Differential Regulation of Pro-Inflammatory Cytokines During Wound Healing in Normal and Glucocorticoid-Treated Mice

Hübner, Griseldis; Brauchle, Maria; Smola, Hans; Madlener, Marianne; Fässler, Reinhard; Werner, Sabine

doi:10.1006/cyto.1996.0074

Cited by 430 publications

(325 citation statements)

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“…We previously demonstrated a strong induction of the expression of KGF (Werner et al, 1992), TGF-b and TNF-a (HuÈ bner et al, 1996) in the same wound healing model. Furthermore, a strong expression of epidermal growth factor receptor ligands in the healing wound has also been demonstrated (Todd et al, 1991; Figure 6 Expression of CAD and HPRT in 5 day full-thickness excisional wounds.…”

Section: Discussionmentioning

confidence: 73%

Growth factor – regulated expression of enzymes involved in nucleotide biosynthesis: a novel mechanism of growth factor action

1999

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Keratinocyte growth factor (KGF) is a potent and speci®c mitogen for epithelial cells, including the keratinocytes of the skin. We investigated the mechanisms of action of KGF by searching for genes which are regulated by this growth factor in cultured human keratinocytes. Using the di erential display RT ± PCR technology we identi®ed the gene encoding adenylosuccinate lyase [EC 4.3 [EC 3.5.2.3]). Expression of all of these enzymes was upregulated after treatment with KGF and also with epidermal growth factor (EGF), indicating that these mitogens stimulate nucleotide production by induction of these enzymes. To determine a possible in vivo correlation between the expression of KGF, EGF and the enzymes mentioned above, we analysed the expression of the enzymes during cutaneous wound repair, where high levels of these mitogens are present. Indeed, we found a strong mRNA expression of all of these enzymes in the EGF-and KGF-responsive keratinocytes of the hyperproliferative epithelium at the wound edge, indicating that their expression might also be regulated by growth factors during wound healing.

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Section: Discussionmentioning

confidence: 73%

Growth factor – regulated expression of enzymes involved in nucleotide biosynthesis: a novel mechanism of growth factor action

1999

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“…It is recognised that inflammatory cells are essential for normal wound healing; neutrophil-deficient mice demonstrate impaired wound healing [38]. One advantage of this baboon model is the absence of infection, so the inflammatory cells present are part of the process of granulation tissue formation, not removal of bacteria.…”

Section: Discussionmentioning

confidence: 99%

A novel primate model of delayed wound healing in diabetes: dysregulation of connective tissue growth factor

et al. 2009

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Aims/hypothesis Chronic non-healing wounds are a common complication of diabetes. Prolonged inflammation and decreased matrix accumulation may contribute. Connective tissue growth factor (CTGF) is induced during normal wound healing, but its regulation in diabetic wounds is unknown. We developed a primate model for the study of in vivo wound healing in baboons with long diabetes duration. Methods Drum implants were placed subcutaneously into thighs of diabetic and non-diabetic control baboons. After 2 and 4 weeks the skin incision sites were removed for measurement of breaking strength and epithelial thickness.Drum implants were removed for analysis of granulation tissue and inflammatory cells, CTGF and tissue inhibitor of matrix metalloproteinase (TIMP-1). Degradation of added CTGF by wound fluid was also examined. Results Healed incision site skin was stiffer (less elastic) in diabetic baboons and epithelial remodelling was slower compared with controls. Granulation tissue from diabetic baboons was reduced at 2 and 4 weeks, with increased vessel lumen areas at 4 weeks. Macrophages were reduced while neutrophils persisted in diabetic tissue. In diabetic wound tissue at 4 weeks there was less CTGF induced, as shown by immunohistochemistry, compared with controls. In contrast, Electronic supplementary material The online version of this article

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“…In the early phases of wound healing, there is an upregulation of the pro-inflammatory cytokines IL-1␣, IL-1␤, and TNF-␣. 29 This is assumed to be a component of the stress response that regulates protective processes, including caspase-mediated apoptosis, and reduces necrosis-associated pathology, which terminates the burn-induced inflammatory cascade and minimizes damage. Furthermore, cytokine release stimulates growth factor synthesis necessary to the wound healing process.…”

Section: Discussionmentioning

confidence: 99%

“…This prolonged local inflamma- tory response at the wound site may hinder and delay the ongoing process of wound healing. 10,29,32 A potential mechanism for this effect may be the activation of keratinocyte and fibroblast apoptosis via increases in local TNF-␣ protein levels, known to activate the caspase cascade and apoptosis. The IGF-1-induced decreases in local TNF-␣ levels may be responsible for decreases in the number of keratinocytes that commit to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Liposomal IGF-1 gene transfer modulates pro- and anti-inflammatory cytokine mRNA expression in the burn wound

et al. 2001

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Differential Regulation of Pro-Inflammatory Cytokines During Wound Healing in Normal and Glucocorticoid-Treated Mice

Cited by 430 publications

References 0 publications

Growth factor – regulated expression of enzymes involved in nucleotide biosynthesis: a novel mechanism of growth factor action

Growth factor – regulated expression of enzymes involved in nucleotide biosynthesis: a novel mechanism of growth factor action

A novel primate model of delayed wound healing in diabetes: dysregulation of connective tissue growth factor

Liposomal IGF-1 gene transfer modulates pro- and anti-inflammatory cytokine mRNA expression in the burn wound

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