Neuropeptide, Mast Cell, and Myofibroblast Expression After Rabbit Deep Flexor Tendon Repair

Berglund, Maria; Hildebrand, Kevin A.; Zhang, Mei; Hart, David A.; Wiig, Monica

doi:10.1016/j.jhsa.2010.06.031

Cited by 19 publications

(12 citation statements)

References 44 publications

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“…This finding was also reported by another original study that evaluated the density of mast cells in patellar tendons of individuals who had symptomatic chronic tendinopathy for more than three months when compared with tendons of healthy individuals [25]. Furthermore, the occurrence of increased population of mast cells was reported in deep flexor tendons of the legs of rabbits that were in the process of healing and fibrosis [36], as the increase of mast cells is related to the event of soft tissue remodeling after chronic injury, with the function of releasing profibrotic factors and tryptase that shape this process [25], [37].…”

Section: Discussionsupporting

confidence: 77%

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

et al. 2013

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This study aims to demonstrate how the state of chronic hyperglycemia from experimental Diabetes Mellitus can influence the homeostatic imbalance of tendons and, consequently, lead to the characteristics of tendinopathy. Twenty animals were randomly divided into two experimental groups: control group, consisting of healthy rats and diabetic group constituted by rats induced to Diabetes Mellitus I. After twenty-four days of the induction of Diabetes type I, the Achilles tendon were removed for morphological evaluation, cellularity, number and cross-sectional area of blood vessel, immunohistochemistry for Collagen type I, VEGF and NF-κB nuclear localization sequence (NLS) and nitrate and nitrite level. The Achilles tendon thickness (µm/100g) of diabetic animals was significantly increased and, similarly, an increase was observed in the density of fibrocytes and mast cells in the tendons of the diabetic group. The average number of blood vessels per field, in peritendinous tissue, was statistically higher in the diabetic group 3.39 (2.98) vessels/field when compared to the control group 0.89 (1.68) vessels/field p = 0.001 and in the intratendinous region, it was observed that blood vessels were extremely rare in the control group 0.035 (0.18) vessels/field and were often present in the tendons of the diabetic group 0.89 (0.99) vessels/field. The immunohistochemistry analysis identified higher density of type 1 collagen and increased expression of VEGF as well as increased immunostaining for NFκB p50 NLS in the nucleus in Achilles tendon of the diabetic group when compared to the control group. Higher levels of nitrite/nitrate were observed in the experimental group induced to diabetes. We conclude that experimental DM induces notable structural, inflammatory and vascular changes in the Achilles tendon which are compatible with the process of chronic tendinopathy.

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Section: Discussionsupporting

confidence: 77%

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

et al. 2013

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“…Previous clinical studies based on samples derived from patients suffering from AT rupture have provided limited support for an increase in MC numbers during healing (Scott et al 2008). Moreover, an increase in MC density has been suggested after rabbit deep flexor tendon repair (Berglund et al 2010) and in the tendinopathy seen in the calcaneal tendon overuse rat model (Pingel et al 2013). However, the present study is to our knowledge the first to document increased MC numbers in experimentally-induced tendon rupture in a rat model for Achilles tendon rupture.…”

Section: Discussioncontrasting

confidence: 64%

Increased mast cell degranulation and co-localization of mast cells with the NMDA receptor-1 during healing after Achilles tendon rupture

et al. 2017

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The role of inflammation and the mechanism of tendon healing after rupture has historically been a matter of controversy. The purpose of the present study is to investigate the role of mast cells and their relation to the NMDA receptor-1 (a glutamate receptor) during healing after Achilles tendon rupture. Eight female Sprague Dawley rats had their right Achilles tendon transected. Three weeks after rupture, histological quantification of mast cell numbers and their state of degranulation was assessed by histochemistry. Co-localization of mast cell tryptase (a mast cell marker) and NMDA receptor-1 was determined by immunofluorescence. The intact left Achilles tendon was used as control. An increased number of mast cells and a higher proportion of degranulated mast cells were found in the healing Achilles tendon compared to the intact. In addition, increased co-localization of mast cell tryptase and NMDA receptor-1 was seen in the areas of myotendinous junction, mid-tendon proper and bone tendon junction of the healing versus the intact tendon. These findings introduce a possible role for mast cells in the healing phase after Achilles tendon rupture.

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“…Following a tendon rupture, elevated levels of TGF-β1 have been documented [65], [66]. We tested in this study whether supplementation with TGF-β1 would cause a change in matrix gene expression in de-tensioned tissue, i.e.…”

Section: Discussionmentioning

confidence: 99%

Release of Tensile Strain on Engineered Human Tendon Tissue Disturbs Cell Adhesions, Changes Matrix Architecture, and Induces an Inflammatory Phenotype

et al. 2014

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Mechanical loading of tendon cells results in an upregulation of mechanotransduction signaling pathways, cell-matrix adhesion and collagen synthesis, but whether unloading removes these responses is unclear. We investigated the response to tension release, with regard to matrix proteins, pro-inflammatory mediators and tendon phenotypic specific molecules, in an in vitro model where tendon-like tissue was engineered from human tendon cells. Tissue sampling was performed 1, 2, 4 and 6 days after surgical de-tensioning of the tendon construct. When tensile stimulus was removed, integrin type collagen receptors showed a contrasting response with a clear drop in integrin subunit α11 mRNA and protein expression, and an increase in α2 integrin mRNA and protein levels. Further, specific markers for tendon cell differentiation declined and normal tendon architecture was disturbed, whereas pro-inflammatory molecules were upregulated. Stimulation with the cytokine TGF-β1 had distinct effects on some tendon-related genes in both tensioned and de-tensioned tissue. These findings indicate an important role of mechanical loading for cellular and matrix responses in tendon, including that loss of tension leads to a decrease in phenotypical markers for tendon, while expression of pro-inflammatory mediators is induced.

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Neuropeptide, Mast Cell, and Myofibroblast Expression After Rabbit Deep Flexor Tendon Repair

Cited by 19 publications

References 44 publications

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

Experimental Diabetes Induces Structural, Inflammatory and Vascular Changes of Achilles Tendons

Increased mast cell degranulation and co-localization of mast cells with the NMDA receptor-1 during healing after Achilles tendon rupture

Release of Tensile Strain on Engineered Human Tendon Tissue Disturbs Cell Adhesions, Changes Matrix Architecture, and Induces an Inflammatory Phenotype

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