Concentration Kinetics of Serum MMP-9 and TIMP-1 after Blunt Multiple Injuries in the Early Posttraumatic Period

Brumann, M.; Kusmenkov, Thomas; Ney, Ludwig; Kanz, Karl‐Georg; Leidel, Bernd A.; Biberthaler, Peter; Mutschler, Wolf; Bogner, V.

doi:10.1155/2012/435463

Cited by 16 publications

(13 citation statements)

References 29 publications

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“…Brumann et al [26] found the highest MMP-9 levels immediately after admission in polytrauma casualties, whereas TIMP-1 were increased significantly during the whole 72-hour study period after a low admission level. These enzyme concentration kinetics are in concordance with our results.…”

Section: Discussionmentioning

confidence: 96%

Dynamic changes of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 after burn injury

Nagy

Szélig

Rendeki

et al. 2015

Journal of Critical Care

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Section: Discussionmentioning

confidence: 96%

Dynamic changes of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 after burn injury

Nagy

Szélig

Rendeki

et al. 2015

Journal of Critical Care

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“…MMP-9 (a 92 kDa gelatinase) is a type IV collagenase implicated in various aspects of inflammation including accumulation of inflammatory cells, healing of tissue injury, and remodeling processes (Brumann et al 2012). It is produced by epithelial and endothelial cells, fibroblasts, platelets, neutrophils, eosinophils, and macrophages (Iyer et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Carbonic anhydrase enzyme as a potential therapeutic target for experimental trichinellosis

et al. 2016

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Trichinellosis is a globally distributed helminthic infection. There is a considerable interest in developing new anti-helminthic drugs affecting all the developmental stages of Trichinella. Acetazolamide (carbonic anhydrase (CA) inhibitor) involves a novel mechanism of action by inhibiting such an essential enzyme for parasite metabolism. This work aimed to study the effect of acetazolamide against different stages of T. spiralis in experimental animals. Mice were divided into three groups: group I: infected and treated with acetazolamide on day 2 post infection (P.I.), group II: infected and treated with acetazolamide on day 12 P.I., and group III: infected non-treated. From each group, small intestine and muscles were removed for histopathological and immunohistochemical studies. Also, total adult and muscle larval count were estimated. We found that acetazolamide was effective in reduction of both adult and muscle larval counts. When given early, the effect was more pronounced on the adults (62.7 %). However, the efficacy of the drug against muscle larvae was increased when given late (63 %). Improvement of the intestinal histopathological changes was observed in all the treated groups. Degeneration of encysted larvae with minimal pathologic changes of infected skeletal muscle was observed in the treated groups. Expression of matrix metalloproteinase-9 showed a statistically significant decrease in the intestinal and muscle tissues in all treated groups as compared to the control group. In conclusion, the present study revealed that acetazolamide, carbonic anhydrase inhibitor, could be a promising drug against both adults and larvae of T. spiralis.

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“…Compared to its normotensive control, the Wistar Kyoto Rat (WKY), MMP levels, specifically MMP-2 and MMP-9, in the SHR are elevated (Chen et al, 2012; DeLano & Schmid-Schönbein, 2008; Tran et al, 2010), leading to ectodomain receptor cleavage and cellular dysfunctions (Chen et al, 2010; Delano et al, 2011; DeLano & Schmid-Schönbein, 2008; Rodrigues et al, 2010; Tran et al, 2010) generating its co-morbidities, such as insulin resistance. Levels of the endogenous tissue inhibitors of metalloproteinases (TIMPs), such as TIMP-1 and TIMP-2 with the ability to inhibit MMP-9 and MMP-2, respectively (Bernardo & Fridman, 2003; Brumann et al, 2012) are undetermined and will be presented in this report.…”

Section: Introductionmentioning

confidence: 99%

Cleavage and reduced CD36 ectodomain density on heart and spleen macrophages in the Spontaneously Hypertensive Rat

Santamaria

Chen

Chow

et al. 2014

Microvascular Research

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Metabolic disease is accompanied by a range of cellular defects (“comorbidities”) whose origin is uncertain. To investigate this pathophysiological phenomenon we used the Spontaneously Hypertensive Rat (SHR), which besides an elevated arterial blood pressure also has many other comorbidities, including a defective glucose and lipid metabolism. We have shown that this model of metabolic disease has elevated plasma matrix metalloproteinase (MMP) activity, which cleaves the extracellular domain of membrane receptors. We hypothesize here that the increased MMP activity also leads to abnormal cleavage of the scavenger receptor and fatty acid transporter CD36. To test this idea, chronic pharmaceutical MMP inhibition (CGS27023A) of the SHR and its normotensive control, the Wistar Kyoto Rat (WKY), was used to determine if inhibition of MMP activity serves to maintain CD36 receptor density and function. Surface density of CD36 on macrophages from the heart, spleen, and liver was determined in WKY, SHR, CGS-treated WKY (CGS WKY), and CGS-treated SHR (CGS SHR) by immunohistochemistry with an antibody against the CD36 ectodomain. The extracellular CD36 density was lower in SHR heart and spleen macrophages compared to that in the WKY. MMP inhibition by CGS served to restore the reduced CD36 density on SHR cardiac and splanchnic macrophages to levels of the WKY. To examine CD36 function, culture assays with murine macrophages (RAW 264.7) after incubation in fresh WKY or SHR plasma were used to test for adhesion of light-weight donor red blood cell (RBC) by CD36. This form of RBC adhesion to macrophages was reduced after incubation in SHR compared WKY plasma. Analysis of the supernatant macrophage media by Western blot shows a higher level of CD36 extracellular protein fragments following exposure to SHR plasma compared to WKY. MMP inhibition in the SHR plasma compared to untreated plasma, served to increase the RBC adhesion to macrophages and decrease the number of receptor fragments in the macrophage media. In conclusion, these studies bring to light that plasma in the SHR model of metabolic disease has an unchecked MMP degrading activity which causes cleavage of a variety of membrane receptors, including CD36, which attenuates several cellular functions typical for the metabolic disease, including RBC adhesion to the scavenger receptor CD36. In addition to other cell dysfunctions chronic MMP inhibition restores CD36 in the SHR.

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Concentration Kinetics of Serum MMP-9 and TIMP-1 after Blunt Multiple Injuries in the Early Posttraumatic Period

Cited by 16 publications

References 29 publications

Dynamic changes of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 after burn injury

Dynamic changes of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 after burn injury

Carbonic anhydrase enzyme as a potential therapeutic target for experimental trichinellosis

Cleavage and reduced CD36 ectodomain density on heart and spleen macrophages in the Spontaneously Hypertensive Rat

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