נגישות
menu      
חיפוש מתקדם
תחביר
חפש...
הספר "אוצר וולקני"
אודות
תנאי שימוש
ניהול
קהילה:
אסיף מאגר המחקר החקלאי
פותח על ידי קלירמאש פתרונות בע"מ -
MiR-138 promotes the migration of cultured chicken embryonic hypothalamic cells by targeting reelin
Year:
2013
Source of publication :
Neuroscience
Authors :
מאירי, נעם
;
.
קיסיליוק, טטיאנה
;
.
Volume :
238
Co-Authors:
Kisliouk, T., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan 50250, Israel
Meiri, N., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan 50250, Israel
Facilitators :
From page:
114
To page:
124
(
Total pages:
11
)
Abstract:
Neuronal network remodeling during critical periods of sensory development might be accompanied by alterations in hypothalamic cell populations. MicroRNAs play a central role in regulating neuronal function, including neural stem cell proliferation, and neuronal migration, maturation and integration into viable circuits by modulating different mRNA targets. Here we investigated the role of miR-138 in cell proliferation and migration in a neuron-enriched hypothalamic cell culture prepared from chicks on embryonic day 16. Ectopic expression of miR-138 enhanced hypothalamic cell migration, but did not affect cell proliferation. As a potential mechanism for miR-138's effect on cell migration, we investigated reelin (Reln) as a direct target of miR-138. Luciferase reporter assay and Ago2-immunoprecipitation experiments confirmed direct binding of miR-138 to the Reln 3'-untranslated region. Ectopic miR-138 abolished Reln levels in hypothalamic cells and enhanced their migration, similar to Reln-antisense DNA. Furthermore, inhibition of Reln expression by miR-138 led to decreased phosphorylation level of the key component of Reln-regulated signaling cascades, Disabled 1. These findings describe miR-138 as a novel regulator of hypothalamic cell migration, acting at least in part via inhibition of Reln expression and leading to the inactivation of Reln signals. © 2013 IBRO.
Note:
Related Files :
animal cell
Animals
animal tissue
Cell Proliferation
Extracellular Matrix Proteins
immunoprecipitation
unclassified drug
עוד תגיות
תוכן קשור
More details
DOI :
10.1016/j.neuroscience.2013.02.020
Article number:
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
20708
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:38
Scientific Publication
MiR-138 promotes the migration of cultured chicken embryonic hypothalamic cells by targeting reelin
238
Kisliouk, T., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan 50250, Israel
Meiri, N., Institute of Animal Science, ARO, The Volcani Center, Bet Dagan 50250, Israel
MiR-138 promotes the migration of cultured chicken embryonic hypothalamic cells by targeting reelin
Neuronal network remodeling during critical periods of sensory development might be accompanied by alterations in hypothalamic cell populations. MicroRNAs play a central role in regulating neuronal function, including neural stem cell proliferation, and neuronal migration, maturation and integration into viable circuits by modulating different mRNA targets. Here we investigated the role of miR-138 in cell proliferation and migration in a neuron-enriched hypothalamic cell culture prepared from chicks on embryonic day 16. Ectopic expression of miR-138 enhanced hypothalamic cell migration, but did not affect cell proliferation. As a potential mechanism for miR-138's effect on cell migration, we investigated reelin (Reln) as a direct target of miR-138. Luciferase reporter assay and Ago2-immunoprecipitation experiments confirmed direct binding of miR-138 to the Reln 3'-untranslated region. Ectopic miR-138 abolished Reln levels in hypothalamic cells and enhanced their migration, similar to Reln-antisense DNA. Furthermore, inhibition of Reln expression by miR-138 led to decreased phosphorylation level of the key component of Reln-regulated signaling cascades, Disabled 1. These findings describe miR-138 as a novel regulator of hypothalamic cell migration, acting at least in part via inhibition of Reln expression and leading to the inactivation of Reln signals. © 2013 IBRO.
Scientific Publication
You may also be interested in