Gene expression of inflammatory mediators induced by jararhagin on endothelial cells
Antigens, Differentiation, T-Lymphocyte
0301 basic medicine
Cell Survival
Endothelial cells
Jararhagin
Gene Expression
Apoptosis
Toxicology
Nitric Oxide
Cell Line
03 medical and health sciences
Matrix Metalloproteinase 10
Antigens, CD
Crotalid Venoms
Human Umbilical Vein Endothelial Cells
Animals
Humans
Bothrops
Lectins, C-Type
Snake venom metalloproteinase
Inflammation
Interleukin-8
Inflammatory response
Metalloendopeptidases
Microarray Analysis
Gene expression
Inflammation Mediators
E-Selectin
DOI:
10.1016/j.toxicon.2012.07.004
Publication Date:
2012-08-07T14:32:10Z
AUTHORS (8)
ABSTRACT
Snake venom metalloproteinases (SVMP) are abundant toxins in venoms of viper snakes and play a relevant role the complex multifactorial tissue damage characteristic Viperidae envenoming. Jararhagin, SVMP isolated from Bothrops jararaca venom, induces fast onset hemorrhagic lesions acting directly on capillary vessels, which disrupted by toxin adhesion degradation extracellular matrix proteins like collagen IV. Jararhagin also triggers inflammatory response, where endothelial cells activated, resulting enhanced rolling circulating leukocytes, nitric oxide generation, prostacyclin production pro-inflammatory cytokines release. decreases viability inducing apoptosis (in vitro studies). In present study we attempted to correlate effect sub-apoptotic doses jararhagin human umbilical vein (HUVECs) gene expression mediators, using microarray assay, real time PCR detection specific HUVEC surface or released medium. was effective activate up-regulate different mediators such as E-selectin, VCAM-1, IL-8, CD69, Ang-2 MMP-10. Despite increase genes coding for molecules, did not induce increased concentrations VCAM-1 IL-8 produced cells. conclusion, is able transcription however this stimulus sufficient result consequent effectors molecules IL-8. The courses these events, well important points be addressed herein.
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