Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes
Authors
Balint, VandaStanisavljević Ninković, Danijela
Anastasov, Nataša
Lazić, Stefan
Kovačević-Grujičić, Nataša
Stevanović, Milena
Lazić, Andrijana
Krstić, Aleksandra
Pejić, Jelena
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Astrocytes are the main homeostatic cells in the central nervous system (CNS) that provide mechanical,
metabolic, and trophic support to neurons. Disruption of their physiological role or acquisition of
senescence-associated phenotype can contribute to the CNS dysfunction and pathology. However, molecular
mechanisms underlying the complex physiology of astrocytes are explored insufficiently. Recent studies have
shown that miRNAs are involved in the regulation of astrocyte function through different mechanisms.
Although miR-21 has been reported as an astrocytic miRNA with an important role in astrogliosis, no link
between this miRNA and cellular senescence of astrocytes has been identified. To address the role of miR-21
in astrocytes, with special focus on cellular senescence, we used NT2/A (astrocytes derived from NT2/D1
cells). Downregulation of miR-21 expression in both immature and mature NT2/A by the antisense
technology induced the arrest of cell growth and premature cell...ular senescence, as indicated by senescence
hallmarks such as increased expression of cell cycle inhibitors p21 and p53 and augmented senescenceassociated
β-galactosidase activity. Additionally, in silico analysis predicted many of the genes, previously
shown to be upregulated in astrocytes with the irradiation-induced senescence, as miR-21 targets. Taken
together, our results point to miR-21 as a potential regulator of astrocyte senescence. To the best of our
knowledge, these are the first data showing the link between miR-21 and cellular senescence of astrocytes.
Since senescent astrocytes are associated with different CNS pathologies, development of novel therapeutic
strategies based on miRNA manipulation could prevent senescence and may improve the physiological
outcome.
Keywords:
RA-induced neural differentiation / miR-21 downregulation / miR-21 targets / SA-β-gal activity / cellular senescenceSource:
RAD International concerence on radiation in various fields of research, 2022, Spring Edition, 90-Note:
- BOOK OF ABSTRACTS: 10th JUBILEE INTERNATIONAL CONFERENCE ON RADIATION IN VARIOUS FIELDS OF RESEARCH Jun 13-17, 2022, Herceg Novi - Montenegro
URI
https://doi.org/10.21175/rad.spr.abstr.book.2022.22.1https://imagine.imgge.bg.ac.rs/handle/123456789/1864
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Institut za molekularnu genetiku i genetičko inženjerstvoTY - CONF AU - Balint, Vanda AU - Stanisavljević Ninković, Danijela AU - Anastasov, Nataša AU - Lazić, Stefan AU - Kovačević-Grujičić, Nataša AU - Stevanović, Milena AU - Lazić, Andrijana AU - Krstić, Aleksandra AU - Pejić, Jelena PY - 2022 UR - https://doi.org/10.21175/rad.spr.abstr.book.2022.22.1 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/1864 AB - Astrocytes are the main homeostatic cells in the central nervous system (CNS) that provide mechanical, metabolic, and trophic support to neurons. Disruption of their physiological role or acquisition of senescence-associated phenotype can contribute to the CNS dysfunction and pathology. However, molecular mechanisms underlying the complex physiology of astrocytes are explored insufficiently. Recent studies have shown that miRNAs are involved in the regulation of astrocyte function through different mechanisms. Although miR-21 has been reported as an astrocytic miRNA with an important role in astrogliosis, no link between this miRNA and cellular senescence of astrocytes has been identified. To address the role of miR-21 in astrocytes, with special focus on cellular senescence, we used NT2/A (astrocytes derived from NT2/D1 cells). Downregulation of miR-21 expression in both immature and mature NT2/A by the antisense technology induced the arrest of cell growth and premature cellular senescence, as indicated by senescence hallmarks such as increased expression of cell cycle inhibitors p21 and p53 and augmented senescenceassociated β-galactosidase