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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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Representative immunohistochemical staining for ARPC5 protein expression in the cortical layer III and IV of control rats and hypothyroidism rats during development, 400×. (a): P1 control. ARPC5 was diffusely expressed and predominantly found in neurites (⇒ red). (b):P1 hypothyroidism. The distribution and cellular location were similar to P1 control group. (c): P15 control. ARPC5 was found in neurites. The intensity of ARPC5 staining was higher in control rats (⇒ red). (d): P15 hypothyroidism. ARPC5 was found in neurites. The intensity of ARPC5 staining was lower in hypothyroid rats (⇒ red).
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Figure 4: Representative immunohistochemical staining for ARPC5 protein expression in the cortical layer III and IV of control rats and hypothyroidism rats during development, 400×. (a): P1 control. ARPC5 was diffusely expressed and predominantly found in neurites (⇒ red). (b):P1 hypothyroidism. The distribution and cellular location were similar to P1 control group. (c): P15 control. ARPC5 was found in neurites. The intensity of ARPC5 staining was higher in control rats (⇒ red). (d): P15 hypothyroidism. ARPC5 was found in neurites. The intensity of ARPC5 staining was lower in hypothyroid rats (⇒ red).

Mentions: ARPC5 was expressed diffusely throughout the six layers of the frontal cortex and was predominantly found in neurites. Cortical layer III and IV were emphatically studied. No difference was found in the intensity of ARPC5 staining in rats with hypothyroidism compared with control rats at P1 (Z = -0.522, P= 0.602) (Table 4). The intensity of ARPC5 staining was lower in rats with hypothyroidism than in control rats at P15 (Z = -2.450, P=0.014) (Table 5 and Fig. 4).


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)

Representative immunohistochemical staining for ARPC5 protein expression in the cortical layer III and IV of control rats and hypothyroidism rats during development, 400×. (a): P1 control. ARPC5 was diffusely expressed and predominantly found in neurites (⇒ red). (b):P1 hypothyroidism. The distribution and cellular location were similar to P1 control group. (c): P15 control. ARPC5 was found in neurites. The intensity of ARPC5 staining was higher in control rats (⇒ red). (d): P15 hypothyroidism. ARPC5 was found in neurites. The intensity of ARPC5 staining was lower in hypothyroid rats (⇒ red).
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Related In: Results  -  Collection

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Figure 4: Representative immunohistochemical staining for ARPC5 protein expression in the cortical layer III and IV of control rats and hypothyroidism rats during development, 400×. (a): P1 control. ARPC5 was diffusely expressed and predominantly found in neurites (⇒ red). (b):P1 hypothyroidism. The distribution and cellular location were similar to P1 control group. (c): P15 control. ARPC5 was found in neurites. The intensity of ARPC5 staining was higher in control rats (⇒ red). (d): P15 hypothyroidism. ARPC5 was found in neurites. The intensity of ARPC5 staining was lower in hypothyroid rats (⇒ red).
Mentions: ARPC5 was expressed diffusely throughout the six layers of the frontal cortex and was predominantly found in neurites. Cortical layer III and IV were emphatically studied. No difference was found in the intensity of ARPC5 staining in rats with hypothyroidism compared with control rats at P1 (Z = -0.522, P= 0.602) (Table 4). The intensity of ARPC5 staining was lower in rats with hypothyroidism than in control rats at P15 (Z = -2.450, P=0.014) (Table 5 and Fig. 4).

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