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- Author: Masashi Suzuki x
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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University of Tsukuba, Tennodai, Tsukuba, Ibaraki 305-8572, Japan
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The highly ordered process of wound healing involves the coordinated regulation of cell proliferation and migration and tissue remodeling, predominantly by polypeptide growth factors. Consequently, the slowing of wound healing that occurs in the aged may be related to changes in the activity of these various regulatory factors. To gain additional insight into these issues, we quantified the absolute copy numbers of mRNAs encoding all the fibroblast growth factors (FGFs), their receptors (FGFRs) and two other growth factors in the dorsal skin of young and aged mice during the healing of full-thickness skin excisional wounds. In young adult mice (8 weeks old), FGF7, FGF10 and FGF22 mRNAs were all strongly expressed in healthy skin, and levels of FGF7 and 10 but not 22 increased 2- to 3.5-fold over differing time courses after wounding. The levels of FGF9, 16, 18 and especially 23 mRNAs were moderate or low in healthy skin but increased 2- to 33-fold after wounding. Among the four FGFRs, expression of only FGFR1 mRNA was augmented during wound healing. Expression of transforming growth factor-β and hepatocyte growth factor was also high in healthy skin and was upregulated during healing. Notably, in aged mice (35 weeks old), where healing proceeded more slowly than in the young, both the basal and wound-induced mRNA expression of most of these genes was reduced. While these results confirm the established notion that FGFR2 IIIB ligands (FGF7 and FGF10) are important for wound healing, they also suggest that decreased expression of multiple FGF ligands contributes to the slowing of wound healing in aged mice and indicate the potential importance of further study of the involvement of FGF9, 16, 18 and 23 in the wound healing process.
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Monocyte chemoattractant protein-1 (MCP-1) and angiotensin II (Ang II) in adipose tissue are thought to induce systemic insulin resistance in rodents; but the precise mechanism is not fully clarified. We examined the mechanism of Ang II-induced and/or tumor necrosis factor-α (TNF-α)-induced MCP-1 production from 3T3-L1 preadipocytes. The MCP-1 protein and MCP-1 mRNA expression in 3T3-L1 preadipocytes were increased significantly by stimulation with TNF-α. We found no significant increase in MCP-1 concentrations by Ang II alone; but it enhanced the TNF-α-induced MCP-1 mRNA expression in a dose-dependent manner. Then, we examined the effect of Ang II and/or TNF-α on phosphorylation of extracellular signal-regulated kinase (ERK), p38MAPK, and IκB-α. Ang II and TNF-α clearly enhanced ERK and p38MAPK phosphorylation. IκB-α phosphorylation was enhanced by TNF-α, but not by Ang II. The MCP-1 mRNA expression induced by TNF-α and co-stimulation with Ang II was inhibited by either ERK inhibitor, p38MAPK inhibitor or NF-κB inhibitor. Moreover, Ang II enhanced the activation of AP-1 (c-fos) induced by TNF-α. Our results suggest that Ang II may serve as an additional stimulus on the TNF-α-induced MCP-1 production through the ERK-and p38MAPK-dependent pathways probably due to AP-1 activation.
