PMID- 30539387
OWN - NLM
STAT- MEDLINE
DCOM- 20191224
LR  - 20191224
IS  - 1559-0720 (Electronic)
IS  - 0163-4984 (Linking)
VI  - 191
IP  - 1
DP  - 2019 Sep
TI  - Abnormal Iodine Nutrition-Induced ER Stress Upregulates MCP-1 Expression Through 
      P38/MAPK Signaling Pathway in Thyroid Cells.
PG  - 98-103
LID - 10.1007/s12011-018-1610-9 [doi]
AB  - Iodine is an important chemical for thyroid hormone synthesis. The association 
      between iodine nutrition status and the risk of disease present U-shaped curve, 
      as either low or high iodine nutrition status will increase the risk of thyroid 
      diseases. Endoplasmic reticulum stress (ER stress), which can induce over 
      expressions of inflammation factors, like monocyte chemo-attractant protein-1 
      (MCP-1), is related to the pathogenesis of thyroid disease. However, the 
      correlations among iodine, MCP-1 and ER stress are not entirely clear during the 
      pathogenesis of thyroid diseases. Present study aims to investigate how iodine 
      nutrition status influences MCP-1 expression through P38/MAPK pathway as well as 
      the roles of ER stress in this process. Human thyroid cells (Nthy-ori-3-1) was 
      used as a cell model in this study. The expressions of p-P38, PERK, IRE1, ATF6, 
      and MCP-1 were detected after the cells were treated with iodine at different 
      concentrations with or without ER stress inhibitor (4-PBA) or P38/MAPK blocker 
      (SB203580). The expressions of p-P38, PERK, IRE1, ATF6, and MCP-1 in Nthy-ori-3-1 
      cells treated with iodine at abnormal concentrations were all significantly 
      higher than those in cells treated with iodine at normal concentration. However, 
      addition of ER stress blocker, 4-PBA in the abnormal-iodine treated cells, 
      decreased the expressions of p-P38, PERK, IRE1, ATF6, and MCP-1. Similarly, 
      P38/MAPK activity inhibitor, SB203580, also decreased the expressions of p-P38 
      and MCP-1. Abnormal iodine nutrition status triggered ER stress and upregulated 
      MCP-1 expression through P38/MAPK signaling pathway in thyrocyte.
FAU - Chen, Xiaoshan
AU  - Chen X
AD  - The Second Clinical Medical College of Fujian Medical University, Quanzhou, 
      362000, Fujian, People's Republic of China.
FAU - Huang, Huibin
AU  - Huang H
AUID- ORCID: 0000-0001-6487-7029
AD  - Department of Endocrinology, The Second affiliated Hospital of Fujian Medical 
      University, NO.34 North Zhongshan Road, Quanzhou City, Fujian Province, People's 
      Republic of China. huibinhuang@aliyun.com.
FAU - Liang, Bo
AU  - Liang B
AD  - Department of Endocrinology, The Second affiliated Hospital of Fujian Medical 
      University, NO.34 North Zhongshan Road, Quanzhou City, Fujian Province, People's 
      Republic of China.
FAU - Zhou, Jingxiong
AU  - Zhou J
AD  - Department of Endocrinology, The Second affiliated Hospital of Fujian Medical 
      University, NO.34 North Zhongshan Road, Quanzhou City, Fujian Province, People's 
      Republic of China.
LA  - eng
GR  - 81370886/the National Natural Science Foundation of China/
GR  - 2014Y0017/Key scientific project of Fujian Province/
GR  - 2018-CX-33/Innovative medical research project of Fujian Province/
PT  - Journal Article
DEP - 20181211
PL  - United States
TA  - Biol Trace Elem Res
JT  - Biological trace element research
JID - 7911509
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 9679TC07X4 (Iodine)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Cell Line
MH  - Chemokine CCL2/*biosynthesis
MH  - Endoplasmic Reticulum Stress/*drug effects
MH  - Humans
MH  - Iodine/*pharmacology
MH  - MAP Kinase Signaling System/*drug effects
MH  - Thyroid Gland/cytology/*metabolism
MH  - Up-Regulation/*drug effects
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
OTO - NOTNLM
OT  - ER stress
OT  - Inflammatory
OT  - Iodine
OT  - MCP-1
OT  - P38/MAPK
OT  - Thyroid cells
EDAT- 2018/12/13 06:00
MHDA- 2019/12/25 06:00
CRDT- 2018/12/13 06:00
PHST- 2018/09/18 00:00 [received]
PHST- 2018/12/06 00:00 [accepted]
PHST- 2018/12/13 06:00 [pubmed]
PHST- 2019/12/25 06:00 [medline]
PHST- 2018/12/13 06:00 [entrez]
AID - 10.1007/s12011-018-1610-9 [pii]
AID - 10.1007/s12011-018-1610-9 [doi]
PST - ppublish
SO  - Biol Trace Elem Res. 2019 Sep;191(1):98-103. doi: 10.1007/s12011-018-1610-9. Epub 
      2018 Dec 11.