著者

山本 雅久 河原 三明 安孫子 宜光

出版者

公益社団法人 日本口腔インプラント学会

雑誌

日本口腔インプラント学会誌 (ISSN:09146695)

巻号頁・発行日

vol.15, no.3, pp.323-329, 2002-09-30 (Released:2015-08-20)

参考文献数

27

被引用文献数

1

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The recent advent of improved low-level laser irradiation (LLLI) therapy has promoted interest in clinical implantology. It has been reported that LLLI on bony implant sites might have positive effects on the integration of implants. The biostimulatory effect of cell proliferation and bone formation by LLLI has been investigated, but little is known about the molecular basis of biostimulatory mechanisms. Since LLLI will be useful to support implant therapy, it is important to elucidate the mechanism of the biostimulatory effect of LLLI on bone formation. We previously constructed the cDNA library of mouse osteoblastic cells (MC 3 T 3-E 1), which enhanced gene expression by LLLI using a subtracted gene cloning technology. In the present study, we further analyzed the DNA nucleotide sequence of gene clones, and focused on a gene clone designated MCL-174. The nucleotide sequence of MCL-174 insert was determined and assessed in the standard nucleotide-nucleotide BLAST (blastn) homology-search using NCBI DNA databases. DNA nucleotide sequences of clone MCL-174 inserted DNA exhibited 99% homology with Mus musculus annexin Ⅲ gene. Reverse-transcription PCR analysis showed that the mRNA level was enhanced by LLLI. These findings suggest that LLLI may enhance mRNA transcription and play a role in stimulating proliferation of osteoblasts through the enhancement of annexin Ⅲ gene expression. Annexin Ⅲ was detected in secretory ameloblasts and odontoblasts, and it was thought to be involved in the regulation of cell calcium. These findings suggest that the biostimulatory effect of LLLI on bone formation may relate through gene expression of annexin Ⅲ.

著者

三俣 昌子 江角 眞理子 楠美 嘉晃 安孫子 宜光 東 浩介

出版者

日本大学

雑誌

基盤研究(C)

巻号頁・発行日

2008

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第一に血流下における内皮の増殖と粥状硬化発症の関連を検討した。層流性ずり応力に比べ乱流性ずり応力は内皮の増殖と単球接着を増加させた。内皮の増殖を抑制するp21^<Sdi/Cip/Waf1>(p21)は乱流による単球接着増加、内皮のTXNIP,VCAM-1,CCL5,CXCL10,L-selectin発現を抑制した。血流下でp21は単独で、または内皮の増殖抑制を介して、内皮のレドックスバランスを抗酸化状態へ導き、接着や遊走因子発現を阻止し、単球接着を抑制して抗粥状硬化性に作用すると思われる。第二に、粥状硬化発症への歯周病菌(Pg)の関与を検討した。ヒト大動脈のAtheromaのマクロファージにPg由来r40kDa蛋白が存在し、Fatty streak,DIT、冠動脈のAtheromaには認めなかった。Pg由来LPSで刺激した単球の培養上清は内皮のTLR2 mRNAを発現させ好炎症性に作用した。