PMID- 25418681
OWN - NLM
STAT- MEDLINE
DCOM- 20150316
LR  - 20200315
IS  - 1365-2184 (Electronic)
IS  - 0960-7722 (Print)
IS  - 0960-7722 (Linking)
VI  - 48
IP  - 1
DP  - 2015 Feb
TI  - Cyclic mechanical stress modulates neurotrophic and myelinating gene expression 
      of Schwann cells.
PG  - 59-66
LID - 10.1111/cpr.12151 [doi]
AB  - OBJECTIVES: This study aimed to investigate the response of Schwann cells to 
      cyclic compressive and tensile stresses of different durations of stimulation. 
      MATERIALS AND METHODS: RSC96 cells were subjected to cyclic tensile stress or 
      compressive stress; for either, cells in five groups were treated for 0, 1, 2, 24 
      and 48 h respectively. Enzyme-linked immunosorbent assay was conducted to detect 
      secretion of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), 
      neurotrophin-3 and neurotrophin-4 in the culture medium. Real-time PCR was 
      conducted to quantify mRNA expression of neurotrophins including NGF, BDNF, 
      neurotrophin-3 and neurotrophin-4, and myelin-related genes including Sox10, 
      Krox20, neuregulin 1, NCAM, N-cadherin, P0, MAG and MBP. Immunofluorescent 
      staining was performed to visualize Krox20 and F-actin in the tensile groups. 
      RESULTS: Within 24 h, cells treated with cyclic tensile stress expressed and 
      secreted significantly more BDNF, while cyclic compression down-regulated BDNF 
      expression. Cells treated with both tensile and compressive stress down-regulated 
      expression of NRG1, NCAM, Krox20 and Sox10 at all time points. Expression of 
      N-cadherin was not affected by either stretch or compression. F-actin was 
      down-regulated by tensile stress. CONCLUSIONS: Both tensile and compressive 
      loading down-regulated expression of several important myelin-related Schwann 
      cells genes and thus facilitated demyelination. Tensile stress meanwhile promoted 
      secretion of BDNF by Schwann cells within 24 h, which may contribute to 
      maintenance and repair of damaged axons. These effects of mechanical stress might 
      have been mediated by the actin cytoskeleton.
CI  - (c) 2014 John Wiley & Sons Ltd.
FAU - Zhang, L
AU  - Zhang L
AD  - State Key Laboratory of Oral Diseases, West China School of Stomatology, Sichuan 
      University, Chengdu, 610041, China.
FAU - Yang, X
AU  - Yang X
FAU - Yue, Y
AU  - Yue Y
FAU - Ye, J
AU  - Ye J
FAU - Yao, Y
AU  - Yao Y
FAU - Fu, Y
AU  - Fu Y
FAU - Li, G
AU  - Li G
FAU - Yao, Q
AU  - Yao Q
FAU - Lin, Y
AU  - Lin Y
FAU - Gong, P
AU  - Gong P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141124
PL  - England
TA  - Cell Prolif
JT  - Cell proliferation
JID - 9105195
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Early Growth Response Protein 2)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics
MH  - Cell Adhesion Molecules/metabolism
MH  - Cell Line
MH  - Early Growth Response Protein 2/metabolism
MH  - *Gene Expression Regulation
MH  - Humans
MH  - Myelin Sheath/*metabolism
MH  - Rats
MH  - Schwann Cells/*metabolism
MH  - *Stress, Mechanical
PMC - PMC6496414
EDAT- 2014/11/25 06:00
MHDA- 2015/03/17 06:00
PMCR- 2014/11/24
CRDT- 2014/11/25 06:00
PHST- 2014/04/01 00:00 [received]
PHST- 2014/09/12 00:00 [accepted]
PHST- 2014/11/25 06:00 [entrez]
PHST- 2014/11/25 06:00 [pubmed]
PHST- 2015/03/17 06:00 [medline]
PHST- 2014/11/24 00:00 [pmc-release]
AID - CPR12151 [pii]
AID - 10.1111/cpr.12151 [doi]
PST - ppublish
SO  - Cell Prolif. 2015 Feb;48(1):59-66. doi: 10.1111/cpr.12151. Epub 2014 Nov 24.