activity. Additionally, in silico analysis predicted many of the genes, previously shown to be upregulated in astrocytes with the irradiation-induced senescence, as miR-21 targets. Taken together, our results point to miR-21 as a potential regulator of astrocyte senescence. To the best of our knowledge, these are the first data showing the link between miR-21 and cellular senescence of astrocytes. Since senescent astrocytes are associated with different CNS pathologies, development of novel therapeutic strategies based on miRNA manipulation could prevent senescence and may improve the physiological outcome. C3 - RAD International concerence on radiation in various fields of research T1 - Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes IS - Spring Edition SP - 90 DO - 10.21175/rad.spr.abstr.book.2022.22.1 ER -
@conference{ author = "Balint, Vanda and Stanisavljević Ninković, Danijela and Anastasov, Nataša and Lazić, Stefan and Kovačević-Grujičić, Nataša and Stevanović, Milena and Lazić, Andrijana and Krstić, Aleksandra and Pejić, Jelena", year = "2022", abstract = "Astrocytes are the main homeostatic cells in the central nervous system (CNS) that provide mechanical, metabolic, and trophic support to neurons. Disruption of their physiological role or acquisition of senescence-associated phenotype can contribute to the CNS dysfunction and pathology. However, molecular mechanisms underlying the complex physiology of astrocytes are explored insufficiently. Recent studies have shown that miRNAs are involved in the regulation of astrocyte function through different mechanisms. Although miR-21 has been reported as an astrocytic miRNA with an important role in astrogliosis, no link between this miRNA and cellular senescence of astrocytes has been identified. To address the role of miR-21 in astrocytes, with special focus on cellular senescence, we used NT2/A (astrocytes derived from NT2/D1 cells). Downregulation of miR-21 expression in both immature and mature NT2/A by the antisense technology induced the arrest of cell growth and premature cellular senescence, as indicated by senescence hallmarks such as increased expression of cell cycle inhibitors p21 and p53 and augmented senescenceassociated β-galactosidase activity. Additionally, in silico analysis predicted many of the genes, previously shown to be upregulated in astrocytes with the irradiation-induced senescence, as miR-21 targets. Taken together, our results point to miR-21 as a potential regulator of astrocyte senescence. To the best of our knowledge, these are the first data showing the link between miR-21 and cellular senescence of astrocytes. Since senescent astrocytes are associated with different CNS pathologies, development of novel therapeutic strategies based on miRNA manipulation could prevent senescence and may improve the physiological outcome.", journal = "RAD International concerence on radiation in various fields of research", title = "Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes", number = "Spring Edition", pages = "90", doi = "10.21175/rad.spr.abstr.book.2022.22.1" }
Balint, V., Stanisavljević Ninković, D., Anastasov, N., Lazić, S., Kovačević-Grujičić, N., Stevanović, M., Lazić, A., Krstić, A.,& Pejić, J.. (2022). Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes. in RAD International concerence on radiation in various fields of research(Spring Edition), 90. https://doi.org/10.21175/rad.spr.abstr.book.2022.22.1
Balint V, Stanisavljević Ninković D, Anastasov N, Lazić S, Kovačević-Grujičić N, Stevanović M, Lazić A, Krstić A, Pejić J. Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes. in RAD International concerence on radiation in various fields of research. 2022;(Spring Edition):90. doi:10.21175/rad.spr.abstr.book.2022.22.1 .
Balint, Vanda, Stanisavljević Ninković, Danijela, Anastasov, Nataša, Lazić, Stefan, Kovačević-Grujičić, Nataša, Stevanović, Milena, Lazić, Andrijana, Krstić, Aleksandra, Pejić, Jelena, "Inhibition of miR-21 promotes cellular senescence in NT2-derived astrocytes" in RAD International concerence on radiation in various fields of research, no. Spring Edition (2022):90, https://doi.org/10.21175/rad.spr.abstr.book.2022.22.1 . .