scholarly journals myc and src oncogenes have complementary effects on cell proliferation and expression of specific extracellular matrix components in definitive chondroblasts.

1985 ◽  
Vol 5 (3) ◽  
pp. 538-544 ◽  
Author(s):  
S Alema ◽  
F Tato ◽  
D Boettiger
Keyword(s):  
Cell Proliferation ◽  
Neoplastic Transformation ◽  
Type Ii Collagen ◽  
Proliferative Potential ◽  
Type Ii ◽  
Proliferative Capacity ◽  
Myc Oncogene ◽  
Viral Oncogenes ◽  
Extracellular Matrix Components ◽  
Infected Cells

The effects of the avian viral oncogenes src and myc were compared for their ability to alter the differentiated phenotype and the proliferative capacity of definitive chondroblasts. As previously demonstrated, viruses carrying the src oncogene suppressed the synthesis of the chondroblast-specific products, type II collagen and cartilage-specific sulfated proteoglycan. In contrast, infection with MC29 and HB1 viruses, which carry the myc oncogene, did not suppress the synthesis of these normal differentiated cell products, but the infected cells exhibited an increased proliferative potential. The MH2 virus, which carries both the myc and mil oncogenes, both induced the suppression of these chondroblast-specific products and increased cell proliferation. The implications of these results for cooperation between oncogenes and the multi-oncogene models for neoplastic transformation are discussed.

myc and src oncogenes have complementary effects on cell proliferation and expression of specific extracellular matrix components in definitive chondroblasts

1985 ◽  
Vol 5 (3) ◽  
pp. 538-544
Author(s):  
S Alema ◽  
F Tato ◽  
D Boettiger
Keyword(s):  
Cell Proliferation ◽  
Neoplastic Transformation ◽  
Type Ii Collagen ◽  
Proliferative Potential ◽  
Type Ii ◽  
Proliferative Capacity ◽  
Myc Oncogene ◽  
Viral Oncogenes ◽  
Extracellular Matrix Components ◽  
Infected Cells

The effects of the avian viral oncogenes src and myc were compared for their ability to alter the differentiated phenotype and the proliferative capacity of definitive chondroblasts. As previously demonstrated, viruses carrying the src oncogene suppressed the synthesis of the chondroblast-specific products, type II collagen and cartilage-specific sulfated proteoglycan. In contrast, infection with MC29 and HB1 viruses, which carry the myc oncogene, did not suppress the synthesis of these normal differentiated cell products, but the infected cells exhibited an increased proliferative potential. The MH2 virus, which carries both the myc and mil oncogenes, both induced the suppression of these chondroblast-specific products and increased cell proliferation. The implications of these results for cooperation between oncogenes and the multi-oncogene models for neoplastic transformation are discussed.

Effects of bio-mimic collagen II-g-hyaluronic acid copolymers on chondrocyte maintenance

2019 ◽  
Vol 34 (4-5) ◽  
pp. 373-385
Author(s):  
Kuan Wei Lee ◽  
Tang-Ching Kuan ◽  
Ming Wei Lee ◽  
Chen Show Yang ◽  
Lain-Chyr Hwang ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Hyaluronic Acid ◽  
Specific Binding ◽  
Type Ii Collagen ◽  
Polymerase Chain Reaction Analysis ◽  
Collagen Fibrils ◽  
Type Ii ◽  
Human Cartilage

Extracellular matrix has an important part of the role in tissue engineering and regenerative medicine, so it is necessary to understand the various interactions between cells and extracellular matrix. Type II collagen and hyaluronic acid are the major structural components of the extracellular matrix of articular cartilage, and they are involved in fibril formation, entanglement and binding. The aim of this study was to prepare type II collagen fibrils with surface grafted with hyaluronic acid modified at the reducing end. The topographic pattern of type II collagen fibrils showed a significant change after the surface coupling of hyaluronic acid according to atomic force microscopy scanning. The presence of hyaluronic acid on the type II collagen fibrillar surface was confirmed by the specific binding of nanogold labelled with lectin. No significant increase in cell proliferation was detected by a WST-1 assay. According to histochemical examination, the maintenance of the round shape of chondrocytes and increased glycosaminoglycan secretion revealed that these cell pellets with Col II- g-hyaluronic acid molecules contained un-dedifferentiated chondrocytes in vitro. In the mixture with the 220-kDa Col II- g-hyaluronic acid copolymer, the expression of type II collagen and aggrecan genes in chondrocytes increased as demonstrated by real-time polymerase chain reaction analysis. Experimental results show that the amount of hyaluronic acid added during culturing of chondrocytes can maintain the functionality of chondrocytes and thus allow for increased cell proliferation that is suitable for tissue repair of human cartilage.

