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We investigated whether transforming growth factor-beta (TGF-beta) stimulates the induction of heat shock protein (HSP) 27 and HSP70 in osteoblast-like MC3T3-E1 cells and the mechanism underlying the induction. TGF-beta increased the level of HSP27 but had no effect on the HSP70 level. TGF-beta stimulated the accumulation of HSP27 dose-dependently, and induced an increase in the level of mRNA for HSP27. TGF-beta induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase. The HSP27 accumulation induced by TGF-beta was significantly suppressed by PD98059, an inhibitor of the upstream kinase of p44/p42 MAP kinase, or SB203580, an inhibitor of p38 MAP kinase. PD98059 and SB203580 suppressed the TGF-beta-stimulated increase in the level of mRNA for HSP27. Retinoic acid, a vitamin A (retinol) metabolite, which alone had little effect on the HSP27 level, markedly enhanced the HSP27 accumulation stimulated by TGF-beta. Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27. The amplification of TGF-beta-stimulated HSP27 accumulation by retinoic acid was reduced by PD98059 or SB203580. Retinoic acid failed to affect the TGF-beta-induced phosphorylation of p44/p42 MAP kinase or p38 MAP kinase. These results strongly suggest that p44/p42 MAP kinase and p38 MAP kinase take part in the pathways of the TGF-beta-stimulated HSP27 induction in osteoblasts, and that retinoic acid upregulates the TGF-beta-stimulated HSP27 induction at a point downstream from p44/p42 MAP kinase and p38 MAP kinase.

Irritation fibromas are very common hyperplastic lesions of the oral mucosa, although there have been few studies of large numbers of cases. Clinicopathological features of this type of lesion were examined in 129 lesions in 124 patients, consisting of 47 males and 77 females. The peak incidence of the lesion was in the 6th decade of life. The lesions occurred in the tongue (n=66), the buccal mucosa (n=42), the labial mucosa (n=14), and the hard palate (n=7). All of the lesions were excised totally, and no recurrence was reported in any of the cases. Histologically, the lesions were divided into "radiating" type (n=105) and "circular" type (n=24) according to Barker & Lucas (1967). The incidence of the lesions in the buccal and labial mucosae was higher in the circular type of lesions (83.3%) than in the radiating type of lesions (34.3%), with a significant statistical difference (p<0.05). This supports the hypothesis that a low level of trauma or mechanical irritation might produce a radiating lesion on fixed mucosa and a circular lesion on mobile mucosa.

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