PMID- 30261648
OWN - NLM
STAT- MEDLINE
DCOM- 20190110
LR  - 20211204
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 19
IP  - 10
DP  - 2018 Sep 26
TI  - Combined Fluid Shear Stress and Melatonin Enhances the ERK/Akt/mTOR Signal in 
      Cilia-Less MC3T3-E1 Preosteoblast Cells.
LID - 10.3390/ijms19102929 [doi]
LID - 2929
AB  - We investigated whether combined fluid shear stress (FSS) and melatonin 
      stimulated signal transduction in cilia-less MC3T3-E1 preosteoblast cells. 
      MC3T3-E1 cells were treated with chloral hydrate or nocodazole, and 
      mechanotransduction sensor primary cilia were removed. p-extracellular 
      signal(-)regulated kinase (ERK) and p-Akt with/without melatonin increased with 
      nocodazole treatment and decreased with chloral hydrate treatment, whereas p-ERK 
      and p-Akt in FSS with/without melatonin increased in cilia-less groups compared 
      to cilia groups. Furthermore, p-mammalian target of rapamycin (mTOR) with 
      FSS-plus melatonin increased in cilia-less groups compared to only melatonin 
      treatments in cilia groups. Expressions of Bcl-2, Cu/Zn-superoxide dismutase 
      (SOD), and catalase proteins were higher in FSS with/without melatonin with 
      cilia-less groups than only melatonin treatments in cilia groups. Bax protein 
      expression was high in FSS-plus melatonin with chloral hydrate treatment. In 
      chloral hydrate treatment with/without FSS, expressions of Cu/Zn-SOD, Mn-SOD, and 
      catalase proteins were high compared to only-melatonin treatments. In nocodazole 
      treatment, Mn-SOD protein expression without FSS was high, and catalase protein 
      level with FSS was low, compared to only melatonin treatments. These data show 
      that the combination with FSS and melatonin enhances ERK/Akt/mTOR signal in 
      cilia-less MC3T3-E1, and the enhanced signaling in cilia-less MC3T3-E1 osteoblast 
      cells may activate the anabolic effect for the preservation of cell structure and 
      function.
FAU - Kim, Chi Hyun
AU  - Kim CH
AD  - Department of Biomedical Engineering, College of Health Science, Yonsei 
      University, Wonju, Gangwon 26493, Korea. chihyun@yonsei.ac.kr.
FAU - Jeung, Eui-Bae
AU  - Jeung EB
AUID- ORCID: 0000-0001-8936-916X
AD  - Laboratory of Veterinary Biochemistry and Molecular Biology, College of 
      Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, 
      Korea. ebjeung@chungbuk.ac.kr.
FAU - Yoo, Yeong-Min
AU  - Yoo YM
AUID- ORCID: 0000-0003-1732-8494
AD  - Laboratory of Veterinary Biochemistry and Molecular Biology, College of 
      Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, 
      Korea. yyeongm@hanmail.net.
LA  - eng
PT  - Journal Article
DEP - 20180926
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Antioxidants)
RN  - 0 (Tubulin Modulators)
RN  - 418M5916WG (Chloral Hydrate)
RN  - EC 1.15.1.1 (Superoxide Dismutase-1)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - JL5DK93RCL (Melatonin)
RN  - SH1WY3R615 (Nocodazole)
SB  - IM
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Cell Line
MH  - Chloral Hydrate/pharmacology
MH  - Cilia/metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Hydrodynamics
MH  - Melatonin/*pharmacology
MH  - Mice
MH  - Nocodazole/pharmacology
MH  - Osteoblasts/*drug effects/metabolism
MH  - Protein Kinases/*metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction/*drug effects
MH  - *Stress, Mechanical
MH  - Superoxide Dismutase-1/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Tubulin Modulators/pharmacology
PMC - PMC6213863
OTO - NOTNLM
OT  - MC3T3-E1 cells
OT  - chloral hydrate
OT  - fluid shear stress
OT  - melatonin
OT  - nocodazole
OT  - primary cilia
COIS- The authors declare no conflict of interest.
EDAT- 2018/09/29 06:00
MHDA- 2019/01/11 06:00
PMCR- 2018/10/01
CRDT- 2018/09/29 06:00
PHST- 2018/08/30 00:00 [received]
PHST- 2018/09/22 00:00 [revised]
PHST- 2018/09/23 00:00 [accepted]
PHST- 2018/09/29 06:00 [entrez]
PHST- 2018/09/29 06:00 [pubmed]
PHST- 2019/01/11 06:00 [medline]
PHST- 2018/10/01 00:00 [pmc-release]
AID - ijms19102929 [pii]
AID - ijms-19-02929 [pii]
AID - 10.3390/ijms19102929 [doi]
PST - epublish
SO  - Int J Mol Sci. 2018 Sep 26;19(10):2929. doi: 10.3390/ijms19102929.