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1.
Acta Histochem ; 118(7): 729-735, 2016 Sep.
Article in English | MEDLINE | ID: mdl-27640084

ABSTRACT

Membrane type 1-matrix metalloproteinase (MT1-MMP) is involved in numerous biological processes, including morphogenesis. However, the role of MT1-MMP in the development of the vertebrate intestine is poorly understood. This study aimed to evaluate the expression of MT1-MMP in the intestine of rats and chickens along the embryonic and postnatal periods using immunohistochemistry. Results revealed a remarkable spatiotemporal correlation between MT1-MMP expression and intestinal villi morphogenesis in both vertebrates. However, the villi morphogenesis process was found to be different in chickens to that of rats. Moreover, extensive MT1-MMP labeling was observed in the entire villus epithelium from birth until the complete maturation of the small intestinal mucosa in both vertebrates. From these results, we suggest that MT1-MMP contributes to intestinal development, particularly to villi morphogenesis, in both vertebrates. However, further studies are necessary to confirm the role of MT1-MMP in this cellular process. In addition, we performed validation of the primary antibody against human MT1-MMP for adult chickens.


Subject(s)
Gene Expression Regulation, Neoplastic/physiology , Intestines/embryology , Intestines/growth & development , Matrix Metalloproteinase 14/metabolism , Vertebrates/metabolism , Animals , Chickens , Immunohistochemistry/methods , Intestines/cytology , Male , Rats, Wistar , Tumor Cells, Cultured
2.
J Periodontal Res ; 49(1): 85-92, 2014 Feb.
Article in English | MEDLINE | ID: mdl-23586845

ABSTRACT

BACKGROUND AND OBJECTIVE: It has been demonstrated that periodontitis induces a systemic inflammation, which may impair endothelial function. Cyclooxygenase-2 (COX-2) is an important enzyme in the inflammatory process and is responsible for prostacyclin production. We hypothesised that in periodontitis, an increase in vascular COX-2 expression may occur, which in turn may have a role in vascular homeostasis. Thus, we evaluated the vascular effects of COX-2 inhibition in an experimental rat model of periodontitis. MATERIAL AND METHODS: Experimental periodontitis was induced in rats by placing a cotton ligature around the cervix of both sides of the mandibular first molars and maxillary second molars. Sham-operated rats had the ligature removed immediately after the procedure. Mesenteric vessels were obtained for the study of COX-2 expression, and blood samples were collected for nitric oxide quantification. In another set of experiments, animals received etoricoxib (10 mg/kg/d, v.o.) or vehicle, and alveolar bone loss and cardiovascular parameters were evaluated. RESULTS: We observed an increase in COX-2 expression in mesenteric vessels harvested from animals with periodontitis, which was accompanied by a reduction in nitric oxide content. Etoricoxib treatment impaired the endothelium-dependent reduction in blood pressure in rats with periodontitis. CONCLUSION: Periodontitis increases vascular COX-2 expression, which is important in the maintenance of vascular homeostasis in this model. Despite the limitations of an animal study, these findings may have important implications regarding the safety of using selective COX-2 inhibitors in patients with periodontitis.


Subject(s)
Arterial Pressure/physiology , Cyclooxygenase 2/physiology , Periodontitis/enzymology , Alveolar Bone Loss/enzymology , Alveolar Bone Loss/prevention & control , Animals , Anti-Inflammatory Agents/pharmacology , Arterial Pressure/drug effects , Cyclooxygenase 2/drug effects , Cyclooxygenase 2 Inhibitors/pharmacology , Disease Models, Animal , Endothelium, Vascular/drug effects , Endothelium, Vascular/enzymology , Etoricoxib , Heart Rate/drug effects , Male , Mesenteric Arteries/enzymology , Nitric Oxide/blood , Periodontitis/prevention & control , Pyridines/pharmacology , Random Allocation , Rats, Wistar , Sulfones/pharmacology , Vasoconstrictor Agents/pharmacology , Vasodilator Agents/pharmacology
3.
J Periodontal Res ; 49(5): 634-41, 2014 Oct.
Article in English | MEDLINE | ID: mdl-24251721

