Detection of vascular endothelial growth factor (VEGF) in moderate osteoarthritis in a rabbit model

Jansen, H.; Meffert, Rainer H.; Birkenfeld, Falk; Petersen, Wolf

doi:10.1016/j.aanat.2012.01.006

Cited by 39 publications

(31 citation statements)

References 21 publications

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“…1B) was unexpected. Lafont et al (2008) earlier reported a rather moderate, approximately 3-fold induction, of this gene, which may be an underestimation due to their microarray-based analysis or result from the fact that these authors analyzed healthy human chondrocytes from osteosarcomas, since VEGF expression is known to be higher in OA (Jansen et al, 2012). The fold-change of GDF10 and COX-2 expression in the present study is in nice agreement with earlier reported QPCR data (Lafont et al, 2008).…”

Section: Discussionsupporting

confidence: 94%

TGF-β2 is involved in the preservation of the chondrocyte phenotype under hypoxic conditions

Das

Timur

Edip

et al. 2015

Annals of Anatomy - Anatomischer Anzeiger

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Section: Discussionsupporting

confidence: 94%

TGF-β2 is involved in the preservation of the chondrocyte phenotype under hypoxic conditions

Das

Timur

Edip

et al. 2015

Annals of Anatomy - Anatomischer Anzeiger

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“…It is speculated that due to the effect of the abnormal stress, the blood vessel can break through the calcified cartilage and tidemark and damage the microenvironment of articular cartilage independent from the subchondral bone (10). On the other hand, the intravascular cells can secrete various factors and cause damage on the chondrocyte normal physiological functions (11). Further, the vascular invasion is also a physical disruption for the normal arrangement of the chondrocyte and collagen fibers (12).…”

Section: Discussionmentioning

confidence: 99%

Significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis

Liu¹,

Dai²,

Wang³

et al. 2017

Experimental and Therapeutic Medicine

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We studied the significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis (TMJOA). Fifteen 8-week-old female Sprague-Dawley rats were selected to establish TMJOA models of gradually induced occlusal disorders. Five rats were sacrificed at 4, 8 and 16 weeks, and histological exam was conducted along with micro-computed tomography observation on the condyle specimen. The distribution and number of new blood vessels breaking were observed through the tidemark through CD34 immunofluorescence staining. The proliferation of chondrocytes were detected through Ki67 immunohistochemical staining, and the differentiation functions of chondrocytes were observed through PTHrP and IHH immunohistochemical staining. The degradation functions of cartilage matrix were observed through matrix metalloproteinase (MMP)-9 immunohistochemical staining to detect the expression of vascular growth promotion and inhibition factors with vascular endothelial growth factor (VEGF), CTGF and CHM-1 immunohistochemical staining and screen differentially expressed genes through gene chip analysis method. It was found that the condyle tissue full thickness, fiber layer thickness and calcified cartilage layer thickness were significantly increased with time (P<0.05). Bone mineral density, trabecular thickness and Tb.Sp were also increased significantly with time, BS/BV and trabecular number were decreased significantly with time (P<0.05). The new blood vessels reached the deep layer of calcified cartilage until the tide line was broken and non-calcified cartilage was invaded. The number of vessels were increased significantly with time (P<0.05). Ki67, PTHrP and IHH-positive rates were increased significantly (P<0.05). MMP-9, VEGF, CTGF and CHM-1 were increased significantly (P<0.05). VEGF, CTGF and CHM-1 mRNA were upregulated differentially with the expressed genes. In conclusion, the new blood vessels may be important in the pathogenesis of TMJOA.

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“…Its pathological phenotypes include articular cartilage impairment, subchondral bone sclerosis, bone resorption/formation imbalance, osteophyte formation, and inflammation of the synovial membrane12. Its symptoms include pain, stiffness and swelling of involved joints, and muscle weakness.…”

mentioning

confidence: 99%

Epigenetic modifications of interleukin-6 in synovial fibroblasts from osteoarthritis patients

Yang

Zhou

Wang

et al. 2017

Sci Rep

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Osteoarthritis (OA) is the most common degenerative disease of the synovial joint. The synovial membrane is responsible for the inflammatory reaction leading to the secretion of macrophage-derived pro-inflammatory cytokines, such as IL-6. Suppressing IL-6 over-expression in synovial fibroblasts (SF) is a promising method to prevent OA development and progression, in which the prerequisite is the elucidation of the molecular mechanisms underlying IL-6 over-expression in SF. Currently, there are few reports concerning epigenetic modifications in IL-6 in OA SF. In the present study, we attempted to investigate this phenomenon. SF over-expressing IL-6 was collected from OA patients. DNA hypomethylation and histone hyperacetylation were observed in the IL-6 promoter regions in OA SF compared with normal SF. No differences in the status of H3K9 di-methylation, H3K27 tri-methylation and H3K4 tri-methylation were observed in the IL-6 promoter regions between normal and OA SF. DNA (cytosine-5-)-methyltransferase 3 alpha (Dnmt3a) overexpression and anacardic acid (histone acetyltransferase inhibitor) treatment increased DNA methylation and decreased histone acetylation in the IL-6 promoter, and IL-6 over-expression in OA SF was suppressed. These observations provide deeper insight into the pathogenesis of OA and can be used to design new drugs and develop new therapeutic methods to treat OA.

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Detection of vascular endothelial growth factor (VEGF) in moderate osteoarthritis in a rabbit model

Cited by 39 publications

References 21 publications

TGF-β2 is involved in the preservation of the chondrocyte phenotype under hypoxic conditions

TGF-β2 is involved in the preservation of the chondrocyte phenotype under hypoxic conditions

Significance of new blood vessels in the pathogenesis of temporomandibular joint osteoarthritis

Epigenetic modifications of interleukin-6 in synovial fibroblasts from osteoarthritis patients

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