Collagen Components of Bovine Fetal and Guinea Pig Cochlear Bone and Human Stapes

1988 ◽  
Vol 97 (3) ◽  
pp. 318-321 ◽  
Author(s):  
Thomas M. Chiang ◽  
Taizo Takeda ◽  
T. J. Yoo ◽  
Saryu Dixit ◽  
Tsukasa Ishibe ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Amino Acid ◽  
Guinea Pig ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Immunoblot Assay ◽  
Inner Ear Disease ◽  
Fetal Bovine ◽  
Autoimmune Inner Ear Disease

Collagenous components were isolated chemically from fetal bovine or guinea pig cochlear bone and human stapes after stapedectomy, and the purified protein was characterized by immunoblot assay and amino acid analysis. The results of this study suggest that these are mixtures of type I and type II collagens. The presence of type II collagen in the human stapes also was demonstrated by immunohistologic methods using monoclonal antibody. The presence of type II collagen in these tissues is significant, since it has been postulated as an autoantigen in autoimmune inner ear disease.

Effect of Anti-Inflammatory Drugs on Collagen-Induced Autoimmune Inner Ear Disease

1988 ◽  
Vol 97 (2) ◽  
pp. 153-158 ◽  
Author(s):  
Naohiro Sudo ◽  
T. J. Yoo
Keyword(s):  
Inner Ear ◽  
Type Ii Collagen ◽  
Serum Levels ◽  
Type Ii ◽  
Therapeutic Value ◽  
Inner Ear Disease ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Temporal Bones ◽  
Autoimmune Inner Ear Disease

Animals that had collagen-induced autoimmune inner ear disease were treated with anti-inflammatory drugs: Solu-Medrol (steroid), sulindac (nonsteroid), or a combination of both. Temporal bones from drug-treated animals were examined for histopathologic and immunohistochemical changes, and sera were examined for levels of circulating antibody to type II collagen. Therapy was beneficial to the animals whether the drugs were administered alone or in combination; however, fewer lesions were observed in animals given either drug alone. Further, animals treated with steroid alone showed the least amount of inner ear damage. Immunohistochemical changes and serum levels of antibodies against type II collagen correlated with the pathologic changes. These findings suggest that both steroidal and nonsteroidal anti-inflammatory drugs may have potential therapeutic value in the treatment of autoimmune ear disease.

Type VI collagen expression is upregulated in the early events of chondrocyte differentiation

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 245-251
Author(s):  
R. Quarto ◽  
B. Dozin ◽  
P. Bonaldo ◽  
R. Cancedda ◽  
A. Colombatti
Keyword(s):  
Suspension Culture ◽  
Type I Collagen ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Type Vi Collagen ◽  
Full Spectrum ◽  
Collagen Expression ◽  
Hypertrophic Chondrocyte

Dedifferentiated chondrocytes cultured adherent to the substratum proliferate and synthesize large amounts of type I collagen but when transferred to suspension culture they decrease proliferation, resume the chondrogenic phenotype and the synthesis of type II collagen, and continue their maturation to hypertrophic chondrocyte (Castagnola et al., 1986, J. Cell Biol. 102, 2310–2317). In this report, we describe the developmentally regulated expression of type VI collagen in vitro in differentiating avian chondrocytes. Type VI collagen mRNA is barely detectable in dedifferentiated chondrocytes as long as the attachment to the substratum is maintained, but increases very rapidly upon passage of the cells into suspension culture reaching a peak after 48 hours and declining after 5–6 days of suspension culture. The first evidence of a rise in the mRNA steady-state levels is obtained already at 6 hours for the alpha 3(VI) chain. Immunoprecipitation of metabolically labeled cells with type VI collagen antibodies reveals that the early mRNA rise is paralleled by an increased secretion of type VI collagen in cell media. Induction of type VI collagen is not the consequence of trypsin treatment of dedifferentiated cells since exposure to the actin-disrupting drug cytochalasin or detachment of the cells by mechanical procedures has similar effects. In 13-day-old chicken embryo tibiae, where the full spectrum of the chondrogenic differentiation process is represented, expression of type VI collagen is restricted to the articular cartilage where chondrocytes developmental stage is comparable to stage I (high levels of type II collagen expression).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals TGF-  type I receptor kinase inhibitor down-regulates rheumatoid synoviocytes and prevents the arthritis induced by type II collagen antibody

2006 ◽  
Vol 19 (2) ◽  
pp. 117-126 ◽  
Author(s):  
M. Sakuma ◽  
K. Hatsushika ◽  
K. Koyama ◽  
R. Katoh ◽  
T. Ando ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Receptor Kinase

scholarly journals Autoimmunity to type II collagen an experimental model of arthritis.

