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HDAC3 But not HDAC2 Mediates Visual Experience-Dependent Radial Glia Proliferation in the Developing Xenopus Tectum

View Article: PubMed Central - PubMed

ABSTRACT

Radial glial cells (RGs) are one of the important progenitor cells that can differentiate into neurons or glia to form functional neural circuits in the developing central nervous system (CNS). Histone deacetylases (HDACs) has been associated with visual activity dependent changes in BrdU-positive progenitor cells in the developing brain. We previously have shown that HDAC1 is involved in the experience-dependent proliferation of RGs. However, it is less clear whether two other members of class I HDACs, HDAC2 and HDAC3, are involved in the regulation of radial glia proliferation. Here, we reported that HDAC2 and HDAC3 expression were developmentally regulated in tectal cells, especially in the ventricular layer of the BLBP-positive RGs. Pharmacological blockade using an inhibitor of class I HDACs, MS-275, decreased the number of BrdU-positive dividing progenitor cells. Specific knockdown of HDAC3 but not HDAC2 decreased the number of BrdU- and BLBP-labeled cells, suggesting that the proliferation of radial glia was selectively mediated by HDAC3. Visual deprivation induced selective augmentation of histone H4 acetylation at lysine 16 in BLBP-positive cells. Furthermore, the visual deprivation-induced increase in BrdU-positive cells was partially blocked by HDAC3 downregulation but not by HDAC2 knockdown at stage 49 tadpoles. These data revealed a specific role of HDAC3 in experience-dependent radial glia proliferation during the development of Xenopus tectum.

No MeSH data available.


Related in: MedlinePlus

Class I HDAC inhibitor decreases the proliferative rate of radial glia cells. (A) Representative images showing the co-labeling for BrdU+ and BLBP+ in control (A1–A3) and MS-275-treated (10 μM, A4–A6) tecta. The BLBP+ cell bodies locate along the midline of the ventricular layer of the tectum (arrows) and the endfeet reside along the edge of neuropil (arrow heads). Scale: 50 μm. (B–C) Summary data showing that the numbers of BrdU+ and BLBP+ cells were dramatically decreased in MS-275-treated tecta compared to the control tecta. (BrdU: Ctrl, 163.2 ± 7.9, N = 5, MS-275, 98.2 ± 10.9, N = 4; BLBP: Ctrl, 179.2 ± 7.2, N = 5, MS-275, 137.2 ± 14.6, N = 4; *p < 0.05, **p < 0.01).
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Figure 2: Class I HDAC inhibitor decreases the proliferative rate of radial glia cells. (A) Representative images showing the co-labeling for BrdU+ and BLBP+ in control (A1–A3) and MS-275-treated (10 μM, A4–A6) tecta. The BLBP+ cell bodies locate along the midline of the ventricular layer of the tectum (arrows) and the endfeet reside along the edge of neuropil (arrow heads). Scale: 50 μm. (B–C) Summary data showing that the numbers of BrdU+ and BLBP+ cells were dramatically decreased in MS-275-treated tecta compared to the control tecta. (BrdU: Ctrl, 163.2 ± 7.9, N = 5, MS-275, 98.2 ± 10.9, N = 4; BLBP: Ctrl, 179.2 ± 7.2, N = 5, MS-275, 137.2 ± 14.6, N = 4; *p < 0.05, **p < 0.01).

Mentions: To test whether class I HDACs was involved in RG proliferation in the optic tectum, tadpoles at stage 46 were exposed to Entinostat (MS-275, 10 μM, Selleck), a class I HDACs inhibitor (Hu et al., 2003; Bahari-Javan et al., 2012) in Steinberg’s solution for 48 h. The tadpoles were incubated with BrdU for 2 h and immunostained with anti-BrdU and anti-BLBP antibodies (Figure 2A). We observed that the numbers of BrdU+ and BLBP+ RGs were dramatically reduced in the MS-275-treated tadpoles (Figures 2B,C). These data indicated that class I HDAC activity was required for the proliferation of RGs.


