CCN2, which may be a critical event that determines the distribution of CCN2 in cartilage.

DOI： 10.1242/jcs.101956

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Other Link： http://journals.biologists.com/jcs/article-pdf/doi/10.1242/jcs.101956/2043789/jcs101956.pdf

Role of low-density lipoprotein receptor related protein 1 (LRP1) in CCN2/connective tissue growth factor (CTGF) protein transport in chondrocytes

Kawata., K, Kubota, S, Eguchi, T, Aoyama, E, Moritani, N, Kondo, S, Nishida, T, Takigawa, M

J Cell Sci 15 2965 - 2972 2012

Effect of CCN2 on FGF2-Induced Proliferation and MMP9 and MMP13 Productions by Chondrocytes Reviewed

Takashi Nishida, Satoshi Kubota, Eriko Aoyama, Danilo Janune, Azusa Maeda, Masaharu Takigawa

ENDOCRINOLOGY 152 ( 11 ) 4232 - 4241 2011.11

Language：English Publishing type：Research paper (scientific journal) Publisher：ENDOCRINE SOC

CCN2 (also known as connective tissue growth factor) interacts with several growth factors involved in endochondral ossification via its characteristic four modules and modifies the effect of such growth factors. Presently we investigated whether CCN2 interacts with fibroblast growth factor 2 (FGF2). Solid-phase binding assay, immunoprecipitation-Western blot analysis, and surface plasmon resonance (SPR) spectroscopy revealed that the C-terminal module of CCN2 (CT) directly bound to FGF2 with a dissociation constant of 5.5 nM. Next, we examined the combinational effects of CCN2 and FGF2 on the proliferation of and matrix metalloproteinase (MMP)-9 and -13 productions by cultured chondrocytes. FGF2 promoted not only the proliferation but also the production of MMP9 and -13, however, combined of FGF2 with CT module nullified the enhancement of both MMP productions and proliferation. To clarify the mechanism, we investigated the binding of CCN2 or its CT module to FGF receptor 1. As a result, we found that CCN2 bound to FGF receptor 1 with a dissociation constant of 362 nM, whereas the CT module did not. In addition, when we tested FGF signaling in chondrocytic HCS-2/8 cells stimulated by the combination of FGF2 with CT module, the level of ERK1/2, p38 MAPK, and c-Jun N-terminal kinase phosphorylation was decreased compared with that found with FGF2 alone. These findings suggest that CCN2 may regulate the proliferation and matrix degradation of chondrocytes by forming a complex with FGF2 as a novel modulator of FGF2 functions. (Endocrinology 152: 4232-4241, 2011)

DOI： 10.1210/en.2011-0234

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軟骨細胞における血小板由来増殖因子受容体様(PDGFRL)遺伝子の発現(Expression of platelet-derived growth factor receptor-like (PDGFRL) gene in chondrocytes)

河田かずみ, 久保田聡, 江口傑徳, 青山絵理子, 森谷徳文, 岡森彦, 川木晴美, 滝川正春

日本生化学会大会プログラム・講演要旨集 84回 3P - 0351 2011.9

軟骨細胞に対する、CCN2モジュールの単独・結合下での影響に関する評価(Evaluation of independent and combinational effect of CCN2 modules on chondorocytic cells)

El Kdaer Tarek Abd, Kubota Satoshi, Nishida Takashi, Hattori Takako, Aoyama Eriko, Janune Danilo, Kuboki Takuo, Takigawa Masaharu

日本骨代謝学会学術集会プログラム抄録集 29回 248 - 248 2011.7

FGF2刺激による軟骨細胞増殖促進及びMMP13酵素活性上昇に与えるCCN2/CTGFの影響

西田崇, 粕山拓郎, 前田あずさ, 青山絵理子, 久保田聡, 滝川正春

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 83回・33回 1P - 0291 2010.12

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