scholarly journals Aqueous extract of Arctium lappa L. root (burdock) enhances chondrogenesis in human bone marrow-derived mesenchymal stem cells

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
King-Chuen Wu ◽  
Hung-Kai Weng ◽  
Yun-Shang Hsu ◽  
Pin-Jia Huang ◽  
Yang-Kao Wang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Aqueous Extract ◽  
Chondrogenic Differentiation ◽  
Type Ii Collagen ◽  
Induction Medium ◽  
Type Ii ◽  
Arctium Lappa

Abstract Background Arctium lappa L. root (burdock root) has long been recommended for the treatment of different diseases in traditional Chinese medicine. Burdock root possesses anti-oxidative, anti-inflammatory, anti-cancer, and anti-microbial activities. The aim of the study was to elucidate whether aqueous extract of burdock root regulates mesenchymal stem cell proliferation and differentiation. Methods Human bone marrow-derived mesenchymal stem cells in 2D high density culture and in 3D micromass pellets were treated with chondrogenic induction medium and chondral basal medium in the absence or presence of aqueous extract of burdock root. The chondrogenic differentiation was accessed by staining glucosaminoglycans, immunostaining SOX9 and type II collagen and immuonblotting of SOX9, aggrecan and type II collagen. Results Treatment of aqueous extract of burdock root increased the cell proliferation of hMSCs. It did not have significant effect on osteogenic and adipogenic differentiation, but significantly enhanced chondrogenic induction medium-induced chondrogenesis. The increment was dose dependent, as examined by staining glucosaminoglycans, SOX9, and type II collagen and immunobloting of SOX9, aggrecan and type II collagen in 2D and 3D cultures. In the presence of supplemental materials, burdock root aqueous extract showed equivalent chondrogenic induction capability to that of TGF-β. Conclusions The results demonstrate that aqueous extract of Arctium lappa L. root promotes chondrogenic medium-induced chondrogenic differentiation. The aqueous extract of burdock root can even be used alone to stimulate chondrogenic differentiation. The study suggests that the aqueous extract of burdock root can be used as an alternative strategy for treatment purposes.

scholarly journals Functional Lateral Shift of the Mandible Effects on the Expression of ECM in Rat Temporomandibular Cartilage

2009 ◽  
Vol 79 (4) ◽  
pp. 652-659 ◽  
Author(s):  
Tanapan Wattanachai ◽  
Ikuo Yonemitsu ◽  
Sawa Kaneko ◽  
Kunimichi Soma
Keyword(s):  
Extracellular Matrix ◽  
Experimental Period ◽  
Type Ii Collagen ◽  
Lateral Shift ◽  
Control Group ◽  
Type Ii ◽  
Early Puberty ◽  
Condylar Cartilage ◽  
Cartilage Extracellular Matrix ◽  
Extracellular Matrix Components

Abstract Objective: To test the hypothesis that the effects of mechanical stress from a functional lateral shift of the mandible have no effect on the expression of two main condylar cartilage extracellular matrix components, type II collagen and aggrecan, in rats from early puberty to young adulthood. Materials and Methods: Functional lateral shift of the mandible was induced in experimental groups of 5-week-old male Wistar rats, using guiding appliances. The rats were sacrificed at 3, 7, 14, and 28 days post appliance attachment. The condyles were immunohistochemically evaluated for type II collagen and aggrecan (the immunoreactive areas were quantified). Results: As compared with the control group, on the contralateral condyles, the immunoreactivity of the experimental groups was significantly increased from 7 to 14 days. While on the ipsilateral condyles, the immunoreactive areas were significantly decreased throughout the experimental period. Conclusion: A functional lateral shift of the mandible modulated the condylar cartilage extracellular matrix differently on each side of the condyle, which affected condylar morphology, growth, biomechanical properties, and even the susceptibility of the condylar cartilage to pathogenesis.

scholarly journals Differential localization of mRNAs of collagen types I and II in chick fibroblasts, chondrocytes, and corneal cells by in situ hybridization using cDNA probes.

