MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation

A. Nigro, R. Menon, A. Bergamaschi, Y. M. Clovis, A. Baldi, M. Ehrmann, G. Comi, D. De Pietri Tonelli, C. Farina, G. Martino, L. Muzio

Research output: Contribution to journalArticle

Abstract

The precise mechanisms by which microRNAs (miRNAs) contribute to the dynamic regulation of gene expression during the forebrain development are still partly elusive. Here we show that the depletion of miRNAs in the cerebral cortex and hippocampus, via genetic inactivation of Dicer after the onset of forebrain neurogenesis, profoundly impairs the morphological and proliferative characteristics of neural stem and progenitor cells. The cytoarchitecture and self-renewal potential of radial glial (RG) cells located within the cerebral cortex and the hippocampus were profoundly altered, thus causing a significant derangement of both the post natal dorsal sub-ventricular zone and the dentate gyrus. This effect was attributed to the High-temperature requirement A serine peptidase 1 (HtrA1) gene product whose overexpression in the developing forebrain recapitulated some of the aspects of the Dicer -/- phenotype. MiR-30e and miR-181d were identified as posttranscriptional negative regulators of HtrA1 by binding to its 3′ untranslated region. In vivo overexpression of miR-30e and miR-181d in Dicer -/- forebrain rescued RG proliferation defects.

Original languageEnglish
Article numbere360
JournalCell Death and Disease
Volume3
Issue number8
DOIs
Publication statusPublished - Aug 2012

Fingerprint

Prosencephalon
Neuroglia
Serine
Peptide Hydrolases
Cell Proliferation
Temperature
MicroRNAs
Cerebral Cortex
Hippocampus
Ependymoglial Cells
Neural Stem Cells
Neurogenesis
Dentate Gyrus
Gene Expression Regulation
3' Untranslated Regions
Stem Cells
Phenotype
Genes

Keywords

  • Dicer
  • HtrA1
  • MiR-181d
  • MiR-30e
  • Neurogenesis

ASJC Scopus subject areas

  • Cell Biology
  • Immunology
  • Cancer Research
  • Cellular and Molecular Neuroscience
  • Medicine(all)

Cite this

Nigro, A., Menon, R., Bergamaschi, A., Clovis, Y. M., Baldi, A., Ehrmann, M., ... Muzio, L. (2012). MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation. Cell Death and Disease, 3(8), [e360]. https://doi.org/10.1038/cddis.2012.98

MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation. / Nigro, A.; Menon, R.; Bergamaschi, A.; Clovis, Y. M.; Baldi, A.; Ehrmann, M.; Comi, G.; De Pietri Tonelli, D.; Farina, C.; Martino, G.; Muzio, L.

In: Cell Death and Disease, Vol. 3, No. 8, e360, 08.2012.

Research output: Contribution to journalArticle

Nigro, A, Menon, R, Bergamaschi, A, Clovis, YM, Baldi, A, Ehrmann, M, Comi, G, De Pietri Tonelli, D, Farina, C, Martino, G & Muzio, L 2012, 'MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation', Cell Death and Disease, vol. 3, no. 8, e360. https://doi.org/10.1038/cddis.2012.98
Nigro A, Menon R, Bergamaschi A, Clovis YM, Baldi A, Ehrmann M et al. MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation. Cell Death and Disease. 2012 Aug;3(8). e360. https://doi.org/10.1038/cddis.2012.98
Nigro, A. ; Menon, R. ; Bergamaschi, A. ; Clovis, Y. M. ; Baldi, A. ; Ehrmann, M. ; Comi, G. ; De Pietri Tonelli, D. ; Farina, C. ; Martino, G. ; Muzio, L. / MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation. In: Cell Death and Disease. 2012 ; Vol. 3, No. 8.
@article{9e8f890e54e947fdb243c3154564cb70,
title = "MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation",
abstract = "The precise mechanisms by which microRNAs (miRNAs) contribute to the dynamic regulation of gene expression during the forebrain development are still partly elusive. Here we show that the depletion of miRNAs in the cerebral cortex and hippocampus, via genetic inactivation of Dicer after the onset of forebrain neurogenesis, profoundly impairs the morphological and proliferative characteristics of neural stem and progenitor cells. The cytoarchitecture and self-renewal potential of radial glial (RG) cells located within the cerebral cortex and the hippocampus were profoundly altered, thus causing a significant derangement of both the post natal dorsal sub-ventricular zone and the dentate gyrus. This effect was attributed to the High-temperature requirement A serine peptidase 1 (HtrA1) gene product whose overexpression in the developing forebrain recapitulated some of the aspects of the Dicer -/- phenotype. MiR-30e and miR-181d were identified as posttranscriptional negative regulators of HtrA1 by binding to its 3′ untranslated region. In vivo overexpression of miR-30e and miR-181d in Dicer -/- forebrain rescued RG proliferation defects.",
keywords = "Dicer, HtrA1, MiR-181d, MiR-30e, Neurogenesis",
author = "A. Nigro and R. Menon and A. Bergamaschi and Clovis, {Y. M.} and A. Baldi and M. Ehrmann and G. Comi and {De Pietri Tonelli}, D. and C. Farina and G. Martino and L. Muzio",
year = "2012",
month = "8",
doi = "10.1038/cddis.2012.98",
language = "English",
volume = "3",
journal = "Cell Death and Disease",
issn = "2041-4889",
publisher = "Nature Publishing Group",
number = "8",

