Expression of cytokines, growth factors and apoptosis-related signal molecules in chronic pressure ulcer wounds healing

  • Jiang L
  • Dai Y
  • Cui F
 et al. 
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Abstract

OBJECTIVES Many complex mechanisms responsible for the pathogenesis of pressure ulcers (PUs) currently remain poorly understood. The objective of this study was to discover the major roles for inflammatory cytokines, growth factors and several apoptosis-related signal molecules in chronic PU wound. METHODS We investigated expression of inflammatory cytokines, growth factors and their corresponding receptors, and the apoptosis signal of caspase-3 in chronic stage III/IV chronic PU wound, acute wounds as well as normal skin controls. Tissues were stained by hematoxylin and eosin (HE) for histopathology and Masson's trichrome for collagen. Vascular endothelial growth factor (VEGF), fibroblast growth factors 2 (bFGF) and caspase-3 were detected by immunohistochemical analysis. Expression of mRNAs for interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), VEGF, KDR, bFGF and FGFR1 was determined by real-time reverse transcription PCR. RESULTS Stage III and IV chronic PUs stained had increased inflammatory cell infiltration and decreased collagen compared with controls. Levels of mRNAs for inflammatory cytokines IL-1β and TNF-α were elevated in PUs compared with acute wounds and normal skin. VEGF and bFGF, together with their receptors KDR and FGFR1, respectively, were significantly decreased compared with controls. However, the expression levels of caspase-3 were elevated in the PUs. CONCLUSION Our series of studies have shown that chronic PUs displayed high levels of inflammation and disruption of the collagen matrix, along with increased indications of apoptosis and decreased levels of growth factors and their receptors. These characteristics can be used to comprehensively evaluate the etiology and treatment of chronic PUs.

Author-supplied keywords

  • apoptosis
  • growth factors
  • inflammatory cytokines
  • pressure ulcers

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Authors

  • L. Jiang

  • Y. Dai

  • F. Cui

  • Y. Pan

  • H. Zhang

  • J. Xiao

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