PMID- 22595232
OWN - NLM
STAT- MEDLINE
DCOM- 20121126
LR  - 20211203
IS  - 1873-5487 (Electronic)
IS  - 0188-4409 (Linking)
VI  - 43
IP  - 4
DP  - 2012 May
TI  - Perinatal iodine deficiency and hypothyroidism increase cell apoptosis and alter 
      doublecortin and reelin protein expressions in rat cerebellum.
PG  - 255-64
LID - 10.1016/j.arcmed.2012.05.002 [doi]
AB  - BACKGROUND AND AIMS: Adequate thyroid hormone is critical for cerebellar 
      development. Developmental hypothyroidism induced by iodine deficiency during the 
      perinatal period results in permanent impairments of cerebellar development with 
      an unclear mechanism. In the present study we investigated effects of perinatal 
      iodine deficiency and hypothyroidism on cerebellar cell apoptosis, doublecortin 
      (Dcx) and reelin. Apoptosis is an essential part of neural development. Dcx and 
      reelin are two important molecules involved in neuronal migration, structure, and 
      development in cerebellum. METHODS: Two developmental rat models were created by 
      administering dam rats with either iodine-deficient diet or propylthiouracil 
      (PTU, 5 ppm or 15 ppm)-added drinking water from gestational day (GD) 6 until 
      postnatal day (PND) 28. TUNEL assay and protein levels of Dcx and reelin in 
      cerebella were assessed on PND14, 21 and 28. RESULTS: Apoptotic cells were 
      increased in the iodine-deficient and PTU-treated rats. Dcx protein levels in the 
      cerebella of iodine-deficient and PTU-treated rats were significantly 
      downregulated on PND14. Interestingly, iodine deficiency and PTU treatment 
      upregulated the levels of Dcx protein on PND21 and 28. Reelin expressions in 
      iodine-deficient and PTU-treated rats were significantly decreased on PND14 and 
      21. On PND28, reelin expressions of three treated groups were still lower than 
      control group, although without significant difference. CONCLUSIONS: These 
      findings may implicate alterations in cell apoptosis and levels of Dcx and reelin 
      in the impairments of cerebellar development induced by developmental iodine 
      deficiency and hypothyroidism.
CI  - Copyright (c) 2012 IMSS. Published by Elsevier Inc. All rights reserved.
FAU - Wang, Yi
AU  - Wang Y
AD  - Department of Occupational and Environmental Health, School of Public Health, 
      China Medical University, Shenyang, PR China.
FAU - Zhong, Jiapeng
AU  - Zhong J
FAU - Xu, Hongde
AU  - Xu H
FAU - Wei, Wei
AU  - Wei W
FAU - Dong, Jing
AU  - Dong J
FAU - Yu, Fei
AU  - Yu F
FAU - Wang, Yuan
AU  - Wang Y
FAU - Gong, Jian
AU  - Gong J
FAU - Shan, Zhongyan
AU  - Shan Z
FAU - Teng, Weiping
AU  - Teng W
FAU - Chen, Jie
AU  - Chen J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120515
PL  - United States
TA  - Arch Med Res
JT  - Archives of medical research
JID - 9312706
RN  - 0 (Cell Adhesion Molecules, Neuronal)
RN  - 0 (Dcx protein, rat)
RN  - 0 (Doublecortin Domain Proteins)
RN  - 0 (Doublecortin Protein)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neuropeptides)
RN  - 0 (Reelin Protein)
RN  - 0 (Reln protein, rat)
RN  - 0 (Thyroid Hormones)
RN  - 721M9407IY (Propylthiouracil)
RN  - 9679TC07X4 (Iodine)
RN  - EC 3.4.21.- (Serine Endopeptidases)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis
MH  - Cell Adhesion Molecules, Neuronal/*biosynthesis/genetics
MH  - Cerebellum/embryology/growth & development/metabolism/*pathology
MH  - Doublecortin Domain Proteins
MH  - Doublecortin Protein
MH  - Extracellular Matrix Proteins/*biosynthesis/genetics
MH  - Female
MH  - Gene Expression Regulation, Developmental
MH  - Hypothyroidism/chemically induced/etiology/genetics/metabolism/*pathology
MH  - Iodine/*deficiency
MH  - Male
MH  - Microtubule-Associated Proteins/*biosynthesis/genetics
MH  - Nerve Tissue Proteins/*biosynthesis/genetics
MH  - Neuropeptides/*biosynthesis/genetics
MH  - Pregnancy
MH  - Pregnancy Complications/chemically induced/genetics/metabolism/*pathology
MH  - Propylthiouracil/toxicity
MH  - Rats
MH  - Rats, Wistar
MH  - Reelin Protein
MH  - Serine Endopeptidases/*biosynthesis/genetics
MH  - Thyroid Hormones/blood/physiology
EDAT- 2012/05/19 06:00
MHDA- 2012/12/10 06:00
CRDT- 2012/05/19 06:00
PHST- 2011/11/29 00:00 [received]
PHST- 2012/04/20 00:00 [accepted]
PHST- 2012/05/19 06:00 [entrez]
PHST- 2012/05/19 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
AID - S0188-4409(12)00127-0 [pii]
AID - 10.1016/j.arcmed.2012.05.002 [doi]
PST - ppublish
SO  - Arch Med Res. 2012 May;43(4):255-64. doi: 10.1016/j.arcmed.2012.05.002. Epub 2012 
      May 15.