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The role of αvβ6 integrin in epidermal wound healing Al-Dahlawi, Salwa
Abstract
The αvβ6 integrin is an exclusively epithelial integrin that is highly expressed during fetal development. In adult tissue αvβ6 integrin is re-expressed during inflammation, carcinogenesis and in wound healing. The objective of this study was to investigate whether compromised wound healing by hydrocortisone treatment is altered in mice deficient or overexpressing the β6 subunit in comparison to wild type littermates. Three groups of age and sex matched mice were used; wild type (WT), β6 integrin deficient (β6√-), and human β6 integrin overexpressing transgenic mice (hβ6Fl). Each group was subdivided into untreated (control) and treatment groups. Treatment groups received a daily intraperitoneal injection of 1 mg of hydrocortisone for 13 days. Excisional 4 mm wounds were made on the dorsal surface of the mice and wound healing was evaluated daily. Comparisons between different groups were made from the histological analysis of three and ten days wound healing. Aged (22- month-old) β6 integrin deficient (β6√-) animals showed a significant delay in wound healing when compared to their aged matched wild type animals. The most significant delay was observed at the stages where significant granulation tissue formation is occurring (four to seven days post wounding). Hydrocortisone treatment significantly delayed wound healing in wild type and β6 integrin deficient mice in comparison to the untreated controls. However, hydrocortisone treatment in human P6 integrin overexpressing (hβ6Fl) animals did not cause a significant delay in wound healing. The results of this study indicated that the presence of αvβ6 integrin plays an important role in wound healing in animals compromised by either age or stress.
Item Metadata
Title |
The role of αvβ6 integrin in epidermal wound healing
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
2004
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Description |
The αvβ6 integrin is an exclusively epithelial integrin that is highly expressed during
fetal development. In adult tissue αvβ6 integrin is re-expressed during inflammation,
carcinogenesis and in wound healing. The objective of this study was to investigate
whether compromised wound healing by hydrocortisone treatment is altered in mice
deficient or overexpressing the β6 subunit in comparison to wild type littermates.
Three groups of age and sex matched mice were used; wild type (WT), β6 integrin
deficient (β6√-), and human β6 integrin overexpressing transgenic mice (hβ6Fl). Each
group was subdivided into untreated (control) and treatment groups. Treatment
groups received a daily intraperitoneal injection of 1 mg of hydrocortisone for 13
days. Excisional 4 mm wounds were made on the dorsal surface of the mice and
wound healing was evaluated daily. Comparisons between different groups were
made from the histological analysis of three and ten days wound healing. Aged (22-
month-old) β6 integrin deficient (β6√-) animals showed a significant delay in wound
healing when compared to their aged matched wild type animals. The most significant
delay was observed at the stages where significant granulation tissue formation is
occurring (four to seven days post wounding). Hydrocortisone treatment significantly
delayed wound healing in wild type and β6 integrin deficient mice in comparison to
the untreated controls. However, hydrocortisone treatment in human P6 integrin
overexpressing (hβ6Fl) animals did not cause a significant delay in wound healing.
The results of this study indicated that the presence of αvβ6 integrin plays an
important role in wound healing in animals compromised by either age or stress.
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Extent |
23218388 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-11-24
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0099758
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
2004-05
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Media
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Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.