کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9110813 | 1155370 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cytokine gene expression in a murine wound healing model
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
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چکیده انگلیسی
Inflammatory mediators have been shown to play a major role in the complex series of co-ordinated events that occur in wound healing responses following injury. However, to date most of the studies carried out have addressed the expression, interactions and role of only one or two cytokines that are thought to be involved in wound repair. This study has evaluated, in murine skin samples taken at 0, 3, 12, 18, 24, 48, 72, 120 and 168 h post-wounding, the expression of a wide range of cytokines with potential for a role in wound repair. Various techniques (reverse transcription polymerase chain reaction (RT-PCR), bioassays and ELISA) were used to evaluate cytokine expression in these samples at both the mRNA and protein expressions level. Semi-quantitative analysis using RT-PCR revealed that IL-1β, IP10, bFGF, and TGFβ3 up-regulated in wounded samples, compared to non-injured control samples. Expression of mRNA for other cytokines and inflammatory mediators, IL-1α, IL-6, TGFβ1, TNFα, MIP-1α, MIP-2, JE, KC, PDGFα and PDGFβ, were found to be down-regulated in injured adult murine samples compared to normal control samples. Interestingly we failed to find evidence of mRNA expression for the cytokines IL-2, IL-4, IL-12, GM-CSF, IFNγ and RANTES, in both non-injured and injured samples. These observations were also generally supported by the results obtained using bioassays for IL-1 and IL-6 and ELISA for IL-1α, IL-1β, IL-6, TNFα, and IFNγ.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 31, Issue 6, 21 September 2005, Pages 429-438
Journal: Cytokine - Volume 31, Issue 6, 21 September 2005, Pages 429-438
نویسندگان
Donna Bryan, Kenneth B. Walker, Mark Ferguson, Robin Thorpe,