HDAC3 But not HDAC2 Mediates Visual Experience-Dependent Radial Glia Proliferation in the Developing Xenopus Tectum
Class I HDAC inhibitor decreases the proliferative rate of radial glia cells. (A) Representative images showing the co-labeling for BrdU+ and BLBP+ in control (A1–A3) and MS-275-treated (10 μM, A4–A6) tecta. The BLBP+ cell bodies locate along the midline of the ventricular layer of the tectum (arrows) and the endfeet reside along the edge of neuropil (arrow heads). Scale: 50 μm. (B–C) Summary data showing that the numbers of BrdU+ and BLBP+ cells were dramatically decreased in MS-275-treated tecta compared to the control tecta. (BrdU: Ctrl, 163.2 ± 7.9, N = 5, MS-275, 98.2 ± 10.9, N = 4; BLBP: Ctrl, 179.2 ± 7.2, N = 5, MS-275, 137.2 ± 14.6, N = 4; *p < 0.05, **p < 0.01).
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Figure 2: Class I HDAC inhibitor decreases the proliferative rate of radial glia cells. (A) Representative images showing the co-labeling for BrdU+ and BLBP+ in control (A1–A3) and MS-275-treated (10 μM, A4–A6) tecta. The BLBP+ cell bodies locate along the midline of the ventricular layer of the tectum (arrows) and the endfeet reside along the edge of neuropil (arrow heads). Scale: 50 μm. (B–C) Summary data showing that the numbers of BrdU+ and BLBP+ cells were dramatically decreased in MS-275-treated tecta compared to the control tecta. (BrdU: Ctrl, 163.2 ± 7.9, N = 5, MS-275, 98.2 ± 10.9, N = 4; BLBP: Ctrl, 179.2 ± 7.2, N = 5, MS-275, 137.2 ± 14.6, N = 4; *p < 0.05, **p < 0.01).
Mentions: To test whether class I HDACs was involved in RG proliferation in the optic tectum, tadpoles at stage 46 were exposed to Entinostat (MS-275, 10 μM, Selleck), a class I HDACs inhibitor (Hu et al., 2003; Bahari-Javan et al., 2012) in Steinberg’s solution for 48 h. The tadpoles were incubated with BrdU for 2 h and immunostained with anti-BrdU and anti-BLBP antibodies (Figure 2A). We observed that the numbers of BrdU+ and BLBP+ RGs were dramatically reduced in the MS-275-treated tadpoles (Figures 2B,C). These data indicated that class I HDAC activity was required for the proliferation of RGs.

View Article: PubMed Central - PubMed

ABSTRACT

Radial glial cells (RGs) are one of the important progenitor cells that can differentiate into neurons or glia to form functional neural circuits in the developing central nervous system (CNS). Histone deacetylases (HDACs) has been associated with visual activity dependent changes in BrdU-positive progenitor cells in the developing brain. We previously have shown that HDAC1 is involved in the experience-dependent proliferation of RGs. However, it is less clear whether two other members of class I HDACs, HDAC2 and HDAC3, are involved in the regulation of radial glia proliferation. Here, we reported that HDAC2 and HDAC3 expression were developmentally regulated in tectal cells, especially in the ventricular layer of the BLBP-positive RGs. Pharmacological blockade using an inhibitor of class I HDACs, MS-275, decreased the number of BrdU-positive dividing progenitor cells. Specific knockdown of HDAC3 but not HDAC2 decreased the number of BrdU- and BLBP-labeled cells, suggesting that the proliferation of radial glia was selectively mediated by HDAC3. Visual deprivation induced selective augmentation of histone H4 acetylation at lysine 16 in BLBP-positive cells. Furthermore, the visual deprivation-induced increase in BrdU-positive cells was partially blocked by HDAC3 downregulation but not by HDAC2 knockdown at stage 49 tadpoles. These data revealed a specific role of HDAC3 in experience-dependent radial glia proliferation during the development of Xenopus tectum.

No MeSH data available.


Related in: MedlinePlus