1986 ◽  
Vol 102 (6) ◽  
pp. 2302-2309 ◽  
Author(s):  
M Hayashi ◽  
Y Ninomiya ◽  
J Parsons ◽  
K Hayashi ◽  
B R Olsen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Situ Hybridization ◽  
Epithelial Cells ◽  
Type Ii Collagen ◽  
Type I ◽  
Type Ii ◽  
Collagen Types ◽  
Paraffin Sections ◽  
Extracellular Matrix Components

We have employed a highly specific in situ hybridization protocol that allows differential detection of mRNAs of collagen types I and II in paraffin sections from chick embryo tissues. All probes were cDNA restriction fragments encoding portions of the C-propeptide region of the pro alpha-chain, and some of the fragments also encoded the 3'-untranslated region of mRNAs of either type I or type II collagen. Smears of tendon fibroblasts and those of sternal chondrocytes from 17-d-old chick embryos as well as paraffin sections of 10-d-old whole embryos and of the cornea of 6.5-d-old embryos were hybridized with 3H-labeled probes for either type I or type II collagen mRNA. Autoradiographs revealed that the labeling was prominent in tendon fibroblasts with the type I collagen probe and in sternal chondrocytes with the type II collagen probe; that in the cartilage of sclera and limbs from 10-d-old embryos, the type I probe showed strong labeling of fibroblast sheets surrounding the cartilage and of a few chondrocytes in the cartilage, whereas the type II probe labeled chondrocytes intensely and only a few fibroblasts; and that in the cornea of 6.5-d-old embryos, the type I probe labeled the epithelial cells and fibroblasts in the stroma heavily, and the endothelial cells slightly, whereas the type II probe labeled almost exclusively the epithelial cells except for a slight labeling in the endothelial cells. These data indicate that embryonic tissues express these two collagen genes separately and/or simultaneously and offer new approaches to the study of the cellular regulation of extracellular matrix components.

scholarly journals Down-regulation of microRNA-216b inhibits IL-1β-induced chondrocyte injury by up-regulation of Smad3

2017 ◽  
Vol 37 (2) ◽  
Author(s):  
Jiye He ◽  
Jiahong Zhang ◽  
Dongliang Wang
Keyword(s):  
Cell Proliferation ◽  
Type Ii Collagen ◽  
Joint Disease ◽  
Luciferase Reporter ◽  
Type Ii ◽  
Articular Chondrocyte ◽  
Down Regulation ◽  
Protein Levels ◽  
Normal Tissues ◽  
Smad3 Expression

Osteoarthritis (OA) is the most common type of joint disease, leading to a major cause of pain and disability. OA is characterized by the continuous degradation of articular cartilage, mainly resulting in an imbalance between synthesis and degradation of articular chondrocyte extracellular matrix (ECM). Aberrant miR-216b expression has been found in multiple cancers. However, the level of miR-216b in OA cartilage and its role in progression of this disease are still unknown. In the present study, the functional roles of miR-216b and its expression in OA tissues and interleukin-1β (IL-1β)-induced chondrocytes were examined. We found that the level of miR-216b was significantly higher and Smad3 expression was obviously lower in OA cartilage and IL-1β-induced chondrocytes than in normal tissues and cells. Furthermore, a bioinformatics analysis and luciferase reporter assay identified Smad3 as a direct target gene of miR-216b, and Smad3 expression was reduced by miR-216b overexpression at both the mRNA and protein levels. A functional analysis demonstrated that miR-216b down-regulation obviously alleviated the IL-1β-induced inhibition in cell proliferation, type II collagen, and aggrecan down-regulation and matrix metalloproteinase-13 (MMP-13) up-regulation, while miR-216b overexpression had the opposite effects. Knockdown of Smad3 by siRNA reversed the effects of the miR-216b inhibitor on cell proliferation, the expressions of type II collagen, aggrecan, and MMP-13. Our results suggested that miR-216b contributes to progression of OA by directly targeting Smad3, providing a potential therapeutic target for treatment of OA.

Sign in / Sign up

Export Citation Format

Share Document