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Caspase 3 activity in isolated fetal rat lung fibroblasts and rat periodontal ligament fibroblasts: cigarette smoke induced alterations

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dc.contributor.author Ahmed, Asra
dc.contributor.author Thliveris, James A
dc.contributor.author Shaw, Anthony
dc.contributor.author Sowa, Michael
dc.contributor.author Gilchrist, James
dc.contributor.author Scott, James E
dc.date.accessioned 2013-12-11T08:18:44Z
dc.date.available 2013-12-11T08:18:44Z
dc.date.issued 2013-12-06
dc.identifier.citation Tobacco Induced Diseases. 2013 Dec 06;11(1):25
dc.identifier.uri http://hdl.handle.net/1993/22299
dc.description.abstract Abstract Background Cigarette smoking is the leading cause of preventable death and has been implicated in pathogenesis of pulmonary, oral and systemic diseases. Smoking during pregnancy is a risk factor for the developing fetus and may be a major cause of infant mortality. Moreover, the oral cavity, and all cells within are the first to be exposed to cigarette smoke and may be a possible source for the spread of toxins to other organs of the body. Fibroblasts in general are morphologically heterogeneous connective tissue cells with diverse functions. Apoptosis or programmed cell death is a crucial process during embryogenesis and for the maintenance of homeostasis throughout life. Deregulation of apoptosis has been implicated in abnormal lung development in the fetus and disease progression in adults. Caspases are proteases which belong to the family of cysteine aspartic acid proteases and are key components for downstream amplification of intracellular apoptotic signals. Of 14 known caspases, caspase-3 is the key executioner of apoptosis. In the present study we explored the hypothesis that cigarette smoke (CS) extract activates caspase-3 in two types of fibroblasts, both of which would be exposed directly to cigarette smoke, isolated fetal rat lung fibroblasts and adult rat periodontal ligament (PDL) fibroblasts. Methods Isolated fetal rat lung fibroblasts and adult PDLs were used. Cells were exposed to different concentrations of CS for 60 min. Caspase-3 activity and its inhibition by Z-VAD-fmk were measured by caspase-3 fluorometric assay. The effect of CSE on cellular viability was measured using the MTT formazan assay. Caspase-3 expression was detected by western blot analysis and cellular localization of caspase-3 was determined by immunofluorescence using fluorescence microscopy. Results It was observed in fetal rat lung fibroblast cells that CSE extract significantly (p<0.05) increased caspase-3 activity and decrease cell proliferation. However, no significant changes in activity or viability were observed in PDLs. Conclusions This indicates CS activates caspase-3 the key regulatory point in apoptosis in fetal rat lung fibroblast cells suggesting that smoking during pregnancy may alter the developmental program of fetal lung, jeopardizing the establishment of critical cellular mechanisms necessary to expedite pulmonary maturation at birth.of critical cellular mechanisms necessary to expedite pulmonary maturation at birth.
dc.rights info:eu-repo/semantics/openAccess
dc.title Caspase 3 activity in isolated fetal rat lung fibroblasts and rat periodontal ligament fibroblasts: cigarette smoke induced alterations
dc.type Journal Article
dc.type info:eu-repo/semantics/article
dc.language.rfc3066 en
dc.description.version Peer Reviewed
dc.rights.holder Asra Ahmed et al.; licensee BioMed Central Ltd.
dc.date.updated 2013-12-11T08:18:44Z
dc.identifier.doi http://dx.doi.org/10.1186/1617-9625-11-25


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