Department of Pathology, Chosun University, School of Dentistry, Seoseok-dong, Dong-gu, Gwangju, Korea.
Biol Pharm Bull. 2011;34(4):486-9. doi: 10.1248/bpb.34.486.
Transforming growth factor β1 (TGF-β1) regulates cellular functions including cell growth, differentiation, and migration. However, signal transduction pathways of TGF-β1 are mostly undefined in human periodontal ligament (hPDL) cells. In this study, we investigated TGF β1-induced migration focusing on heat shock protein 27 (Hsp27) activation. The cellular response to TGF-β1 by hPDL cells was measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and Western blot analysis. Cell migration was determined by counting migrated cells using a Chemotaxis Cell Migration Assay kit. TGF-β1 induced cell migration and increased the phosphorylation of Hsp27 and p38 mitogen-activated protein kinase (MAPK) in hPDL cells. Inhibiting p38 MAPK with SB203580 blocked TGF-β1-induced Hsp27 activation and cell migration. These findings suggest that TGF-β1-induced Hsp27 may promote the migration of hPDL cells via p38 MAPK mediated signaling. Hsp27 may be a potential target for the periodontal regeneration process related to cell migration.
转化生长因子 β1(TGF-β1)调节细胞功能,包括细胞生长、分化和迁移。然而,TGF-β1 的信号转导途径在人牙周韧带(hPDL)细胞中大多尚未确定。在这项研究中,我们研究了 TGF-β1 诱导的迁移,重点关注热休克蛋白 27(Hsp27)的激活。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)测定法和 Western blot 分析测量 hPDL 细胞对 TGF-β1 的细胞反应。通过使用趋化细胞迁移测定试剂盒计数迁移的细胞来确定细胞迁移。TGF-β1 诱导细胞迁移,并增加 hPDL 细胞中 Hsp27 和 p38 丝裂原活化蛋白激酶(MAPK)的磷酸化。用 SB203580 抑制 p38 MAPK 阻断了 TGF-β1 诱导的 Hsp27 激活和细胞迁移。这些发现表明,TGF-β1 诱导的 Hsp27 可能通过 p38 MAPK 介导的信号通路促进 hPDL 细胞的迁移。Hsp27 可能是与细胞迁移相关的牙周再生过程的潜在靶标。