Matrix metaloproteases (MMPS) belong to a main group of proteases which have roll in extracellular matrix degradation. Their activities such as wounds healing and angiogenesis are very important in physiological conditions, but they are transient and under the control of endogenous blockers. In pathological processes such as in case of disease and after physical and mechanical stresses, expression and activity of these proteolysic increases, due to preinflammatory cytokines secretion and lead to collagen and gelatin degradation and disruption of micro anatomical structure of tissues. In these circumstances, along with the time, this can lead to worse inflammation and displaying many of disease such as cardiac injuries and damage to blood vessels epithelium, forward cancer cells development and osteoporosis. In should be noted that, because of the novelty this topic about (MMPS) and their responses to physical activities, there is not any consensus between researchers. The aim of this research was to investigate effects of one exhaustive endurance exercise session on MMP2 and MMP9 activities (the most complex and the most abundant enzymes) in male well trained and untrained peoples. So 11 elite male endurance runners which have trained at least for 5 years in clubs or national team camps (age: 22.27±3.87; Vo2max: 60.68±6.19) and 10 untrained male subject (age: 23±4.04; Vo2max: 37.90±5.90) participated voluntarily in this research. Blood samples were collected from two groups in three phase which they include: basal levels (20 minutes before exercise), 20 and 24 hour after end of exercise. Then the variables were measured by means of gelatin zymography technique and collected data were analyzed with ANOVA and post-hoc and independent T student tests. The result showed that blood MMP2 and MMP9 levels increased following of one exhaustive aerobic activity session (P<0.001). It should be noted that despite of significant decrease of MMP2 and MMP9 levels after 24 hour (P<0.001), but their levels were higher than basal levels (P<0.001). In all phases of measurements, changes of MMP2 and MMP9 activities in non-athletes were similar to those in athletes but none of these changes were significant. Moreover, athletes MMP2 and MMP9 activities in pre-exercise, 20 and 24 hour after exercise were significantly higher than non-athletes (P<0.001). Conclusion: With increasing MMPS activities inflammatory responses to physical and mechanical stimuli (one session of exhaustive exercise) has been started in both of subjects (well trained and untrained) which continued up to 34 hours after exercise. In seems that, the rate of mentioned inflammatory indices responses is dependent on the duration and intensity of the exercise.

This study was conducted to examine if allergic contact dermatitis (ACD) alters the expression of MMPs in human dermal fibroblasts. Fibroblasts are the primary source for MMP and matrix production in skin. MMPs are known to involve in a number of physiological and pathological processes. Some published data indicated a gelatinase-like activity in acute and chronic phases of allergic contact dermatitis. However, no exact source of gelatinase activity was demonstrated. Moreover, little is known about the role of MMPs in immune responses. To study and predict the pathophysiological effects of (MMP-2) in allergic contact dermatitic (ACD) patients, we established an in vitro tissue culture survey based on fibroblast explanted from ACD wounds and normal tissues respectively. We also employed a precise proliferation assay [i.e. MTT; 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] to analyze and compare three ACD vs. three normal cell strains. Parallel to MTT assay, we assessed the activity as well as the kinetics of gelatinase (MMP-2) in conditioned media using a zymogeraphy analysis. There was a significant difference in proliferation capacity between mean ACD fibroblast strains vs. mean normal cells, particularly in days 6 to 8 post explanation, 492.5±6.6 vs. 361.75±8.25 respectively. Zymoanalyses indicated significant differences between ACD cells and normal fibroblasts both in time-course and MMP-2 activity per cell fashions, 163.7±16.21 for mean ACD fibroblasts vs. 130±9.09 for normal cells respectively. These data suggest that fibroblasts over proliferated in the process of ACD. Moreover, simultaneous over expression of MMPs observed in ACD fibroblasts vs. normal strains, is indicative of altered fibroblast functionality in the process of allergic contact dermatitis. The activity per cell analysis showed that MMP-2 expression in ACD fibroblasts is independent of cell number, suggesting that either intra- or inter-cellular control signals are also altered and that ACD fibroblasts exhibit hyper-responsiveness to mitogenic or fibrogenic stimulants. Altogether, these data address the chronocity and non-healing tendency of ACD wounds. However, more studies are required to examine possible MMPs inhibition and differential expression of mytogenic, fibrogenic and antifibrogenic cytokines in ACD wound beds. In particular, MMP-2 is postulated to be an aim for further gene therapy protocols.