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Effects of hypothyroidism on expression of CRMP2B and ARPC5 during development of the rat frontal cortex

机译:甲状腺功能减退对大鼠额叶皮质发育过程中CRMP2B和ARPC5表达的影响

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Congenital hypothyroidism (CH) can lead to irreversible central nervous system (CNS) damage. However, the pathogenesis of the developmental brain disorders caused by CH has not been completely elucidated. ARPC5 and CRMP2 are closely associated with neurite outgrowth in brain development. Thus, the aim of the present study was to determine whether CRMP2B and ARPC5 expression is altered in the developing cerebral cortex of rats with CH. Control rats and rats with hypothyroidism were sacrificed at birth and at 15 days postpartum. We performed qRT-PCR to detect differences in the crmp2B and arpc5 mRNA expression in the right half of the frontal cortex of these rats. Western blotting was then used to detect differences in CRMP2B and ARPC5 protein expression. Furthermore, immunohistochemical analysis was performed on the left half of the frontal cortex to detect abnormal localization of CRMP2B and ARPC5. Results showed increased expression of the nuclear short isoform of CRMP2B and decreased expression of full-length CRMP2B and ARPC5 in cortical neurons of rats with hypothyroidism. These findings demonstrate that reduced levels of thyroid hormones can inhibit the expression of full-length CRMP2B and ARPC5 and promote nuclear transformation of the short isoform of CRMP2B. CRMP2B and ARPC5 may participate in CNS injury mediated by hypothyroidism by inducing neurite outgrowth inhibition and cytoskeletal protein disorganization. ? Ivyspring International Publisher.
机译:先天性甲状腺功能减退症(CH)会导致不可逆的中枢神经系统(CNS)损害。然而,由CH引起的发育性脑部疾病的发病机理尚未完全阐明。 ARPC5和CRMP2与大脑发育中的神经突增生密切相关。因此,本研究的目的是确定在CH大鼠的大脑皮层中CRMP2B和ARPC5表达是否改变。在出生时和产后15天处死对照大鼠和甲状腺功能低下的大鼠。我们进行了qRT-PCR,以检测这些大鼠额叶皮质右半部crmp2B和arpc5 mRNA表达的差异。然后使用蛋白质印迹法检测CRMP2B和ARPC5蛋白表达的差异。此外,在额叶皮层的左半部分进行了免疫组织化学分析,以检测CRMP2B和ARPC5的异常定位。结果显示,在甲状腺功能减退症大鼠的皮质神经元中,CRMP2B的核短同工型表达增加,全长CRMP2B和ARPC5的表达减少。这些发现表明降低的甲状腺激素水平可以抑制全长CRMP2B和ARPC5的表达,并促进CRMP2B短异构体的核转化。 CRMP2B和ARPC5可能通过诱导神经突向外生长抑制和细胞骨架蛋白紊乱而参与甲状腺功能减退介导的中枢神经系统损伤。 ?常春藤国际出版社。

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