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Expression of TRPC6 and BDNF in Cortical Lesions From Patients With Focal Cortical Dysplasia.

Zheng DH, Guo W, Sun FJ, Xu GZ, Zang ZL, Shu HF, Yang H - J. Neuropathol. Exp. Neurol. (2016)

Bottom Line: Focal cortical dysplasia (FCD) likely results from abnormal migration of neural progenitor cells originating from the subventricular zone.There was also greater expression of calmodulin-dependent kinase IV (CaMKIV), the downstream factor of TRPC6, in FCD lesions, suggesting that TRPC6 expression promoted dendritic growth and the development of dendritic spines and excitatory synapses via the CaMKIV-CREB pathway in FCD.Thus, overexpression of BDNF and TRPC6 and activation of the TRPC6 signal transduction pathway in cortical lesions of FCD patients may contribute to FC pathogenesis and epileptogenesis.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University (D-HZ, F-J, G-ZX, Z-LZ, H-FS, HY), Chongqing, China; Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University(WG), Xi'an, Shanxi, China; Department of Neurosurgery, General Hospital of Chengdu Military Region(H-FS), Chengdu, Sichuan, China.

No MeSH data available.


Related in: MedlinePlus

Expression of CaMKIV protein in normal CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblots of CaMKIV in total homogenates from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) lesions and CTX samples tissues (n = 10 in each group). (B) Densitometric analyses of the Western blots. There were significantly greater CaMKIV protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus the control samples. Importantly, protein levels of CaMKIV were significantly greater in the FCDIIa and FCDIIb cortical lesions versus FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.
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nlw044-F6: Expression of CaMKIV protein in normal CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblots of CaMKIV in total homogenates from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) lesions and CTX samples tissues (n = 10 in each group). (B) Densitometric analyses of the Western blots. There were significantly greater CaMKIV protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus the control samples. Importantly, protein levels of CaMKIV were significantly greater in the FCDIIa and FCDIIb cortical lesions versus FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.

Mentions: CaMKIV expression was increased in the cortical lesions of the FCDIa, FCDIIa, and FCDIIb cases compared with the CTX cases by Western blotting. The protein detected by immunoblotting was a band of 65 KDa. The CaMKIV bands in the FCDIa, FCDIIa, and FCDIIb samples were more intense than those from the CTX samples (Fig. 6A). CaMKIV protein levels were significantly increased in the FCDIa, FCDIIa, and FCDIIb samples compared with the CTX samples. Importantly, the CaMKIV protein levels were greater in the FCDIIa and FCDIIb samples versus the FCDIa samples (Fig. 6B). No band was detected at the corresponding position in the absorption control (data not shown).FIGURE 6.


Expression of TRPC6 and BDNF in Cortical Lesions From Patients With Focal Cortical Dysplasia.

Zheng DH, Guo W, Sun FJ, Xu GZ, Zang ZL, Shu HF, Yang H - J. Neuropathol. Exp. Neurol. (2016)

Expression of CaMKIV protein in normal CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblots of CaMKIV in total homogenates from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) lesions and CTX samples tissues (n = 10 in each group). (B) Densitometric analyses of the Western blots. There were significantly greater CaMKIV protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus the control samples. Importantly, protein levels of CaMKIV were significantly greater in the FCDIIa and FCDIIb cortical lesions versus FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.
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Related In: Results  -  Collection

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nlw044-F6: Expression of CaMKIV protein in normal CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblots of CaMKIV in total homogenates from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) lesions and CTX samples tissues (n = 10 in each group). (B) Densitometric analyses of the Western blots. There were significantly greater CaMKIV protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus the control samples. Importantly, protein levels of CaMKIV were significantly greater in the FCDIIa and FCDIIb cortical lesions versus FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.
Mentions: CaMKIV expression was increased in the cortical lesions of the FCDIa, FCDIIa, and FCDIIb cases compared with the CTX cases by Western blotting. The protein detected by immunoblotting was a band of 65 KDa. The CaMKIV bands in the FCDIa, FCDIIa, and FCDIIb samples were more intense than those from the CTX samples (Fig. 6A). CaMKIV protein levels were significantly increased in the FCDIa, FCDIIa, and FCDIIb samples compared with the CTX samples. Importantly, the CaMKIV protein levels were greater in the FCDIIa and FCDIIb samples versus the FCDIa samples (Fig. 6B). No band was detected at the corresponding position in the absorption control (data not shown).FIGURE 6.

Bottom Line: Focal cortical dysplasia (FCD) likely results from abnormal migration of neural progenitor cells originating from the subventricular zone.There was also greater expression of calmodulin-dependent kinase IV (CaMKIV), the downstream factor of TRPC6, in FCD lesions, suggesting that TRPC6 expression promoted dendritic growth and the development of dendritic spines and excitatory synapses via the CaMKIV-CREB pathway in FCD.Thus, overexpression of BDNF and TRPC6 and activation of the TRPC6 signal transduction pathway in cortical lesions of FCD patients may contribute to FC pathogenesis and epileptogenesis.

View Article: PubMed Central - PubMed

Affiliation: From the Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University (D-HZ, F-J, G-ZX, Z-LZ, H-FS, HY), Chongqing, China; Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University(WG), Xi'an, Shanxi, China; Department of Neurosurgery, General Hospital of Chengdu Military Region(H-FS), Chengdu, Sichuan, China.

No MeSH data available.


Related in: MedlinePlus