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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 TRPC6 protein in CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblot of TRPC6 in total homogenates of lesions from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) (n = 10 in each series) and the control CTX tissues (n = 10). (B) Densitometric analyses of the Western blots. There was a significant increase in TRPC6 protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus control samples. The TRPC6 protein levels were also significantly greater in the FCDIIa and FCDIIb cortical lesions versus the 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-F2: Expression of TRPC6 protein in CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblot of TRPC6 in total homogenates of lesions from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) (n = 10 in each series) and the control CTX tissues (n = 10). (B) Densitometric analyses of the Western blots. There was a significant increase in TRPC6 protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus control samples. The TRPC6 protein levels were also significantly greater in the FCDIIa and FCDIIb cortical lesions versus the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.

Mentions: To confirm the upregulation of TRPC6 in FCD patients, we assessed TRPC6 protein levels by Western blot. TRPC6 was present as a band of approximately 106 KDa. Increased levels of TRPC6 protein were observed in the FCDIa, FCDIIa, and FCDIIb groups compared with the control samples (Fig. 2A). TRPC6 protein levels were significantly higher in the FCDIa, FCDIIa, and FCDIIb tissues than in the control samples. Moreover, TRPC6 protein levels were significantly greater in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens (Fig. 2B). In the absorption control, no band was detected at the corresponding position (data not shown).FIGURE 2.


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 TRPC6 protein in CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblot of TRPC6 in total homogenates of lesions from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) (n = 10 in each series) and the control CTX tissues (n = 10). (B) Densitometric analyses of the Western blots. There was a significant increase in TRPC6 protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus control samples. The TRPC6 protein levels were also significantly greater in the FCDIIa and FCDIIb cortical lesions versus the 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-F2: Expression of TRPC6 protein in CTX and FCD types Ia, IIa, and IIb. (A) Representative immunoblot of TRPC6 in total homogenates of lesions from FCD types Ia (FCDIa), IIa (FCDIIa), and IIb (FCDIIb) (n = 10 in each series) and the control CTX tissues (n = 10). (B) Densitometric analyses of the Western blots. There was a significant increase in TRPC6 protein levels in the FCDIa, FCDIIa, and FCDIIb tissues versus control samples. The TRPC6 protein levels were also significantly greater in the FCDIIa and FCDIIb cortical lesions versus the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA.
Mentions: To confirm the upregulation of TRPC6 in FCD patients, we assessed TRPC6 protein levels by Western blot. TRPC6 was present as a band of approximately 106 KDa. Increased levels of TRPC6 protein were observed in the FCDIa, FCDIIa, and FCDIIb groups compared with the control samples (Fig. 2A). TRPC6 protein levels were significantly higher in the FCDIa, FCDIIa, and FCDIIb tissues than in the control samples. Moreover, TRPC6 protein levels were significantly greater in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens (Fig. 2B). In the absorption control, no band was detected at the corresponding position (data not shown).FIGURE 2.

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