Author Saiga, Kenta| Furumatsu, Takayuki| Yoshida, Aki| Masuda, Shin| Takihira, Shota| Abe, Nobuhiro| Ozaki, Toshifumi|
Published Date 2010-11-12
Publication Title Biochemical and Biophysical Research Communications
Volume volume402
Issue issue2
Content Type Journal Article
Author Miyake, Yoshiaki| Furumatsu, Takayuki| Kubota, Satoshi| Kawata, Kazumi| Ozaki, Toshifumi| Takigawa, Masaharu|
Published Date 2011-06-03
Publication Title Biochemical and Biophysical Research Communications
Volume volume409
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/41320
FullText URL 64_6_351.pdf
Author Furumatsu, Takayuki| Asahara, Hiroshi|
Abstract Chondrocyte differentiation is the fundamental process in skeletal development. From the mesenchymal condensation of chondroprogenitors to the hypertrophic maturation of chondrocytes, chondrogenesis is sequentially regulated by cross-talk among transcription factors, growth factors, and chromatin structure. The master transcription factor Sry-type HMG box (Sox) 9 has an essential role in the expression of chondrogenic genes through the association with Sox9-binding sites on its target genes. Several transcription factors and coactivators, such as Scleraxis/E47 and p300, cooperatively modulate the Sox9-dependent transcription by interacting with Sox9. The Sox9-related transcriptional apparatus activates its target gene expression through p300-mediated histone acetylation on chromatin. The transforming growth factor (TGF)-β superfamily also plays a key role in chondrocyte differentiation. The TGF-β-regulated Smad3/4 complex activates Sox9-dependent transcription on chromatin by associating with Sox9 itself, and by recruiting p300 onto Sox9. These findings suggest that the epigenetic status including histone modification and chromatin structure, directly influences Sox9-regulated chondrocyte differentiation. In this article, we review the regulators of Sox9 expression itself, modulators of posttranslational Sox9 function, and Sox9-associating factors in the Sox9-dependent epigenetic regulation during chondrogenesis.
Keywords Sox9 TGF-β-Smad3 coactivator p300 scleraxis/E47 chondrogenesis
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2010-12
Volume volume64
Issue issue6
Publisher Okayama University Medical School
Start Page 351
End Page 357
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21173804
Web of Science KeyUT 000285664200001
Author Furumatsu, Takayuki| Ozaki, Toshifumi| Asahara, Hiroshi|
Published Date 2010-08-02
Publication Title 岡山医学会雑誌
Volume volume122
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/40007
FullText URL fulltext.pdf
Author Furumatsu, Takayuki| Ozaki, Toshifumi|
Abstract Epigenetics is an essential mechanism to control gene expression and fundamental cellular processes. DNA methylation in CpG-rich promoters correlates with gene silencing. Histone modification including histone acetylation and deacetylation determines the stability of the chromatin structure. Condensed chromatin (heterochromatin), which has a higher-order histone-DNA structure, prevents the access of transcriptional activators to their target genes. The fundamental unit of eukaryotic chromatin consists of 146 bp of DNA wrapped around a histone octamer. Posttranslational modifications of the histone tail and the chromatin remodeling complex disrupt histone-DNA contacts and induce nucleosome mobilization. Histone acetylation of specific lysine residues in the histone tail plays a crucial role in epigenetic regulation. Histone acetylation is a dynamic process regulated by the antagonistic actions of 2 families of enzymes - the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). The balance between histone acetylation and deacetylation serves as a key epigenetic mechanism for transcription factor-dependent gene expression and the developmental process. We review emerging evidence that DNA methylation, histone acetylation modified by HAT and/or HDAC, and transcription factor-associated molecules contribute to a mechanism that can alter chromatin structure, gene expression, and cellular differentiation during chondrogenesis.
Keywords epigenetics DNA methylation histone acetylation and HAT histone deacetylation and HDAC chondrogenesis
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2010-06
Volume volume64
Issue issue3
Publisher Okayama University Medical School
Start Page 155
End Page 161
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 20596126
Web of Science KeyUT 000279094300001
JaLCDOI 10.18926/AMO/32013
FullText URL fulltext.pdf
Author Ohzawa, Seiya| Takahara, Yasuhiro| Furumatsu, Takayuki| Inoue, Hajime|
Abstract

The authors analyzed the 5-year and 9-year survival in 134 of 165 patients who underwent total knee arthroplasties from 1989 to 1996 in our department. Patients were followed until December 31, 1998, or until the time of death. Diagnoses were rheumatoid arthritis in 81 patients (132 knees) and osteoarthritis in 53 patients (79 knees). The survival of the patients was compared to that of the age- and sex-adjusted general population. Kaplan-Meier survival curves were constructed. Twenty-two patients in the study died before the end of the follow-up. The cumulative 5-year patient survival was 88.7%, and 9-year patient survival was 64.4% for total knee arthroplasty patients. The standardized mortality ratio was 0.11 (95% confidence interval: 0.02-0.40) for the patients with osteoarthritis, and 0.81 (95% confidence interval: 0.52-1.25) for the patients with rheumatoid arthritis. The Cox proportional hazards model showed that the factors of male sex and rheumatoid arthritis were related to a higher mortality rate in the total knee arthroplasty group.

Keywords total knee authroplasy patient survival rheumatoid arthritis
Amo Type Article
Publication Title Acta Medica Okayama
Published Date 2001-11
Volume volume55
Issue issue5
Publisher Okayama University Medical School
Start Page 295
End Page 299
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
File Version publisher
Refereed True
PubMed ID 11688953
Web of Science KeyUT 000171635400006
JaLCDOI 10.18926/AMO/30974
FullText URL fulltext.pdf
Author Ikuma, Hisanori| Abe, Nobuhiro| Uchida, Youichiro| Furumatsu, Takayuki| Fujiwara, Kazuo| Nishida, Keiichiro| Ozaki, Toshifumi|
Abstract

Instability of the knee after the medial collateral ligament (MCL) injury is usually assessed with the manual valgus stress test, even though, in recent years, it has become possible to apply magnetic resonance imaging (MRI) to the assessment of the damage of the ligament. The valgus instability of 24 patients (12 isolated injuries and 12 multiple ligament injuries) who suffered MCL injury between 1993 and 1998 was evaluated with the Hughston and Eilers classification, which involves radiographic assessment under manual valgus stress to the injured knees. We developed a novel system for classifying the degree of injury to the MCL by calculating the percentage of injured area based on MRI and investigated the relationship between this novel MRI classification and the magnitude of valgus instability by the Hughston and Eilers classification. There was a significant correlation between the 2 classifications (p=0.0006). On the other hand, the results using other MRI based classification systems, such as the Mink and Deutsch classificaiton and the Petermann classification, were not correlated with the findings by the Hughston and Eilers classification in these cases (p0.05). Since MRI is capable of assessing the injured ligament in clinical practice, this novel classification system would be useful for evaluating the stability of the knee and choosing an appropriate treatment following MCL injury.

Keywords medial collateral ligament magnetic resonance imaging knee instability novel method
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2008-06
Volume volume62
Issue issue3
Publisher Okayama University Medical School
Start Page 185
End Page 191
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
File Version publisher
Refereed True
PubMed ID 18596835
Web of Science KeyUT 000257130300006
FullText URL K002286.pdf
Author 古松 毅之|
Published Date 2002-03-25
Content Type Thesis or Dissertation
Grant Number 甲第2286号
Granted Date 2002-03-25
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language Japanese