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Walsh, David A.; Pearson, C. I.

doi:10.1186/ar292

Cited by 140 publications

(42 citation statements)

References 53 publications

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“…The increase of neoangiogeneses besides stimulating the repair process may also contribute to thickening and disorganization of the tendon [34]. The VEGF signals enhance the expression of matrix metalloproteinase (MMP) and reduce the tissue inhibitor metalloproteinase leading to a weakening of the normal tendon structure, decrease of the mechanical strain, and consequently the spontaneous rupture [13].…”

Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Receptor-2 Polymorphisms Have Protective Effect against the Development of Tendinopathy in Volleyball Athletes

et al. 2016

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The aim of the study was to investigate whether genetic variants in VEGF and KDR genes can be correlated with susceptibility of tendinopathy in volleyball athletes. This study was conducted at the Brazilian Volleyball Federation, and comprised 179 volleyball athletes: 88 had a confirmed diagnosis of tendinopathy (cases), whereas 91 had no evidence of the disease (controls). The VEGF (-2578C>A, -460T>C and +936C>T) and KDR (-604C>T, 1192G>A and 1719T>A) polymorphisms were determined by TaqMan real-time polymerase chain reaction. The odds ratio (OR) with their 95% confidence intervals (CI) were calculated using an unconditional logistic regression model. The evaluation of demographic and clinical characteristics revealed the athlete age (P < 0.001), years of practice in volleyball (P < 0.001) and presence of pain (P = 0.001) were risk factors for tendinopathy. KDR 1192 GA and GA + AA genotypes were associated with lower risk of tendinopathy (OR: 0.41, 95% CI: 0.19–0.88 and OR: 0.47, 95% CI: 0.23–0.98, respectively). The KDR (-604C>T, 1192G>A and 1719T>A) haplotypes CGA and CAT were associated with decreased tendinopathy risk (OR: 0.46, 95% CI: 0.21–0.99 and OR: 0.23, 95% CI: 0.07–0.76, respectively). With regards to pain, traumatic lesion and away from training due to injury, VEGF and KDR polymorphisms were not associated with clinical symptoms complaints. The present results provide evidence that the KDR polymorphisms were associated with development of tendinopathy, and can contribute to identify new therapeutic targets or personalized training programs to avoid tendinopathy development in athletes.

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Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Receptor-2 Polymorphisms Have Protective Effect against the Development of Tendinopathy in Volleyball Athletes

et al. 2016

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“…Swelling in the joints of arthritis patients has been known to be associated with enhanced infiltration of the inflammatory cells and enhancement in angiogenesis in synovial tissues (24,25). Furthermore, our recent data suggest that OPN is involved in angiogenesis in vivo (23); therefore, we examined the effect of OPN deficiency on the levels of inflammatory cell infiltration and vascularity in the synovial tissues.…”

Section: Opn Deficiency Suppressed Angiogenesis In Synovial Tissue Ofmentioning

confidence: 99%

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice

Yumoto

Ishijima

Rittling

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

194

169

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Rheumatoid arthritis is one of the most critical diseases that impair the quality of life of patients, but its pathogenesis has not yet been fully understood. Osteopontin (OPN) is an extracellular matrix protein containing Arg-Gly-Asp (RGD) sequence, which interacts with ␣v␤3 integrins, promotes cell attachment, and cell migration and is expressed in both synovial cells and chondrocytes in rheumatoid arthritis; however, its functional relationship to arthritis has not been known. Therefore, we investigated the roles of OPN in the pathogenesis of inflammatory process in a rheumatoid arthritis model induced by a mixture of anti-type II collagen mAbs and lipopolysaccharide (mAbs͞LPS). mAbs͞LPS injection induced OPN expression in synovia as well as cartilage, and this expression was associated with joint swelling, destruction of the surface structures of the joint based on scanning electron microscopy, and loss of toluidine blue-positive proteoglycan content in the articular cartilage in wild-type mice. In contrast, OPN deficiency prevented the mice from such surface destruction, loss of proteoglycan in the articular joint cartilage, and swelling of the joints even when the mice were subjected to mAbs͞ LPS injection. Furthermore, mAbs͞LPS injection in wild-type mice enhanced the levels of CD31-positive vessels in synovia and terminal deoxynucleotidyltransferase-mediated UTP end labeling-positive chondrocytes in the articular cartilage, whereas such angiogenesis as well as chondrocyte apoptosis was suppressed significantly in OPNdeficient mice. These results indicated that OPN plays a critical role in the destruction of joint cartilage in the rheumatoid arthritis model in mice via promotion of angiogenesis and induction of chondrocyte apoptosis.

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“…Platelet-derived growth factor (PDGF), which is a potent mitogen for many cell types, including fibroblasts and smooth muscle cells, is strongly expressed in RA synovium. Hepatocyte growth factor/scatter factor (HGF/SC) is also highly expressed in the RA synovium and synovial fluids [7,8]. It promotes migration and proliferation of endothelial cells.…”

mentioning

confidence: 99%

Antiangiogenesis for Rheumatoid Arthritis

Roccaro

Russo²,

Cirulli³

et al. 2005

CDTIA

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Angiogenesis, i.e., the induction of new blood vessels from existing vasculature, is a crucial event in the formation and maintenance of the pannus in rheumatoid arthritis (RA). The arthritis is characterized by destruction of peripheral joints in which the cartilage and bone are destroyed by proliferative synovitis. This is characterized by infiltration of inflammatory cells and formation of new blood vessels. Angiogenesis occurs since the early stage of the disease, and supports progression of the arthritis. It has been demonstrated in animal models of arthritis that inhibition of angiogenesis reduces of the arthritis. This suggests that pharmacological inhibition of angiogenesis may play an important role in the treatment of RA. In particular, disruption of new blood vessels can not only prevent delivery of nutrients to the inflammatory site, but can also lead to vessel regression, hence reversal of disease. To sum up, since angiogenesis is central in maintaining of synovitis in RA, antiangiogenesis probably represents a therapeutic tool. This view is supported by recent studies in animal models of arthritis where antiangiogenic drugs deliver a therapeutic benefit.

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Untitled

Cited by 140 publications

References 53 publications

Vascular Endothelial Growth Factor Receptor-2 Polymorphisms Have Protective Effect against the Development of Tendinopathy in Volleyball Athletes

Vascular Endothelial Growth Factor Receptor-2 Polymorphisms Have Protective Effect against the Development of Tendinopathy in Volleyball Athletes

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice

Antiangiogenesis for Rheumatoid Arthritis

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