PMID- 29792849
OWN - NLM
STAT- MEDLINE
DCOM- 20190924
LR  - 20190925
IS  - 1090-2422 (Electronic)
IS  - 0014-4827 (Linking)
VI  - 369
IP  - 2
DP  - 2018 Aug 15
TI  - The role and mechanism of K(Ca)3.1 channels in human monocyte migration induced 
      by palmitic acid.
PG  - 208-217
LID - S0014-4827(18)30291-X [pii]
LID - 10.1016/j.yexcr.2018.05.020 [doi]
AB  - Monocyte migration into diseased tissues contributes to the pathogenesis of 
      diseases. Intermediate-conductance Ca(2+)-activated K(+) (K(Ca)3.1) channels play 
      an important role in cell migration. However, the role of K(Ca)3.1 channels in 
      mediating monocyte migration induced by palmitic acid (PA) is still unclear. 
      Using cultured THP-1 cells and peripheral blood mononuclear cells from healthy 
      subjects, we investigated the role and signaling mechanisms of K(Ca)3.1 channels 
      in mediating the migration induced by PA. Using methods of Western blotting 
      analysis, RNA interference, cell migration assay and ELISA, we found that 
      PA-treated monocytes exhibited increment of the protein levels of K(Ca)3.1 
      channel and monocyte chemoattractant protein-1 (MCP-1), and the effects were 
      reversed by co-incubation of PA with anti-TLR2/4 antibodies or by specific 
      inhibitors of p38-MAPK, or NF-kappaB. In addition, PA increased monocyte migration, 
      which was abolished by a specific K(Ca)3.1 channel blocker, TRAM-34, or K(Ca)3.1 
      small interfering RNA (siRNA). The expression and secretion of MCP-1 induced by 
      PA was also similarly prevented by TRAM-34 and K(Ca)3.1 siRNA. These results 
      demonstrate for the first time that PA upregulates K(Ca)3.1 channels through 
      TLR2/4, p38-MAPK and NF-kappaB pathway to promote the expression of MCP-1, and then 
      induce the trans-endothelial migration of monocytes.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Ma, Xiao-Zhen
AU  - Ma XZ
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China.
FAU - Pang, Zheng-Da
AU  - Pang ZD
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China.
FAU - Wang, Jun-Hong
AU  - Wang JH
AD  - Department of Endocrinology, The Second Affiliated Hospital, Xi'an Jiaotong 
      University, 157 Fifth West Road, Xi'an 710004, Shaanxi, China.
FAU - Song, Zheng
AU  - Song Z
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China.
FAU - Zhao, Li-Mei
AU  - Zhao LM
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China. Electronic address: dengxl@mail.xjtu.edu.cn.
FAU - Du, Xiao-Jun
AU  - Du XJ
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China; Baker Heart and Diabetes Institute, 75 Commercial Road, 
      Melbourne, Victoria 3004, Australia.
FAU - Deng, Xiu-Ling
AU  - Deng XL
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, Xi'an 
      710061, Shaanxi, China; Cardiovascular Research Centre, School of Basic Medical 
      Sciences, Xi'an Jiaotong University Health Science Center, 76 West Yanta Road, 
      Xi'an 710061, Shaanxi, China. Electronic address: dengxl@mail.xjtu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180521
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Intermediate-Conductance Calcium-Activated Potassium Channels)
RN  - 0 (KCNN4 protein, human)
RN  - 0 (NF-kappa B)
RN  - 0 (Potassium Channel Blockers)
RN  - 0 (Pyrazoles)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (TLR2 protein, human)
RN  - 0 (TLR4 protein, human)
RN  - 0 (TRAM 34)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 2V16EO95H1 (Palmitic Acid)
SB  - IM
MH  - Cell Movement/*drug effects/*physiology
MH  - Chemokine CCL2/metabolism
MH  - Humans
MH  - Intermediate-Conductance Calcium-Activated Potassium Channels/antagonists & 
      inhibitors/genetics/*metabolism
MH  - MAP Kinase Signaling System/drug effects
MH  - Monocytes/*drug effects/*physiology
MH  - NF-kappa B/metabolism
MH  - Palmitic Acid/*pharmacology
MH  - Potassium Channel Blockers/pharmacology
MH  - Pyrazoles/pharmacology
MH  - RNA, Small Interfering/genetics
MH  - Signal Transduction/drug effects
MH  - THP-1 Cells
MH  - Toll-Like Receptor 2/metabolism
MH  - Toll-Like Receptor 4/metabolism
MH  - Up-Regulation/drug effects
OTO - NOTNLM
OT  - Intermediate-conductance Ca(2+)-activated K(+) channels
OT  - MCP-1
OT  - Monocyte migration
OT  - Palmitic acid
EDAT- 2018/05/25 06:00
MHDA- 2019/09/26 06:00
CRDT- 2018/05/25 06:00
PHST- 2018/04/10 00:00 [received]
PHST- 2018/05/18 00:00 [revised]
PHST- 2018/05/20 00:00 [accepted]
PHST- 2018/05/25 06:00 [pubmed]
PHST- 2019/09/26 06:00 [medline]
PHST- 2018/05/25 06:00 [entrez]
AID - S0014-4827(18)30291-X [pii]
AID - 10.1016/j.yexcr.2018.05.020 [doi]
PST - ppublish
SO  - Exp Cell Res. 2018 Aug 15;369(2):208-217. doi: 10.1016/j.yexcr.2018.05.020. Epub 
      2018 May 21.