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1.
Osteoarthritis Cartilage ; 18(1): 88-96, 2010 Jan.
Article in English | MEDLINE | ID: mdl-19932218

ABSTRACT

OBJECTIVE: To characterize the in vivo role epiphycan (Epn) has in cartilage development and/or maintenance. METHODS: Epn-deficient mice were generated by disrupting the Epn gene in mouse embryonic stem cells. Epn/biglycan (Bgn) double-deficient mice were produced by crossing Epn-deficient mice with Bgn-deficient mice. Whole knee joint histological sections were stained using van Gieson or Fast green/Safranin-O to analyze collagen or proteoglycan content, respectively. Microarray analysis was performed to detect gene expression changes within knee joints. RESULTS: Epn-deficient and Epn/Bgn double-deficient mice appeared normal at birth. No significant difference in body weight or femur length was detected in any animal at 1 month of age. However, 9-month Epn/Bgn double-deficient mice were significantly lighter and had shorter femurs than wild type mice, regardless of gender. Male Epn-deficient mice also had significantly shorter femurs than wild type mice at 9 months. Most of the deficient animals developed osteoarthritis (OA) with age; the onset of OA was observed earliest in Epn/Bgn double-deficient mice. Message RNA isolated from Epn/Bgn double-deficient knee joints displayed increased matrix protein expression compared with wild type mice, including other small leucine-rich proteoglycan (SLRP) members such as asporin, fibromodulin and lumican. CONCLUSION: Similar to other previously studied SLRPs, EPN plays an important role in maintaining joint integrity. However, the severity of the OA phenotype in the Epn/Bgn double-deficient mouse suggests a synergy between these two proteins. These data are the first to show a genetic interaction involving class I and class III SLRPs in vivo.


Subject(s)
Knee Joint/chemistry , Osteoarthritis, Knee/physiopathology , Proteoglycans/analysis , Proteoglycans/deficiency , Animals , Blotting, Southern , Body Weight , Collagen/analysis , Femur/anatomy & histology , Immunohistochemistry , Knee Joint/pathology , Mice , Mice, Knockout , Microarray Analysis , Osteoarthritis, Knee/genetics , Phenotype , Polymerase Chain Reaction , Proteoglycans/genetics , RNA, Messenger/analysis
2.
Jpn J Clin Oncol ; 31(3): 122-4, 2001 Mar.
Article in English | MEDLINE | ID: mdl-11336325

ABSTRACT

We report a case of extravasation of an antitumor agent by preoperative magnetic resonance (MR) imaging. MR studies demonstrated a decreased signal intensity on T1- and T2-weighted images and a strong enhancement of contrast media in injured tissue, including subcutaneous adipose tissue and deep fascia, which was cicatrical macroscopically. The MR findings were in good agreement with the macroscopic findings. We believe that MR imaging is useful for estimating deep tissue damage due to extravasation of an antitumor agent.


Subject(s)
Antibiotics, Antineoplastic/adverse effects , Debridement , Extravasation of Diagnostic and Therapeutic Materials/diagnosis , Extravasation of Diagnostic and Therapeutic Materials/surgery , Magnetic Resonance Imaging , Mitomycin/adverse effects , Adipose Tissue/surgery , Aged , Female , Humans , Rectal Neoplasms/drug therapy
3.
Cell Struct Funct ; 22(1): 27-32, 1997 Feb.
Article in English | MEDLINE | ID: mdl-9113387

ABSTRACT

We have recently established a human osteoblastic cell line (SV-HFO) in a culture system, in which the cells are mineralized by treatment with dexamethasone (Dex). Using this system, we examined the effects of all trans-retinoic acid (RA) on the mineralization of the cells. RA inhibited the mineralization, coincident with the inhibition of alkaline phosphatase (ALP). On the other hand, RA induced osteocalcin secretion and had no effect on the expression of the other osteoblastic markers such as type I collagen and osteonectin. To further clarify the mechanism of inhibition of mineralization by RA, we used the retinoic acid receptor (RAR) alpha-selective (Am80), beta-selective (CD2019) and gamma-selective (CD437) agonists instead of RA. RAR alpha- and RAR beta-selective agonists inhibited the mineralization and ALP activity of the cells, while the RAR gamma-selective agonist had no such effects. On the other hand, the RAR gamma-selective agonist induced osteocalcin secretion, but RAR alpha- and RAR beta-selective agonists had no effect on osteocalcin secretion. These results suggested that the inhibitory effect of RA on the mineralization of human osteoblasts is mediated by the activation of RAR alpha and/or RAR beta and that RAR gamma preferentially regulates the expression of osteocalcin without influence on mineralization.


Subject(s)
Alkaline Phosphatase/antagonists & inhibitors , Calcification, Physiologic/drug effects , Dexamethasone/pharmacology , Enzyme Inhibitors/pharmacology , Osteoblasts/metabolism , Tretinoin/pharmacology , Benzoates/pharmacology , Biomarkers , Cell Line , Humans , Naphthalenes/pharmacology , Osteocalcin/metabolism , Receptors, Retinoic Acid/metabolism , Retinoic Acid Receptor alpha , Retinoids/pharmacology , Teratogens/pharmacology , Tetrahydronaphthalenes/pharmacology , Retinoic Acid Receptor gamma
4.
Bone ; 19(4): 363-9, 1996 Oct.
Article in English | MEDLINE | ID: mdl-8894142

ABSTRACT

A human osteoblastic cell line (SV-HFO) established in our laboratory expresses osteoblastic markers, including mineralization in vitro, in response to differentiation-inducing agents such as dexamethasone. In this study, we examined the effects of transforming growth factor beta 1 (TGF-beta 1) on the mineralization of SV-HFO cells and show that TGF-beta 1 inhibited the mineralization of the cells via down regulation of tetranectin and alkaline phosphatase without influencing other osteoblastic markers. To examine precisely the effects of TGF-beta 1 on the process of mineralization, we tentatively divided the whole process of mineralization into four phases: induced ALP activity (days 0-5), maximal ALP activity (days 5-10), early mineralization (days 10-15), and progressive mineralization (days 15-20). These inhibitory effects of TGF-beta 1 on the expression of tetranectin and alkaline phosphatase, like that on mineralization, were observed only when TGF-beta 1 was applied in the early phase of the process of mineralization. On the other hand, the other osteoblastic markers were not influenced by treatment with TGF-beta 1. These results suggest that TGF-beta 1 may inhibit mineralization of osteoblasts by the downregulation of tetranectin and alkaline phosphatase expression in the early phase. Thus, TGF-beta 1 has phase-dependent effects on a human osteoblastic cell line during the process of mineralization.


Subject(s)
Biomarkers, Tumor/biosynthesis , Lectins, C-Type , Osteoblasts/drug effects , Transforming Growth Factor beta/pharmacology , Alkaline Phosphatase/biosynthesis , Alkaline Phosphatase/genetics , Biomarkers, Tumor/genetics , Blood Proteins/biosynthesis , Blood Proteins/genetics , Blotting, Northern , Blotting, Western , Calcification, Physiologic/drug effects , Calcification, Physiologic/physiology , Calcium/metabolism , Cell Line , Cells, Cultured , Gene Expression Regulation/drug effects , Gene Expression Regulation/genetics , Humans , Molecular Weight , Osteoblasts/cytology , Osteoblasts/enzymology , Osteoblasts/metabolism , Osteocalcin/biosynthesis , Osteonectin/biosynthesis , Osteopontin , Phosphorus/metabolism , RNA, Messenger/metabolism , Sialoglycoproteins/biosynthesis , Transcription, Genetic/drug effects , Transcription, Genetic/genetics
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