}

TY - JOUR

T1 - MiR-30e and miR-181d control Radial Glia cell proliferation via HtrA1 modulation

AU - Nigro, A.

AU - Menon, R.

AU - Bergamaschi, A.

AU - Clovis, Y. M.

AU - Baldi, A.

AU - Ehrmann, M.

AU - Comi, G.

AU - De Pietri Tonelli, D.

AU - Farina, C.

AU - Martino, G.

AU - Muzio, L.

PY - 2012/8

Y1 - 2012/8

N2 - The precise mechanisms by which microRNAs (miRNAs) contribute to the dynamic regulation of gene expression during the forebrain development are still partly elusive. Here we show that the depletion of miRNAs in the cerebral cortex and hippocampus, via genetic inactivation of Dicer after the onset of forebrain neurogenesis, profoundly impairs the morphological and proliferative characteristics of neural stem and progenitor cells. The cytoarchitecture and self-renewal potential of radial glial (RG) cells located within the cerebral cortex and the hippocampus were profoundly altered, thus causing a significant derangement of both the post natal dorsal sub-ventricular zone and the dentate gyrus. This effect was attributed to the High-temperature requirement A serine peptidase 1 (HtrA1) gene product whose overexpression in the developing forebrain recapitulated some of the aspects of the Dicer -/- phenotype. MiR-30e and miR-181d were identified as posttranscriptional negative regulators of HtrA1 by binding to its 3′ untranslated region. In vivo overexpression of miR-30e and miR-181d in Dicer -/- forebrain rescued RG proliferation defects.

AB - The precise mechanisms by which microRNAs (miRNAs) contribute to the dynamic regulation of gene expression during the forebrain development are still partly elusive. Here we show that the depletion of miRNAs in the cerebral cortex and hippocampus, via genetic inactivation of Dicer after the onset of forebrain neurogenesis, profoundly impairs the morphological and proliferative characteristics of neural stem and progenitor cells. The cytoarchitecture and self-renewal potential of radial glial (RG) cells located within the cerebral cortex and the hippocampus were profoundly altered, thus causing a significant derangement of both the post natal dorsal sub-ventricular zone and the dentate gyrus. This effect was attributed to the High-temperature requirement A serine peptidase 1 (HtrA1) gene product whose overexpression in the developing forebrain recapitulated some of the aspects of the Dicer -/- phenotype. MiR-30e and miR-181d were identified as posttranscriptional negative regulators of HtrA1 by binding to its 3′ untranslated region. In vivo overexpression of miR-30e and miR-181d in Dicer -/- forebrain rescued RG proliferation defects.

KW - Dicer

KW - HtrA1

KW - MiR-181d

KW - MiR-30e

KW - Neurogenesis

UR - http://www.scopus.com/inward/record.url?scp=84865802078&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84865802078&partnerID=8YFLogxK

U2 - 10.1038/cddis.2012.98

DO - 10.1038/cddis.2012.98

M3 - Article

C2 - 22854828

AN - SCOPUS:84865802078

VL - 3

JO - Cell Death and Disease

JF - Cell Death and Disease

SN - 2041-4889

IS - 8

M1 - e360

ER -