Open AccessHeat shock transcription factor 1 affects kidney tubular cell migration by regulating the TGF‑β1‑Smad2/3 signaling pathway
Author(s) -
Qiang Lou,
Yuanyuan Li,
Beibei Hou,
Yonglian Liu,
Yan Zhang,
Jielu Hao,
Yun Ma
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10689
Subject(s) - hsf1 , gene knockdown , cell migration , microbiology and biotechnology , transforming growth factor , transcription factor , biology , heat shock factor , signal transduction , cancer research , cell , cell cycle , heat shock protein , apoptosis , gene , hsp70 , biochemistry
Cell migration is important for renal recovery from tubular cell injury. Heat shock transcription factor 1 (HSF1) is a well‑studied regulatory factor that is active during acute kidney injury. HSF1 is also involved in the migration process during tumor metastasis. Therefore, we hypothesized that HSF1 may promote the recovery of renal function by affecting kidney tubular cell migration. A wound healing assay was used to examine the cell migration rate. The results demonstrated that the migration of rat kidney proximal tubular cells (RPTCs) was increased following knockdown of HSF1. In addition, the invasion ability of HSF1 knockdown RPTCs was also significantly upregulated. The present study also identified that transforming growth factor‑β1 (TGF‑β1) was highly expressed at the edge of the wound in control cells, and its expression was further increased upon knockdown of HSF1. Inhibition of TGF‑β1 signaling prevented RPTC HSF1 knockdown cell migration, suggesting that HSF1‑regulated RPTC cell migration was dependent on the TGF‑β1 signaling pathway. Furthermore, phosphorylation of TGF‑β1 and Smad2/3 was induced in HSF1 knockdown cells. Together, these results suggest that HSF1 may suppress RPTC migration by inhibiting the activation of the TGF‑β1‑Smad2/3 signaling pathway.