Inhibition of PI3K/Akt pathway impairs G2/M transition of cell cycle in late developing progenitors of the avian embryo retina
PI3K/Akt is an important pathway implicated in the proliferation and survival of cells in the CNS. Here we investigated the participation of the PI3K/Akt signal pathway in cell cycle of developing retinal progenitors. Immunofluorescence assays performed in cultures of chick embryo retinal cells and...
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Published in | PloS one Vol. 8; no. 1; p. e53517 |
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Language | English |
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02.01.2013
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Abstract | PI3K/Akt is an important pathway implicated in the proliferation and survival of cells in the CNS. Here we investigated the participation of the PI3K/Akt signal pathway in cell cycle of developing retinal progenitors. Immunofluorescence assays performed in cultures of chick embryo retinal cells and intact tissues revealed the presence of phosphorylated Akt and 4E-BP1 in cells with typical mitotic profiles. Blockade of PI3K activity with the chemical inhibitor LY 294002 (LY) in retinal explants blocked the progression of proliferating cells through G2/M transition, indicated by an expressive increase in the number of cells labeled for phosphorylated histone H3 in the ventricular margin of the retina. No significant level of cell death could be detected at this region. Retinal explants treated with LY for 24 h also showed a significant decrease in the expression of phospho-Akt, phospho-GSK-3 and the hyperphosphorylated form of 4E-BP1. Although no change in the expression of cyclin B1 was detected, a significant decrease in CDK1 expression was noticed after 24 h of LY treatment both in retinal explants and monolayer cultures. Our results suggest that PI3K/Akt is an active pathway during proliferation of retinal progenitors and its activity appears to be required for proper CDK1 expression levels and mitosis progression of these cells. |
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AbstractList | PI3K/Akt is an important pathway implicated in the proliferation and survival of cells in the CNS. Here we investigated the participation of the PI3K/Akt signal pathway in cell cycle of developing retinal progenitors. Immunofluorescence assays performed in cultures of chick embryo retinal cells and intact tissues revealed the presence of phosphorylated Akt and 4E-BP1 in cells with typical mitotic profiles. Blockade of PI3K activity with the chemical inhibitor LY 294002 (LY) in retinal explants blocked the progression of proliferating cells through G2/M transition, indicated by an expressive increase in the number of cells labeled for phosphorylated histone H3 in the ventricular margin of the retina. No significant level of cell death could be detected at this region. Retinal explants treated with LY for 24 h also showed a significant decrease in the expression of phospho-Akt, phospho-GSK-3 and the hyperphosphorylated form of 4E-BP1. Although no change in the expression of cyclin B1 was detected, a significant decrease in CDK1 expression was noticed after 24 h of LY treatment both in retinal explants and monolayer cultures. Our results suggest that PI3K/Akt is an active pathway during proliferation of retinal progenitors and its activity appears to be required for proper CDK1 expression levels and mitosis progression of these cells. |
Audience | Academic |
Author | Ornelas, Isis Moraes Fragel-Madeira, Lucianne Ventura, Ana Lucia Marques Silva, Thayane Martins |
AuthorAffiliation | Department of Neurobiology, Neuroscience Program, Institute of Biology, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil Seattle Children's Research Institute, United States of America |
AuthorAffiliation_xml | – name: Seattle Children's Research Institute, United States of America – name: Department of Neurobiology, Neuroscience Program, Institute of Biology, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil |
Author_xml | – sequence: 1 givenname: Isis Moraes surname: Ornelas fullname: Ornelas, Isis Moraes organization: Department of Neurobiology, Neuroscience Program, Institute of Biology, Fluminense Federal University, Niterói, Rio de Janeiro, Brazil – sequence: 2 givenname: Thayane Martins surname: Silva fullname: Silva, Thayane Martins – sequence: 3 givenname: Lucianne surname: Fragel-Madeira fullname: Fragel-Madeira, Lucianne – sequence: 4 givenname: Ana Lucia Marques surname: Ventura fullname: Ventura, Ana Lucia Marques |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23301080$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: IMO ALMV. Performed the experiments: IMO TMS LFM. Analyzed the data: IMO TMS LFM ALMV. Contributed reagents/materials/analysis tools: ALMV. Wrote the paper: ALMV. Competing Interests: The authors have declared that no competing interests exist. |
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Snippet | PI3K/Akt is an important pathway implicated in the proliferation and survival of cells in the CNS. Here we investigated the participation of the PI3K/Akt... |
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StartPage | e53517 |
SubjectTerms | 1-Phosphatidylinositol 3-kinase AKT protein Animals Biology Cell Cycle Cell death Cell Division Cell growth Cell Proliferation Cell survival Cells, Cultured Cellular signal transduction Central nervous system Chick Embryo Chromones - pharmacology Cyclin B1 Cyclin B1 - metabolism Cyclin-dependent kinases Explants G2 Phase Gene Expression Regulation, Developmental Histone H3 Histones - metabolism Immunofluorescence Kinases Laboratory animals Localization Microscopy, Fluorescence Mitosis Morpholines - pharmacology Neurobiology Neurosciences Phase transitions Phosphatase Phosphatidylinositol 3-Kinases - metabolism Phosphorylation Proteins Proto-Oncogene Proteins c-akt - metabolism Retina Retina - cytology Retina - embryology Retina - metabolism Retinal cells Signal Transduction Stem Cells - cytology Time Factors Tissues Ventricle |
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Title | Inhibition of PI3K/Akt pathway impairs G2/M transition of cell cycle in late developing progenitors of the avian embryo retina |
URI | https://www.ncbi.nlm.nih.gov/pubmed/23301080 https://www.proquest.com/docview/1289061138/abstract/ https://search.proquest.com/docview/1273348795 https://pubmed.ncbi.nlm.nih.gov/PMC3534656 https://doaj.org/article/24cfcbf6ceff4ff2a4213a1949935fc2 http://dx.doi.org/10.1371/journal.pone.0053517 |
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