ABSTRACT

BACKGROUND AND OBJECTIVE: It has been demonstrated that periodontitis induces systemic inflammation, which may impair endothelial function leading to increased cardiovascular risk. The aim of this study was to evaluate the effect of simvastatin on systemic inflammatory markers and endothelial dysfunction induced by periodontitis. MATERIAL AND METHODS: Wistar rats were subjected to ligature-induced experimental periodontitis. Eight days after the procedure, the ligature and sham groups were randomly assigned to receive simvastatin or vehicle once a day until the 14th day, when the effects of acetylcholine and sodium nitroprusside on blood pressure were evaluated. Blood samples were collected and evaluated for plasma interleukin-6C, -reactive protein and lipids. The maxilla and mandible were removed for bone loss analysis. RESULTS: Simvastatin treatment reduced systemic inflammation and endothelial dysfunction induced by periodontitis. Furthermore, simvastatin improved the blood lipid profile and reduced alveolar bone loss. CONCLUSION: Simvastatin treatment, in addition to the improvement on serum lipid profile, may reduce other predictors of cardiovascular events associated with periodontitis.


Subject(s)
Endothelium, Vascular/drug effects , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Inflammation Mediators/immunology , Periodontitis/immunology , Simvastatin/therapeutic use , Acetylcholine/therapeutic use , Alveolar Bone Loss/immunology , Alveolar Bone Loss/prevention & control , Animals , Arterial Pressure/drug effects , C-Reactive Protein/analysis , C-Reactive Protein/drug effects , Disease Models, Animal , Endothelium, Vascular/immunology , Inflammation , Interleukin-6/blood , Leukocyte Count , Lipids/blood , Male , Nitroprusside/therapeutic use , Periodontitis/prevention & control , Random Allocation , Rats , Rats, Wistar , Vasodilator Agents/therapeutic use
4.
Br J Pharmacol ; 168(2): 389-402, 2013 Jan.
Article in English | MEDLINE | ID: mdl-22889120

ABSTRACT

BACKGROUND AND PURPOSE: Kinins are pro-inflammatory peptides that are released during tissue injury, including that caused by inflammatory bowel disease. Herein, we assessed the role and underlying mechanisms through which the absence of kinin B(1) receptors exacerbates the development of dextran sulfate sodium (DSS)-induced colitis in mice. EXPERIMENTAL APPROACH: B(1) and B(2) receptor antagonists and B(1) receptor knockout mice (B1(-/-) ) were used to assess the involvement of B(1) and B(2) receptor signalling in a DSS-colitis. B(1) receptor, B(2) receptor, occludin and claudin-4 expression, cytokine levels and cell permeability were evaluated in colon from wild-type (WT) and B1(-/-) mice. KEY RESULTS: DSS-induced colitis was significantly exacerbated in B1(-/-) compared with WT mice. IL-1ß, IFN-γ, keratinocyte-derived chemokine and macrophage inflammatory protein-2 were markedly increased in the colon from DSS-treated B1(-/-) compared with DSS-treated WT mice. Treatment of WT mice with a selective B(1) receptor antagonist, DALBK or SSR240612, had no effect on DSS-induced colitis. Of note, B(2) receptor mRNA expression was significantly up-regulated in colonic tissue from the B1(-/-) mice after DSS administration. Moreover, treatment with a selective B(2) receptor antagonist prevented the exacerbation of colitis in B1(-/-) mice following DSS administration. The water- or DSS-treated B1(-/-) mice showed a decrease in occludin gene expression, which was partially prevented by the B(2) receptor antagonist. CONCLUSIONS AND IMPLICATIONS: A loss of B(1) receptors markedly exacerbates the severity of DSS-induced colitis in mice. The increased susceptibility of B1(-/-) may be associated with compensatory overexpression of B(2) receptors, which, in turn, modulates tight junction expression.


Subject(s)
Colitis/metabolism , Receptor, Bradykinin B1/metabolism , Receptor, Bradykinin B2/metabolism , Animals , Bradykinin/analogs & derivatives , Bradykinin/pharmacology , Bradykinin B1 Receptor Antagonists , Bradykinin B2 Receptor Antagonists , Colitis/chemically induced , Colitis/pathology , Cytokines/metabolism , Dextran Sulfate , Dioxoles/pharmacology , Homeostasis , Intestinal Mucosa/metabolism , Intestines/pathology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Peroxidase/metabolism , Receptor, Bradykinin B1/genetics , Sulfonamides/pharmacology , Tight Junctions/metabolism , Up-Regulation
5.
Br J Pharmacol ; 163(6): 1289-301, 2011 Jul.
Article in English | MEDLINE | ID: mdl-21410460

