Title page for etd-0823115-001730


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URN etd-0823115-001730
Author Shu-Mei Huang
Author's Email Address No Public.
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Department Biological Sciences
Year 2015
Semester 1
Degree Ph.D.
Type of Document
Language zh-TW.Big5 Chinese
Title Effects of high glucose on keratinocyte functions: focusing on the impaired diabetic wound healing
Date of Defense 2015-09-18
Page Count 166
Keyword
  • hBD3
  • interleukin-8
  • keratinocyte
  • hBD2
  • high glucose
  • interleukin-22
  • Abstract Diabetes mellitus is characterized by elevated plasma glucose and increased rate of skin infection. Altered immune responses have been suggested to contribute to this prevalent complication. High glucose treatment reduced human β-defensin-3 (hBD3) expression of cultured keratinocytes. This pathogenic process involved inhibition of p38MAPK signaling, an event that resulted from increased formation of advanced glycation end product and showed worse anti-Staphylococcus aureus activity. In addition, high-glucose cultivated keratinocytes expressed reduced levels of human β-defensin-2 (hBD2) and pSTAT-1. Besides the impact on keratinocyte cultured under high glucose, the suboptimal interaction between keratinocytes and inflammatory cells also contributed to impaired diabetic wound healing. High-glucose environment enhanced interleukin (IL)-8 production via EGFR-ERK pathway in a ROS-dependent manner in keratinocytes. Treating diabetic rats with neutrophil inhibitor improved the healing. On the other hands, high glucose cultivated monocytes have significantly reduced production of IL-22, a molecule that is responsible for promoting keratinocyte migration. In summary, high glucose environment impared keratinocyte function directly or indirectly that contributed to impaired diabetic wound healing, and focusing on these defects will present a therapeutic approach to promote diabetic healing.
    Advisory Committee
  • Chen, Gwo-Shing - chair
  • Liu, Jong-Kang - co-chair
  • Ching-Shuang Wu - co-chair
  • Lan, Cheng-Che - co-chair
  • Chao, David - advisor
  • Files
  • etd-0823115-001730.pdf
  • indicate access worldwide
    Date of Submission 2015-09-23

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