PMID- 29691578
OWN - NLM
STAT- MEDLINE
DCOM- 20190104
LR  - 20190104
IS  - 0371-0874 (Print)
IS  - 0371-0874 (Linking)
VI  - 70
IP  - 2
DP  - 2018 Apr 25
TI  - [Effects of thyroid hormone on macrophage dysfunction induced by oxidized 
      low-density lipoprotein].
PG  - 141-148
AB  - It has been recognized that patients with hypothyroidism have higher risks of 
      atherosclerosis and coronary heart disease, however, the mechanisms are largely 
      unknown. Considering that macrophage dysfunction plays an important role in the 
      formation and development of atherosclerosis plaques, this study aimed to 
      investigate the direct effects of thyroid hormone on macrophage functions and to 
      provide new insight for the mechanism of hypothyroid atherosclerosis. RAW264.7 
      cells (mouse leukaemic monocyte macrophage cell line) were incubated with 
      oxidized low-density lipoprotein (oxLDL) to establish macrophage foam cells model 
      in vitro, and the protective effects of different concentration of thyroxine (T4) 
      on the macrophage foam cells function were explored. The proliferation, migration 
      and cell aging of macrophages were detected by MTT method, scratch test and 
      beta-galactosidase staining respectively. The ELISA method was used to detect the 
      secretion of tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 
      (MCP-1), and interleukin-1beta (IL-1beta). Western blot analysis was applied to measure 
      the phosphorylation of focal adhesion kinase (FAK), which was required for the 
      process of proliferation and migration of macrophages. The results showed that 
      oxLDL significantly inhibited the macrophage proliferation and migration, induced 
      cell senescence, and promoted the secretion of TNF-alpha, MCP-1, and IL-1beta; while T4 
      reversed those effects of oxLDL on macrophage in a concentration-dependent 
      manner. Moreover, oxLDL increased the phosphorylation of FAK in macrophage, while 
      T4 concentration-dependently reversed the effect. These results suggest that T4 
      modulates macrophage proliferation, migration, senescence, and secretion of 
      inflammation factors in a concentration-dependent way.
FAU - Ning, Yu
AU  - Ning Y
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Zhang, Ming
AU  - Zhang M
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China. 
      mzcap@163.com.
FAU - DU, Yun-Hui
AU  - DU YH
AD  - Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, 
      Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart 
      Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Zhang, Hui-Na
AU  - Zhang HN
AD  - Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, 
      Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart 
      Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Li, Lin-Yi
AU  - Li LY
AD  - Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, 
      Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart 
      Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Qin, Yan-Wen
AU  - Qin YW
AD  - Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, 
      Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart 
      Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Wen, Wan-Wan
AU  - Wen WW
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
FAU - Zhao, Quan-Ming
AU  - Zhao QM
AD  - Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, 
      Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Sheng Li Xue Bao
JT  - Sheng li xue bao : [Acta physiologica Sinica]
JID - 20730130R
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (oxidized low density lipoprotein)
RN  - EC 2.7.10.2 (Focal Adhesion Kinase 1)
RN  - EC 2.7.10.2 (Ptk2 protein, mouse)
RN  - Q51BO43MG4 (Thyroxine)
SB  - IM
MH  - Animals
MH  - Atherosclerosis
MH  - Chemokine CCL2/metabolism
MH  - Foam Cells/*drug effects/pathology
MH  - Focal Adhesion Kinase 1/metabolism
MH  - Interleukin-1beta/metabolism
MH  - Lipoproteins, LDL/*adverse effects
MH  - Macrophages/*drug effects/pathology
MH  - Mice
MH  - Phosphorylation
MH  - RAW 264.7 Cells
MH  - Thyroxine/*pharmacology
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2018/04/25 06:00
MHDA- 2019/01/05 06:00
CRDT- 2018/04/26 06:00
PHST- 2018/04/26 06:00 [entrez]
PHST- 2018/04/25 06:00 [pubmed]
PHST- 2019/01/05 06:00 [medline]
PST - ppublish
SO  - Sheng Li Xue Bao. 2018 Apr 25;70(2):141-148.