Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids

Ulrich, Dietmar; Ulrich, Franziska; Unglaub, Frank; Piatkowski, Andrzej; Pallua, Norbert

doi:10.1016/j.bjps.2009.04.021

Cited by 99 publications

(87 citation statements)

References 29 publications

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“…TIMP-1 can combine with most MMP active sites, thus inhibiting enzyme activity [30][31] . However, some research has found that the expression of TIMP-1 is significantly higher in the scar tissue of patients with HS than in scar tissues of patients with normotrophic scars 32 . Moreover, targeting TIMP-1 using small interfering RNA has significant therapeutic potential as an approach to treating keloids 33 .…”

Section: Discussionmentioning

confidence: 96%

“…Endostar also decreases the expressions of α-SMA and CTGF in other models [19][20] . Because HS is also associated with increased angiogenesis and ECM [21][22][23] , it was chosen as the object of this study, which showed that Endostar significantly reduced the formation of HS in rabbit ears by down-regulating VEGF and TIMP-1 expressions.…”

Section: Discussionmentioning

confidence: 99%

“…Excessive synthesis or lessened degradation of ECM will result in hypertrophic scars 23 . TIMPs and MMPs play a critical role in the formation, alteration, and degradation of matrix proteins [27][28][29] .…”

Section: Discussionmentioning

confidence: 99%

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Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

2016

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Background: Recombinant human endostatin (Endostar) has been widely used to suppress angiogenesis in carcinoma patients. Hypertrophic scar (HS) tissue, much like a carcinoma, is often associated with angiogenesis. However, there have been few studies conducted on the effects of Endostar on HS or its mechanism. Objective: This paper investigated the effects Endostar on the HS of rabbit ears and studied the effects of Endostar on VEGF and TIMP-1 expression. Methods: Sixteen New Zealand white rabbits were used to establish HS models. Then, rabbit ears containing HS were randomly assigned to either the Endostar group or the control group. The changes of appearance and histology were evaluated using the naked eye, hematoxylin eosin staining, and a scar elevation index. The VEGF and TIMP-1 expressions were detected by immunohistochemical staining, RT-PCR, and western blot. Results: The thickness of the connective tissue in the Endostar group were thinner, the numbers of micro vessels and fibroblasts were fewer, and the collagen fibers were smoother. Moreover, the mRNA and protein expressions of VEGF and TIMP-1 in the Endostar group were significantly lower than those in the control group. Conclusion:The results suggested that Endostar reduced the formation of HS by down-regulation of VEGF and TIMP-1 expressions.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

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Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

2016

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“…This suggests that this pathology is due to injury of this skin layer [8]. One of the causes of keloid formation is abnormal extracellular matrix (ECM) turnover (biosynthesis and degradation) during complex and multifactorial healing of wounds [9]. Keloids do not exhibit the characteristics of malignant tumors, but they often grow beyond the original location [10].…”

Section: Introductionmentioning

confidence: 99%

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

Antończak¹,

Jurzak²,

Adamczyk³

et al. 2017

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Introduction. Tranilast (N-(3',4'-demethoxycinnamoyl)-anthranilic acid)is an anti-allergic drug. Its mechanism of action is based on the inhibition of antigen-induced release of chemical mediators from mast cells and basophils. It also reveals antifibroproliferative activities. These properties of tranilast are used in the treatment of hypertrophic scars and keloids. Keloids are characterized by incorrect extracellular matrix components turnover. Fibroblasts derived from keloids reveal overproduction of collagen type I and decreased degradation of extracellular matrix in comparison with normal fibroblasts. Fibroblast activation protein α (FAP-α) may play an important role in remodeling of extracellular matrix and the invasive properties of keloids. Objective. In the present study, the effect of tranilast on expression of FAP-α gene and its protein was evaluated in normal human dermal fibroblasts and fibroblasts derived from keloids cultured in vitro. Materials and methods. In the first stage of the study, the influence of tranilast on cell viability was estimated. The second stage of the study included the quantitative evaluation of FAP-α mRNA expression in normal and keloid fibroblasts treated with tranilast. The third stage of the study comprised fibroblast activation protein α expression analysis in the examined cells treated with tranilast. Results and conclusions. The expression of FAP-α gene and fibroblast activation protein α is higher in keloid fibroblasts. Tranilast at concentrations of 3 μM and 30 μM up-regulated mRNA FAP-α expression in normal fibroblasts but did not influence keloid fibroblasts. The drug, at concentrations of 30 μM and 300 μM up-regulated fibroblast activation protein α expression in normal fibroblasts and did not influence keloid fibroblasts. Tranilast antiproliferative effect is not associated with FAP-α expression in keloid fibroblasts. Original article/Praca oryginalnaThe effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro Wpływ tranilastu na ekspresję białka aktywującego fibroblasty α (FAP-α) w fibroblastach prawidłowych oraz fibroblastach keloidowych in vitro

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“…But an abnormal activation of proteolysis leads to damaging of native ("undamaged") tissue proteins, favours to the inflammation processes, the progress if which is connected to an intensive destruction of extracellular matrix and migration processes in cells. On the other hand, the insufficient activity of proteinases accompanied by a prolonged and abnormal build-up of matrix components leads to slowing down of healing of the wound and nascence of a coarse tissue of the scar due to abnormal build-up of collagen (Doucet and Overall, 2008;Ulrich et al, 2010). We hypothesized that reduction of total proteolytic activity during the whole period of the experiment can be associated with the imbalance between activity of proteolytic enzymes and level of their inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Changes in blood protein composition under experimental chemical burns of esophageal development in rats

Ishchuk¹,

Raetska²,

Savchuk³

et al. 2015

Biomed Res Ther

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Abstract-Exogenous poisoning with alkalis takes the leading position among causes of acute poisoning. Esophageal burns as a result of accidental swallowing of caustic material are seen frequently in children ages 1 to 8 years. A burn wound is perhaps the most intense stress that a human body can suffer. In the place of chemical trauma localization the processes of synthesis and degradation of proteins increase. As a result the structure and functions of vital organs and immune system suffer. The inflammation process after burn injury is determines the changes in protein expression. In our research we have shown that chemical burn of the esophagus is characterized by decreased level of total proteolytic activity, total protein and development of endogenous intoxication of the body as indicated by elevated MMM level. Obtained results suggest that the development of chemical burns of the esophagus grade 2 is characterized by more substantial changes in the protein composition of blood compared with grade 1. An in-depth study of this disease has a crucial scientific and practical importance for development of pathogenically oriented methods of wound process healing after the chemical esophageal burns depending on the stage and extent of the burn process.

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Matrix metalloproteinases and tissue inhibitors of metalloproteinases in patients with different types of scars and keloids

Cited by 99 publications

References 29 publications

Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

Recombinant human endostatin reduces hypertrophic scar formation in rabbit ear model through down-regulation of VEGF and TIMP-1

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

Changes in blood protein composition under experimental chemical burns of esophageal development in rats

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