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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 mRNA in CTX and in patients with FCD types Ia, IIa, and IIb. (A) Real-time polymerase chain reaction analysis of TRPC6 mRNA expression in CTX, FCDIa, FCDIIa, and FCDIIb (n = 10/group) specimens. Increased TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb samples versus CTX samples. Importantly, the expression of TRPC6 mRNA was significantly increased in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA. (B–I)In situ hybridization analysis of TRPC6 mRNA expression. TRPC6 mRNA expression in CTX samples (B–D). Expression was observed in neurons (arrows in B and C) and glia-like cells (arrowheads in C and D) in the neocortex, white matter (WM), and junction. TRPC6 mRNA expression in FCDIa samples (E, F). Expression was observed in neurons (arrows in E), including microcolumns (insert in E), heterotopic neurons (arrows in F) in the white matter, and glia-like cells (arrowheads in F). TRPC6 mRNA expression in FCDIIa samples (G). Expression was observed in dysmorphic neurons (DNs, arrows in G) and glia-like cells (arrowheads in G). TRPC6 mRNA expression in FCDIIb samples (H, I). Expression was observed in dysmorphic neurons (DNs, arrows in H and inset), balloon cells (BCs, double-arrows in I), and glia-like cells (arrowheads in I and inset). Scale bar: 30 µm.
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nlw044-F1: Expression of TRPC6 mRNA in CTX and in patients with FCD types Ia, IIa, and IIb. (A) Real-time polymerase chain reaction analysis of TRPC6 mRNA expression in CTX, FCDIa, FCDIIa, and FCDIIb (n = 10/group) specimens. Increased TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb samples versus CTX samples. Importantly, the expression of TRPC6 mRNA was significantly increased in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA. (B–I)In situ hybridization analysis of TRPC6 mRNA expression. TRPC6 mRNA expression in CTX samples (B–D). Expression was observed in neurons (arrows in B and C) and glia-like cells (arrowheads in C and D) in the neocortex, white matter (WM), and junction. TRPC6 mRNA expression in FCDIa samples (E, F). Expression was observed in neurons (arrows in E), including microcolumns (insert in E), heterotopic neurons (arrows in F) in the white matter, and glia-like cells (arrowheads in F). TRPC6 mRNA expression in FCDIIa samples (G). Expression was observed in dysmorphic neurons (DNs, arrows in G) and glia-like cells (arrowheads in G). TRPC6 mRNA expression in FCDIIb samples (H, I). Expression was observed in dysmorphic neurons (DNs, arrows in H and inset), balloon cells (BCs, double-arrows in I), and glia-like cells (arrowheads in I and inset). Scale bar: 30 µm.

Mentions: We first studied the expression of TRPC6 mRNA in FCD patients by quantitative PCR. Greater TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb groups compared with the CTX samples (Fig. 1A). Importantly, the mRNA expression levels were significantly higher in the FCDIIa and FCDIIb cortical lesions than in the FCDIa specimens (Fig. 1A). Additionally, we performed in situ hybridization to study the cellular distribution of TRPC6 mRNA in the FCD cases. In the control samples, TRPC6 mRNA was weakly distributed in neurons and cells with a glia-like morphology (Fig. 1B–D). TRPC6 mRNA was widely distributed in neurons and glia-like cells in the FCD tissues (Fig. 1E–I), particularly in the microcolumns, heterotopic neurons, DNs, and BCs (Fig. 1E–I). No positive signal was observed in sections treated with a nonsense probe or without the addition of the specific probe for TRPC6 (data not shown).FIGURE 1.


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 mRNA in CTX and in patients with FCD types Ia, IIa, and IIb. (A) Real-time polymerase chain reaction analysis of TRPC6 mRNA expression in CTX, FCDIa, FCDIIa, and FCDIIb (n = 10/group) specimens. Increased TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb samples versus CTX samples. Importantly, the expression of TRPC6 mRNA was significantly increased in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA. (B–I)In situ hybridization analysis of TRPC6 mRNA expression. TRPC6 mRNA expression in CTX samples (B–D). Expression was observed in neurons (arrows in B and C) and glia-like cells (arrowheads in C and D) in the neocortex, white matter (WM), and junction. TRPC6 mRNA expression in FCDIa samples (E, F). Expression was observed in neurons (arrows in E), including microcolumns (insert in E), heterotopic neurons (arrows in F) in the white matter, and glia-like cells (arrowheads in F). TRPC6 mRNA expression in FCDIIa samples (G). Expression was observed in dysmorphic neurons (DNs, arrows in G) and glia-like cells (arrowheads in G). TRPC6 mRNA expression in FCDIIb samples (H, I). Expression was observed in dysmorphic neurons (DNs, arrows in H and inset), balloon cells (BCs, double-arrows in I), and glia-like cells (arrowheads in I and inset). Scale bar: 30 µm.
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nlw044-F1: Expression of TRPC6 mRNA in CTX and in patients with FCD types Ia, IIa, and IIb. (A) Real-time polymerase chain reaction analysis of TRPC6 mRNA expression in CTX, FCDIa, FCDIIa, and FCDIIb (n = 10/group) specimens. Increased TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb samples versus CTX samples. Importantly, the expression of TRPC6 mRNA was significantly increased in the FCDIIa and FCDIIb cortical lesions compared with the FCDIa specimens. Error bars represent SE; *p < 0.05, **p < 0.01 versus CTX; #p < 0.05 versus FCDIa; ANOVA. (B–I)In situ hybridization analysis of TRPC6 mRNA expression. TRPC6 mRNA expression in CTX samples (B–D). Expression was observed in neurons (arrows in B and C) and glia-like cells (arrowheads in C and D) in the neocortex, white matter (WM), and junction. TRPC6 mRNA expression in FCDIa samples (E, F). Expression was observed in neurons (arrows in E), including microcolumns (insert in E), heterotopic neurons (arrows in F) in the white matter, and glia-like cells (arrowheads in F). TRPC6 mRNA expression in FCDIIa samples (G). Expression was observed in dysmorphic neurons (DNs, arrows in G) and glia-like cells (arrowheads in G). TRPC6 mRNA expression in FCDIIb samples (H, I). Expression was observed in dysmorphic neurons (DNs, arrows in H and inset), balloon cells (BCs, double-arrows in I), and glia-like cells (arrowheads in I and inset). Scale bar: 30 µm.
Mentions: We first studied the expression of TRPC6 mRNA in FCD patients by quantitative PCR. Greater TRPC6 mRNA levels were observed in the FCDIa, FCDIIa, and FCDIIb groups compared with the CTX samples (Fig. 1A). Importantly, the mRNA expression levels were significantly higher in the FCDIIa and FCDIIb cortical lesions than in the FCDIa specimens (Fig. 1A). Additionally, we performed in situ hybridization to study the cellular distribution of TRPC6 mRNA in the FCD cases. In the control samples, TRPC6 mRNA was weakly distributed in neurons and cells with a glia-like morphology (Fig. 1B–D). TRPC6 mRNA was widely distributed in neurons and glia-like cells in the FCD tissues (Fig. 1E–I), particularly in the microcolumns, heterotopic neurons, DNs, and BCs (Fig. 1E–I). No positive signal was observed in sections treated with a nonsense probe or without the addition of the specific probe for TRPC6 (data not shown).FIGURE 1.

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