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ID 117039
Title Alternative
FGF2はヒト歯髄由来間葉系幹細胞においてJNK経路を介してCCL11の発現を抑制する
FGF2 SUPPRESSED CCL11 EXPRESSION IN HUMAN DENTAL PULP-DERIVED MSCs
Author
Kurogoushi, Rika Tokushima University|Tokyo Medical and Dental University
Iwata, Kokoro Tokyo Medical and Dental University
Sugimoto, Asuna Tokyo Medical and Dental University
Miyazaki, Aya Tokushima University
Narwidina, Anrizandy Tokushima University
Kawarabayashi, Keita Tokushima University
Iwamoto, Tsutomu Tokyo Medical and Dental University KAKEN Search Researchers
Keywords
dental pulp-derived mesenchymal stem cells
fibroblast growth factor 2
fibroblast growth factor receptor signal
C-C motif ligand 11
c-Jun N-terminal kinase
Content Type
Thesis or Dissertation
Description
The regulation of the mesenchymal stem cell (MSC) programming mechanism promises great success in regenerative medicine. Tissue regeneration has been associated not only with the differentiation of MSCs, but also with the microenvironment of the stem cell niche that involves various cytokines and immune cells in the tissue regeneration site. In the present study, fibroblast growth factor 2 (FGF2), the principal growth factor for tooth development, dental pulp homeostasis and dentin repair, was reported to affect the expression of cytokines in human dental pulp‑derived MSCs. FGF2 significantly inhibited the expression of chemokine C‑C motif ligand 11 (CCL11) in a time‑ and dose‑dependent manner in the SDP11 human dental pulp‑derived MSC line. This inhibition was diminished following treatment with the AZD4547 FGF receptor (FGFR) inhibitor, indicating that FGF2 negatively regulated the expression of CCL11 in SDP11 cells. Furthermore, FGF2 activated the phosphorylation of p38 mitogen‑activated protein kinase (p38 MAPK), extracellular signal‑regulated kinase 1/2 (ERK1/2) and c‑Jun N‑terminal kinases (JNK) in SDP11 cells. The mechanism of the FGFR‑downstream signaling pathway was then studied using the SB203580, U0126 and SP600125 inhibitors for p38 MAPK, ERK1/2, and JNK, respectively. Interestingly, only treatment with SP600125 blocked the FGF2‑mediated suppression of CCL11. The present results suggested that FGF2 regulated the expression of cytokines and suppressed the expression of CCL11 via the JNK signaling pathway in human dental pulp‑derived MSCs. The present findings could provide important insights into the association of FGF2 and CCL11 in dental tissue regeneration therapy.
Journal Title
Experimental and Therapeutic Medicine
ISSN
17920981
17921015
NCID
AA12610820
Publisher
Spandidos Publications
Volume
22
Issue
6
Start Page
1356
Published Date
2021-09-24
Remark
内容要旨・審査要旨・論文本文の公開
本論文は, 著者RIKA KUROGOUSHIの学位論文として提出され, 学位審査・授与の対象となっている。
Rights
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
ETD
MEXT report number
甲第3615号
Diploma Number
甲口第485号
Granted Date
2022-03-23
Degree Name
Doctor of Dental Science
Grantor
Tokushima University
departments
Oral Sciences
University Hospital