Evidence map›Paper›PMID 25577802›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2015

Thyroid hormone alleviates demyelination induced by cuprizone through its role in remyelination during the remission period.

Mao Zhang, Xiao L Zhan, Zi Y Ma, Xing S Chen, Qi Y Cai, Zhong X Yao

Open access · greenAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Nuclear hormone receptors in demyelinating diseases.Journal of neuroendocrinology · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Mao ZhangDepartment of Physiology, Third Military Medical University, Chongqing 400038, China.
Xiao L ZhanDepartment of Histology and Embryology, Third Military Medical University, Chongqing 400038, China.
Zi Y MaBattalion 14 of Cadet Brigade, Third Military Medical University, Chongqing 400038, China.
Xing S ChenDepartment of Histology and Embryology, Third Military Medical University, Chongqing 400038, China.
Qi Y CaiDepartment of Histology and Embryology, Third Military Medical University, Chongqing 400038, China.
Zhong X YaoDepartment of Physiology, Third Military Medical University, Chongqing 400038, China Department of Histology and Embryology, Third Military Medical University, Chongqing 400038, China yaozhx@yahoo.com yaozhx@hotmail.com.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a disease induced by demyelination in the central nervous system, and the remission period of MS is crucial for remyelination. In addition, abnormal levels of thyroid hormone (TH) have been identified in MS. However, in the clinic, insufficient attention has been paid to the role of TH in the remission period. Indeed, TH not only functions in the development of the brain but also affects myelination. Therefore, it is necessary to observe the effect of TH on remyelination during this period. A model of demyelination induced by cuprizone (CPZ) was used to observe the function of TH in remyelination during the remission period of MS. Through weighing and behavioral tests, we found that TH improved the physical symptoms of mice impaired by CPZ. Supplementation of TH led to the repair of myelin as detected by immunohistochemistry and western blot. In addition, a sufficient TH supply resulted in an increase in myelinated axons without affecting myelin thickness and g ratio in the corpus callosum, as detected by electron microscopy. Double immunostaining with myelin basic protein and neurofilament 200 (NF200) showed that the CPZ-induced impairment of axons was alleviated by TH. Conversely, insufficient TH induced by 6-propyl-2-thiouracil resulted in the enlargement of mitochondria. Furthermore, we found that an adequate supply of TH promoted the proliferation and differentiation of oligodendrocyte lineage cells by immunofluorescence, which was beneficial to remyelination. Further, we found that TH reduced the number of astrocytes without affecting microglia. Conclusively, it was shown that TH alleviated demyelination induced by CPZ by promoting the development of oligodendrocyte lineage cells and remyelination. The critical time for remyelination is the remission period of MS. TH plays a significant role in alleviating demyelination during the remission period in the clinical treatment of MS.

Indexed as

AnimalsAstrocytesAxonsCell DifferentiationCell LineageCell ProliferationCuprizoneDemyelinating DiseasesDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMicrogliaMultiple Sclerosis, Relapsing-RemittingMyelin SheathCuprizoneThyroid Hormonescorpus callosummultiple sclerosismyelinoligodendrocyteThyroid hormone

Identifiers

PMID25577802
PMCPMC4935357
OpenAlexW2055674903

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.