1977 ◽  
Vol 146 (3) ◽  
pp. 857-868 ◽  
Author(s):  
D E Trentham ◽  
A S Townes ◽  
A H Kang
Keyword(s):  
Type Ii Collagen ◽  
Intradermal Injection ◽  
Type I ◽  
Type Ii ◽  
Incomplete Freund’S Adjuvant ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant ◽  
Cartilage Proteoglycans ◽  
Bacterial Preparations ◽  
Helical Region

We have found that intradermal injection of native type II collagen extracted from human, chick or rat cartilage induces an inflammatory arthritis in approximately 40% of rats of several strains whether complete Freund's adjuvant or incomplete Freund's adjuvant is used. Type I or III collagen extracted from skin, cartilage proteoglycans and alpha1(II) chains were incapable of eliciting arthritis, as was type II collagen injected without adjuvant. The disease is a chronic proliferative synovitis, resembling adjuvant arthritis in rats and rheumatoid arthritis in humans. Native type II co-lagen modified by limited pepsin digestion still produces arthritis, suggesting that type-specific determinants residing in the helical region of the molecule are responsible for the induction of disease. Since homologous type II collagen emulsified in oil without bacterial preparations regularly causes the disease, this new animal model of arthritis represents a unique example of experimentally-inducible autoimmunity to a tissue component.

In situ hybridization reveals differential spatial distribution of mRNAs for type I and type II collagen in the chick limb bud

Development ◽  
1988 ◽  
Vol 103 (1) ◽  
pp. 111-118 ◽  
Author(s):  
C.J. Devlin ◽  
P.M. Brickell ◽  
E.R. Taylor ◽  
A. Hornbruch ◽  
R.K. Craig ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Limb Development ◽  
Type I Collagen ◽  
Type Ii Collagen ◽  
Limb Bud ◽  
Type I ◽  
Type Ii ◽  
Mrna Accumulation ◽  
Rna Probes

During limb development, type I collagen disappears from the region where cartilage develops and synthesis of type II collagen, which is characteristic of cartilage, begins. In situ hybridization using antisense RNA probes was used to investigate the spatial localization of type I and type II collagen mRNAs. The distribution of the mRNA for type II collagen corresponded well with the pattern of type II collagen synthesis, suggesting control at the level of transcription and mRNA accumulation. In contrast, the pattern of mRNA for type I collagen remained more or less uniform and did not correspond with the synthesis of the protein, suggesting control primarily at the level of translation or of RNA processing.

scholarly journals Brain type I but not type II IL-1 receptors mediate the effects of IL-1β on behavior in mice

1998 ◽  
Vol 274 (3) ◽  
pp. R735-R740 ◽  
Author(s):  
Sandrine Cremona ◽  
Emmanuelle Goujon ◽  
Keith W. Kelley ◽  
Robert Dantzer ◽  
Patricia Parnet
Keyword(s):  
Monoclonal Antibody ◽  
Immune System ◽  
Behavioral Response ◽  
Behavioral Effect ◽  
Behavioral Effects ◽  
Type I ◽  
Type Ii ◽  
Social Exploration ◽  
Neutralizing Monoclonal Antibody ◽  
The Brain

In the immune system, interleukin (IL)-1β effects are mediated by the type I IL-1 receptors (IL-1RI), whereas the type II IL-1 receptors (IL-1RII) act as inhibitory receptors. IL-1RI and IL-1RII are also present in the brain. To study their functionality in the brain, mice were centrally treated with neutralizing monoclonal antibody (MAb) directed against IL-1RI (35F5, 1 μg) or against IL-1RII (4E2, 2 μg) and were centrally injected with recombinant rat IL-1β at a dose (2 ng) that decreased social exploration. Only 35F5 was effective in abrogating the behavioral effect of IL-1β. Moreover, 4E2 (1 μg icv) did not potentiate the behavioral response to a subthreshold dose of IL-1β (1 ng icv). To examine the ability of brain IL-1RI to mediate the effects of endogenous IL-1β, mice were centrally treated with 35F5 (4 μg) and peripherally injected with IL-1β (1 μg). Like IL-1 receptor antagonist (4 μg icv), 35F5 abrogated the effects of IL-1β. These results suggest that brain IL-1RI mediates the behavioral effects of IL-1β in mice.

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