MMP-1 promoter genotype and haplotype association with posterior tibial tendinopathy

Baroneza, José Eduardo; Godoy‐Santos, Alexandre Leme; Massa, Bruno Sérgio Ferreira; Munhoz, Francielle Boçon de Araujo; Fernandes, Túlio Diniz; Santos, Maria Cristina Leme Godoy dos

doi:10.1016/j.gene.2014.07.001

Cited by 23 publications

(19 citation statements)

References 36 publications

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“…The levels of MMP‐1 increased with loading, correlating with previous studies, which have shown increased MMP‐1 expression in tendinopathic44, 45 or ruptured46 tendons. Further, MMP‐1 expression has recently been shown to increase with overload fatigue inducing exercise in equine tendons 47.…”

Section: Discussionsupporting

confidence: 88%

Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

Spiesz

Thorpe

Chaudhry

et al. 2015

Journal Orthopaedic Research

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The role of inflammation in tendon injury is uncertain and a topic of current interest. In vitro studies of tendon accelerated overload damage can serve as a valuable source of information on the early stages of tendinopathy. Viable fascicle bundles from bovine flexor tendons were subjected to cyclic uniaxial loading from 1–10% strain. Immuno‐staining for inflammatory markers and matrix degradation markers was performed on the samples after mechanical testing. Loaded samples exhibited visible extracellular matrix damage, with disrupted collagen fibers and fiber kinks, and notable damage to the interfascicular matrix. Inflammatory markers COX‐2 and IL‐6 were only expressed in the cyclically loaded samples. Collagen degradation markers MMP‐1 and C1,2C were colocalized in many areas, with staining occurring in the interfascicular matrix or the fascicular tenocytes. These markers were present in control samples, but staining became increasingly intense with loading. Little MMP‐3 or MMP‐13 was evident in control sections. In loaded samples, some sections showed intense staining of these markers, again localized to interfascicular regions. This study suggests that inflammatory markers may be expressed rapidly after tendon overload exercise. Interestingly, both inflammation and damage‐induced matrix remodeling seem to be concentrated in, or in the vicinity of, the highly cellular interfascicular matrix. © 2015 The Authors. Journal of Orthopaedic Research Published by Wiley Periodicals, Inc. J Orthop Res 33:889–897, 2015.

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Section: Discussionsupporting

confidence: 88%

Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

Spiesz

Thorpe

Chaudhry

et al. 2015

Journal Orthopaedic Research

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“…Previous reports indicated that rs1144393 is a risk factor for coronary artery disease [24], and it was associated with hypertension and intima-media thickness [25]. Additionally, the G-to-A substitution in rs1144393 resulted in a greater risk of posterior tibial tendinopathy [22]. These findings suggested that this polymorphism is functional in inflammatory or fibrotic diseases, including RILI.…”

Section: Discussionmentioning

confidence: 86%

MMP-1 promoter polymorphism is associated with risk of radiation-induced lung injury in lung cancer patients treated with radiotherapy

Liu

Tang

et al. 2016

Oncotarget

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Matrix metalloproteinase-1 (MMP-1) has been implicated in several inflammatory and fibrotic diseases. We hypothesized that genetic variations in the MMP1 promoter region are associated with risk of radiation-induced lung injury (RILI). A cohort of 251 lung cancer patients was genotyped for five single nucleotide polymorphisms in the MMP1 promoter region. We found that rs1144393 AG/GG was strongly correlated with an increased occurrence of grade ≥ 2 RILI (p = 0.002). Additionally, patients with the rs1144393 AG/GG genotypes exhibited higher MMP-1 expression than patients with the AA genotype in lung tissues (n = 28, p = 0.022) and plasma samples (n = 40, p = 0.018). Our results indicated that rs1144393 in the MMP1 promoter region can be a predictor of grade ≥ 2 RILI in lung cancer patients treated with thoracic radiation.

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“…In addition, Baroneza and colleagues described association of MMP-1 polymorphisms with posterior tibial tendinopathy. MMP-1 polymorphisms may alter collagen types I and III of tendon, which contribute with higher risk of tendinopathy development [6]. …”

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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MMP-1 promoter genotype and haplotype association with posterior tibial tendinopathy

Cited by 23 publications

References 36 publications

Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

Tendon extracellular matrix damage, degradation and inflammation in response to in vitro overload exercise

MMP-1 promoter polymorphism is associated with risk of radiation-induced lung injury in lung cancer patients treated with radiotherapy

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

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