Department of Pathology, School of Dentistry Chosun University, Gwangju 501-759, Korea.
J Endod. 2010 Aug;36(8):1332-5. doi: 10.1016/j.joen.2010.04.010. Epub 2010 Jun 19.
Transforming growth factor beta1 (TGFbeta1) regulates cellular functions including cell growth, differentiation, angiogenesis, migration, and metastasis. The TGFbeta1 signal transduction pathways are mostly undefined in mouse dental papilla-derived MDPC-23 cells. In this study, we investigated TGFbeta1-induced migration focusing on heat shock protein 27 (Hsp27) activation.
Cellular responses mediated by TGFbeta1 in MDPC-23 cells were measured by Western blot and MTT assays. Cell migration was determined by counting migrated cells using the chemotaxis cell migration assay.
TGFbeta1 induced cell migration and increased the phosphorylation of Hsp27 and p38 MAPK in MDPC-23 cells. However, TGFbeta1 did not affect Akt/NF-kappaB signaling to regulate the migration of MDPC-23 cells. Inhibiting p38 MAPK with SB203580 blocked TGFbeta1-induced Hsp27 activation and cell migration.
Hsp27 phosphorylation followed by p38 MAPK activation was required for TGFbeta1-induced migration, and Hsp27 itself contributed to MDPC-23 cell migration.
转化生长因子β1(TGFβ1)调节细胞功能,包括细胞生长、分化、血管生成、迁移和转移。TGFβ1 信号转导途径在小鼠牙乳头来源的 MDPC-23 细胞中大多未被定义。在这项研究中,我们研究了 TGFβ1 诱导的迁移,重点关注热休克蛋白 27(Hsp27)的激活。
通过 Western blot 和 MTT 测定法测量 TGFβ1 在 MDPC-23 细胞中介导的细胞反应。通过趋化细胞迁移测定法计数迁移细胞来确定细胞迁移。
TGFβ1 诱导 MDPC-23 细胞迁移,并增加 Hsp27 和 p38 MAPK 的磷酸化。然而,TGFβ1 不影响 Akt/NF-κB 信号通路来调节 MDPC-23 细胞的迁移。用 SB203580 抑制 p38 MAPK 阻断了 TGFβ1 诱导的 Hsp27 激活和细胞迁移。
TGFβ1 诱导的迁移需要 Hsp27 磷酸化,随后 p38 MAPK 激活,Hsp27 本身有助于 MDPC-23 细胞迁移。