ABSTRACT

BACKGROUND AND PURPOSE: There is increasing evidence that potassium channels are involved in the cardiovascular dysfunction of sepsis. This evidence was obtained after the systemic inflammation, cardiovascular dysfunction and organ damage had developed. Here we have studied the consequences of early interference with potassium channels on development of sepsis. EXPERIMENTAL APPROACH: Sepsis was induced by caecal ligation and puncture (CLP) or sham surgery in Wistar rats. Four hours after surgery, animals received tetraethylammonium (TEA; a non-selective potassium channel blocker) or glibenclamide (a selective ATP-sensitive potassium channel blocker). Twenty-four hours after surgery, inflammatory, biochemical, haemodynamic parameters and survival were evaluated. KEY RESULTS: Sepsis significantly increased plasma NO(x) levels, expression of inducible nitric oxide synthase (NOS-2) protein in lung and thigh skeletal muscle, lung myeloperoxidase, urea, creatinine and lactate levels, TNF-α and IL-1ß, hypotension and hyporesponsiveness to phenylephrine and hyperglycemia followed by hypoglycemia. TEA injected 4 h after surgery attenuated the increased NOS-2 expression, reduced plasma NO(x) , lung myeloperoxidase activity, levels of TNF-α and IL-1ß, urea, creatinine and lactate levels, prevented development of hypotension and hyporesponsiveness to phenylephrine, the alterations in plasma glucose and reduced late mortality by 50%. Glibenclamide did not improve any of the measured parameters and increased mortality rate, probably due to worsening the hypoglycemic phase of sepsis. CONCLUSIONS AND IMPLICATIONS: Early blockade of TEA-sensitive (but not the ATP-sensitive subtype) potassium channels reduced organ damage and mortality in experimental sepsis. This beneficial effect seems to be, at least in part, due to reduction in NOS-2 expression.


Subject(s)
Cardiovascular Diseases/drug therapy , Glyburide/therapeutic use , Potassium Channel Blockers/therapeutic use , Sepsis/complications , Tetraethylammonium/therapeutic use , Animals , Blood Pressure , Female , Gene Expression Regulation, Enzymologic , Heart Rate , Longevity , Lung/drug effects , Lung/metabolism , Muscle, Skeletal/drug effects , Muscle, Skeletal/metabolism , Nitric Oxide Synthase Type II/genetics , Nitric Oxide Synthase Type II/metabolism , Rats , Rats, Wistar , Vasoconstrictor Agents/pharmacology
6.
Toxicon ; 49(5): 663-9, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17188732

ABSTRACT

Lonomia obliqua envenomation induces an intense burning sensation at the site of contact and severe hemorrhage followed by edema and hypotension, and after few days death can occur usually due to acute renal failure. In order to understand more about the envenomation syndrome, the present study investigates the role played by kallikrein-kinin system (KKS) in edematogenic and hypotensive responses to the envenomation by L. obliqua. The incubation of L. obliqua caterpillar bristles extract (LOCBE) with plasma results in kallikrein activation, measured by cromogenic assay using the kallikrein synthetic substrate S-2302 (H-D-Pro-Phe-Arg-pNA). It was also showed that LOCBE was able to release kinins from low-molecular weight kininogen (LMWK). Moreover, it was demonstrated that previous administration of a kallikrein inhibitor (aprotinin) or bradykinin B2 receptor antagonist (HOE-140) significantly reduces the edema and hypotension in response to LOCBE, using mouse paw edema bioassay and mean arterial blood pressure analysis, respectively. The results demonstrate a direct involvement of the KKS in the edema formation and in the fall of arterial pressure that occur in the L. obliqua envenomation syndrome.


Subject(s)
Arthropod Venoms/toxicity , Edema/chemically induced , Hypotension/chemically induced , Insect Bites and Stings/metabolism , Kallikrein-Kinin System/drug effects , Moths/chemistry , Analysis of Variance , Animals , Arthropod Venoms/analysis , Blood Pressure/drug effects , Female , Guinea Pigs , Kininogens , Larva/chemistry , Male , Mice , Oligopeptides , Rats , Rats, Wistar
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