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

Liu CR, Miao J, Zhang YL, Liu YM, Yu BG - Int. J. Biol. Sci. (2013)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Affiliated Hospital of Logistics University of Chinese People's Armed Police Force, Tianjin 300162, China. lcr68@163.com

ABSTRACT
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.

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Western blotting results: (a) Differential expression of CRMP2B protein in the frontal cortex of normal rats and rats with hypothyroidism. (b) Differential expression of ARPC5 protein in the frontal cortex of normal rats and rats with hypothyroidism. (c) The quantification of the bands shown in Fig2a and Fig2b. i: quantification of full-length CRMP2B(64 kDa) protein expression; ii: quantification of CRMP2B (58 kDa) protein expression; iii: quantification of ARPC5 protein expression. *P<0.05 compared with control.
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Figure 2: Western blotting results: (a) Differential expression of CRMP2B protein in the frontal cortex of normal rats and rats with hypothyroidism. (b) Differential expression of ARPC5 protein in the frontal cortex of normal rats and rats with hypothyroidism. (c) The quantification of the bands shown in Fig2a and Fig2b. i: quantification of full-length CRMP2B(64 kDa) protein expression; ii: quantification of CRMP2B (58 kDa) protein expression; iii: quantification of ARPC5 protein expression. *P<0.05 compared with control.

Mentions: No statistically significant difference between the protein expression level of full-length CRMP2B (64 kDa) was observed between rats with hypothyroidism and normal rats at P1 (P = 0.319). In control rats, full-length CRMP2B protein expression was higher at P15 than at P1 (P < 0.001). In rats with hypothyroidism, there was no difference between full-length CRMP2B expression at P1 and P15 (P = 0.342). Full-length CRMP2B protein expression was higher in the frontal cortex of control rats than in hypothyroidism rats at P15 (P = 0.004) (Fig. 2a and 2c-i).


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

Liu CR, Miao J, Zhang YL, Liu YM, Yu BG - Int. J. Biol. Sci. (2013)

Western blotting results: (a) Differential expression of CRMP2B protein in the frontal cortex of normal rats and rats with hypothyroidism. (b) Differential expression of ARPC5 protein in the frontal cortex of normal rats and rats with hypothyroidism. (c) The quantification of the bands shown in Fig2a and Fig2b. i: quantification of full-length CRMP2B(64 kDa) protein expression; ii: quantification of CRMP2B (58 kDa) protein expression; iii: quantification of ARPC5 protein expression. *P<0.05 compared with control.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3584917&req=5

Figure 2: Western blotting results: (a) Differential expression of CRMP2B protein in the frontal cortex of normal rats and rats with hypothyroidism. (b) Differential expression of ARPC5 protein in the frontal cortex of normal rats and rats with hypothyroidism. (c) The quantification of the bands shown in Fig2a and Fig2b. i: quantification of full-length CRMP2B(64 kDa) protein expression; ii: quantification of CRMP2B (58 kDa) protein expression; iii: quantification of ARPC5 protein expression. *P<0.05 compared with control.
Mentions: No statistically significant difference between the protein expression level of full-length CRMP2B (64 kDa) was observed between rats with hypothyroidism and normal rats at P1 (P = 0.319). In control rats, full-length CRMP2B protein expression was higher at P15 than at P1 (P < 0.001). In rats with hypothyroidism, there was no difference between full-length CRMP2B expression at P1 and P15 (P = 0.342). Full-length CRMP2B protein expression was higher in the frontal cortex of control rats than in hypothyroidism rats at P15 (P = 0.004) (Fig. 2a and 2c-i).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Affiliated Hospital of Logistics University of Chinese People's Armed Police Force, Tianjin 300162, China. lcr68@163.com

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus