Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus
Само за регистроване кориснике
2009
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Successful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins red...istribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system.
Кључне речи:
Stress / Hippocampus / Glucocorticoid receptor / Nuclear factor kappa B / Plasticity / ApoptosisИзвор:
Journal of Neural Transmission, 2009, 116, 12, 1579-1589Напомена:
- Link to erratum: http://dx.doi.org/10.1007/s00702-009-0335-5
Повезане информације:
- Повезани садржај
http://dx.doi.org/10.1007/s00702-009-0335-5
DOI: 10.1007/s00702-009-0286-x
ISSN: 0300-9564
PubMed: 19669692
WoS: 000271750300004
Scopus: 2-s2.0-70949092301
Колекције
Институција/група
VinčaTY - JOUR AU - Đorđević, Ana D. AU - Adžić, Miroslav AU - Đorđević, Jelena D. AU - Radojčić, Marija PY - 2009 UR - https://vinar.vin.bg.ac.rs/handle/123456789/3822 AB - Successful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins redistribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system. T2 - Journal of Neural Transmission T1 - Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus VL - 116 IS - 12 SP - 1579 EP - 1589 DO - 10.1007/s00702-009-0286-x ER -
@article{ author = "Đorđević, Ana D. and Adžić, Miroslav and Đorđević, Jelena D. and Radojčić, Marija", year = "2009", abstract = "Successful adaptation to stress involves actions of glucocorticoid receptor (GR), a steroid-dependent transcription factor, abundant in hippocampus. Another transcription factor, nuclear factor kappa B (NF kappa B) is considered as an important stress sensor implicated in adaptive synaptic plasticity. Numerous stress-related genes are regulated by both hippocampal GR and NF kappa B, including neural cell adhesion molecules (NCAM and L1), involved in plasticity, and genes that encode apoptotic proteins (bax and bcl-2). We presumed that the ratio of nuclear NF kappa B to nuclear GR may determine the degree of proplastic or proapoptotic signaling under stress. To test this presumption we have investigated effects of acute, chronic and combined stress on compartmental levels and ratios of NF kappa B and GR proteins, and in parallel, changes in their mRNA expression. In addition, the expression of plasticity (NCAM, L1) and apoptotic (bax, bcl-2) genes, as well as, Bax and Bcl-2 proteins redistribution between mitochondrial and cytoplasmic compartments, were followed. When glucocorticoid levels were low, as found in chronic stress, GR was not efficiently translocated to the nucleus. This resulted in its lower nuclear level relative to the nuclear NF kappa B. Such conditions did not affect proplastic induction of NCAM mRNA, but were related to the onset of proapoptotic signaling illustrated by relocation of mitochondrial Bcl-2 protein to its soluble cytoplasmic form. Because these Bcl-2 rearrangements were not reversed by subsequent acute stress, representing more stable alterations, it is concluded that chronic social isolation of Wistar rats led to the initiation of proapoptotic signaling that may be etiologically related to compromised adaptive response of central nervous system.", journal = "Journal of Neural Transmission", title = "Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus", volume = "116", number = "12", pages = "1579-1589", doi = "10.1007/s00702-009-0286-x" }
Đorđević, A. D., Adžić, M., Đorđević, J. D.,& Radojčić, M.. (2009). Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus. in Journal of Neural Transmission, 116(12), 1579-1589. https://doi.org/10.1007/s00702-009-0286-x
Đorđević AD, Adžić M, Đorđević JD, Radojčić M. Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus. in Journal of Neural Transmission. 2009;116(12):1579-1589. doi:10.1007/s00702-009-0286-x .
Đorđević, Ana D., Adžić, Miroslav, Đorđević, Jelena D., Radojčić, Marija, "Chronic social isolation is related to both upregulation of plasticity genes and initiation of proapoptotic signaling in Wistar rat hippocampus" in Journal of Neural Transmission, 116, no. 12 (2009):1579-1589, https://doi.org/10.1007/s00702-009-0286-x . .