PMID- 26935473
OWN - NLM
STAT- MEDLINE
DCOM- 20161228
LR  - 20211203
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 13
IP  - 4
DP  - 2016 Apr
TI  - CXCR4 antagonist AMD3100 ameliorates thyroid damage in autoimmune thyroiditis in 
      NOD.H‑2h(4) mice.
PG  - 3604-12
LID - 10.3892/mmr.2016.4965 [doi]
AB  - CXC chemokine ligand 12 (CXCL12) and its receptor, CXC chemokine receptor 4 
      (CXCR4), are upregulated in mice with autoimmune thyroid diseases. However, 
      whether this interaction is involved in the pathophysiology of autoimmune 
      thyroiditis (AIT) remains to be elucidated. In the present study, the effects of 
      the CXCR4 antagonist, AMD3100, in an iodine‑induced autoimmune thyroiditis model 
      were investigated. NOD.H‑2h4 mice were randomly separated into a control, AIT and 
      AIT+AMD3100 groups. The mice were fed with 0.05% sodium iodide water for 8 weeks 
      to induce AIT. The AMD3100‑treated mice were administered with the CXCR4 
      antagonist at a dose of 10 mg/kg intraperitoneally three times a week during the 
      experimental period. The percentages of CD19+interleukin (IL)10+ B cells and 
      CD4+IL10+ T cells, and the mRNA expression levels of IL10 in the splenocytes were 
      reduced in the AIT group, compared with the control group, however, they 
      increased following AMD3100 treatment, compared with the untreated AIT group. The 
      percentages of CD4+ T cells, CD8+ T cells, CD19+ B cells and CD8+ interferon 
      (IFN)gamma+ T cells, and the mRNA expression levels of IFNgamma increased in the AIT 
      group, compared with the control group, however, these were reduced in the 
      AMD3100 group, compared with the AIT group. The AMD3100‑treated mice also had 
      lower serum thyroglobulin antibody titers and reduced lymphocytic infiltration in 
      the thyroid, compared with the untreated AIT mice. These results suggested that 
      inhibition of this chemokine axis may offer potential as a therapeutic target for 
      the treatment of AIT.
FAU - Liu, Xin
AU  - Liu X
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Mao, Jinyuan
AU  - Mao J
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Han, Cheng
AU  - Han C
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Peng, Shiqiao
AU  - Peng S
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Li, Chenyan
AU  - Li C
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Jin, Ting
AU  - Jin T
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Fan, Chenling
AU  - Fan C
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Shan, Zhongyan
AU  - Shan Z
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
FAU - Teng, Weiping
AU  - Teng W
AD  - Department of Endocrinology and Metabolism, The Endocrine Institute and Liaoning 
      Provincial Key Laboratory of Endocrine Diseases, The First Hospital of China 
      Medical University, Shenyang, Liaoning 110001, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160302
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Antibodies)
RN  - 0 (Benzylamines)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Cyclams)
RN  - 0 (Heterocyclic Compounds)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CXCR4)
RN  - 130068-27-8 (Interleukin-10)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9010-34-8 (Thyroglobulin)
RN  - F5WR8N145C (Sodium Iodide)
RN  - S915P5499N (plerixafor)
SB  - IM
MH  - Animals
MH  - Antibodies/blood
MH  - Benzylamines
MH  - Chemokine CXCL12/genetics/metabolism
MH  - Cyclams
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Heterocyclic Compounds/*pharmacology
MH  - Interferon-gamma/genetics/metabolism
MH  - Interleukin-10/genetics/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred NOD
MH  - Microscopy, Fluorescence
MH  - RNA, Messenger/metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Receptors, CXCR4/*antagonists & inhibitors/metabolism
MH  - Sodium Iodide/toxicity
MH  - T-Lymphocytes/cytology
MH  - Thyroglobulin/immunology
MH  - Thyroid Gland/*drug effects/metabolism/pathology
MH  - Thyroiditis, Autoimmune/chemically induced/*pathology/veterinary
EDAT- 2016/03/05 06:00
MHDA- 2016/12/29 06:00
CRDT- 2016/03/04 06:00
PHST- 2015/01/22 00:00 [received]
PHST- 2015/11/10 00:00 [accepted]
PHST- 2016/03/04 06:00 [entrez]
PHST- 2016/03/05 06:00 [pubmed]
PHST- 2016/12/29 06:00 [medline]
AID - 10.3892/mmr.2016.4965 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Apr;13(4):3604-12. doi: 10.3892/mmr.2016.4965. Epub 2016 Mar 2.