Excess Thyroid Hormone Inhibits Embryonic Neural Stem/Progenitor Cells Proliferation and Maintenance through STAT3 Signalling Pathway

التفاصيل البيبلوغرافية
العنوان: Excess Thyroid Hormone Inhibits Embryonic Neural Stem/Progenitor Cells Proliferation and Maintenance through STAT3 Signalling Pathway
المؤلفون: Zhengping Yu, Maoquan Li, Mingyue Qu, Shude Chen, Yanwen Zhang, Shangcheng Xu, Xuesen Yang, Min Zhong, Zhou Zhou, Lei Zhang, Yuan Wang, Aimin Wei, Chunhai Chen
المصدر: Neurotoxicity Research. 20:15-25
بيانات النشر: Springer Science and Business Media LLC, 2010.
سنة النشر: 2010
مصطلحات موضوعية: STAT3 Transcription Factor, medicine.medical_specialty, Cell Survival, Neocortex, Biology, Toxicology, Hyperthyroidism, Mice, Internal medicine, medicine, Animals, Enzyme Inhibitors, Phosphorylation, Progenitor cell, STAT3, Cells, Cultured, Embryonic Stem Cells, reproductive and urinary physiology, Cell Proliferation, Mice, Inbred BALB C, General Neuroscience, Thyroid, Janus Kinase 1, Aptamers, Nucleotide, Janus Kinase 2, Embryonic stem cell, Hedgehog signaling pathway, Cell biology, medicine.anatomical_structure, Endocrinology, nervous system, biology.protein, Triiodothyronine, Female, Signal Transduction, Hormone
الوصف: Hyperthyroidism is prevalent during pregnancy, but little is known about the effects of excess thyroid hormone on the development of embryonic neural stem/progenitor cells (NSCs), and the mechanisms underlying these effects. Previous studies indicate that STAT3 plays a crucial role in determining NSC fate during neurodevelopment. In this study, we investigated the effects of a supraphysiological dose of 3,5,3'-L-triiodothyronine (T3) on the proliferation and maintenance of NSCs derived from embryonic day 13.5 mouse neocortex, and the involvement of STAT3 in this process. Our results suggest that excess T3 treatment inhibits NSC proliferation and maintenance. T3 decreased tyrosine phosphorylation of JAK1, JAK2 and STAT3, and subsequently inhibited STAT3-DNA binding activity. Furthermore, proliferation and maintenance of NSCs were decreased by inhibitors of JAKs and STAT3, indicating that the STAT3 signalling pathway is involved in the process of NSC proliferation and maintenance. Taken together, these results suggest that the STAT3 signalling pathway is involved in the process of T3-induced inhibition of embryonic NSC proliferation and maintenance. These findings provide data for understanding the effects of hyperthyroidism during pregnancy on fetal brain development, and the mechanisms underlying these effects.
تدمد: 1476-3524
1029-8428
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dd2cd3b179f80e68428c5e26fdc7861cTest
https://doi.org/10.1007/s12640-010-9214-yTest
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....dd2cd3b179f80e68428c5e26fdc7861c
قاعدة البيانات: OpenAIRE