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Myofibroblast numbers are elevated in human elbow capsules after trauma.

ABSTRACT: Elbow contractures, a frequent problem after injury, can be treated by excision of the joint capsule. However, the underlying changes in the joint capsule are poorly understood. Based on skin healing work, we examined the hypotheses that myofibroblast numbers and expression of a myofibroblast marker alpha-smooth muscle actin, are elevated in patients with posttraumatic joint contractures. Anterior capsules were obtained from six patients who had operative release of posttraumatic contractures greater than 5 months after injury and six elbows of organ donors free of contractures. Immunohistochemical studies revealed that myofibroblast numbers and percentage of total cells that were myofibroblasts were significantly elevated in the joint capsules from patients with contractures (326 +/- 61 cells per field, 36% +/- 4% total cells) when compared with similar tissues of the organ donors (69 +/- 41 cells per field, 9% +/- 4% total cells). Western blot analysis showed that protein levels of alpha-smooth muscle actin were significantly elevated in patients with posttraumatic joint contractures. However, analysis with reverse transcription-polymerase chain reaction determined that messenger ribonucleic acid levels for smooth muscle actin normalized to the housekeeping gene glyceraldehyde-3-phosphate dehydrogenase were not significantly different between the two groups. An association between increased numbers of myofibroblasts and posttraumatic joint contractures has been established in the human elbow capsule. Additional work is required to determine whether myofibroblast regulators may be targets for adjuvant therapies of posttraumatic contractures.

SUBMITTER: Hildebrand KA

PROVIDER: S-EPMC2950171 | biostudies-literature | 2004 Feb

REPOSITORIES: biostudies-literature

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Myofibroblast numbers are elevated in human elbow capsules after trauma.

Hildebrand Kevin A KA Zhang Mei M van Snellenberg Wistara W King Graham J W GJ Hart David A DA

Clinical orthopaedics and related research 20040201 419

Elbow contractures, a frequent problem after injury, can be treated by excision of the joint capsule. However, the underlying changes in the joint capsule are poorly understood. Based on skin healing work, we examined the hypotheses that myofibroblast numbers and expression of a myofibroblast marker alpha-smooth muscle actin, are elevated in patients with posttraumatic joint contractures. Anterior capsules were obtained from six patients who had operative release of posttraumatic contractures gr ...[more]

PMID: 15021153

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Project description:BackgroundPeri-articular injury may result in functional deficits and pain. In particular, post-traumatic elbow stiffness is a debilitating condition, precluding patients from performing activities of daily living. As such, clinicians and basic scientists alike, aim to develop novel therapeutic interventions to prevent and treat elbow stiffness; thereby reducing patient morbidity. Yet, there is a paucity of pre-clinical models of peri-articular stiffness, especially of the upper extremity, necessary to develop and test the efficacy of therapeutics. We set out to develop a pre-clinical murine model of elbow stiffness, resulting from soft tissue injury, with features characteristic of pathology observed in these patients.MethodsA soft tissue peri-elbow injury was inflicted in mice using cardiotoxin. Pathologic tissue repair was induced by creating an investigator-imposed deficiency of plasminogen, a protease essential for musculoskeletal tissue repair. Functional testing was conducted through analysis of grip strength and gait. Radiography, microcomputed tomography, and histological analyses were employed to quantify development of heterotopic ossification.ResultsAnimals with peri-elbow soft tissues injury in conjunction with an investigator-imposed plasminogen deficiency, developed a significant loss of elbow function measured by grip strength (2.387?±?0.136 N vs 1.921?±?0.157 N, ****, p <?0.0001) and gait analysis (35.05?±?2.775 mm vs 29.87?±?2.075 mm, ***, p <?0.0002). Additionally, plasminogen deficient animals developed capsule thickening, delayed skeletal muscle repair, fibrosis, chronic inflammation, and heterotopic ossification; all features characteristic of pathology observed in patients with trauma-induced elbow stiffness.ConclusionA soft tissue injury to the peri-elbow soft tissue with a concomitant deficiency in plasminogen, instigates elbow stiffness and pathologic features similar to those observed in humans. This pre-clinical model is valuable for translational studies designed to investigate the contributions of pathologic features to elbow stiffness or as a high-throughput model for testing therapeutic strategies designed to prevent and treat trauma-induced elbow stiffness.

Project description:Atmospheric CO2 concentrations can determine the number of stomata that form on plant leaves (Woodward & Kelly 1995 New Phyt 131: 311-327). The majority of species exhibit reduced stomatal densities at elevated CO2. However, not all plant species react in the same way to elevated CO2 levels and there is a spectrum of effects: Some species increase stomatal densities, some decrease stomatal densities, and some are unaffected. In addition to which, other environmental factors influence the number of stomata that a plant form. Light intensity has also been shown to affect stomatal numbers in various Arabidopsis ecotypes (Schluter et al. 2003 J Exp Bot 54 (383): 867-874; Lake et al. 2002 J Exp Bot 53 (367): 183-193), by increasing stomatal numbers with increasing light levels. There are many changes in gene expression under elevated CO2 conditions, so pinpointing specific genes involved in the stomatal response to CO2 is difficult. In addition, if there is crosstalk between the various signalling pathways affecting ultimate stomatal numbers this complicates further the task of finding genes specifically involved the stomatal response to CO2. Therefore we propose to look at the interaction of two known influences on stomatal numbers, light and CO2, on one specific ecotype, Col-0. We aim to test the hypothesis that light signals interact the CO2 signals that affect stomatal development. Arabidopsis thaliana Columbia-0 ecotype has previously been shown to decrease stomatal numbers in response to a doubling of ambient CO2 concentrations. Col-0 has also been shown to increase stomatal numbers in response to high light intensities. Therefore we propose to grow A. thaliana Col-0 at three light intensities (50 mmol m-2 s-1, 150 mmol m-2 s-1 and 250 mmol m-2 s-1), in both ambient and elevated (double ambient) atmospheric CO2 concentrations. By looking in more detail at how gene expression differs between plants grown at ambient and elevated CO2 at the same light intensities, and also how gene expression differs between plants grown at the same CO2 concentration but different light intensities, we aim to identify those genes involved in the stomatal developmental response to CO2 and whether genes involved in the light response can also be isolated. Experimenter name = Susannah Bird; Experimenter phone = (0114) 222 4649; Experimenter address = Animal and Plant Science Department; Experimenter address = Alfred Denny Building; Experimenter address = Western Bank; Experimenter address = Sheffield; Experimenter zip/postal_code = S10 2TN; Experimenter country = UK Experiment Overall Design: 6 samples were used in this experiment

Dataset Information

Myofibroblast numbers are elevated in human elbow capsules after trauma.

Publications

Myofibroblast numbers are elevated in human elbow capsules after trauma.

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