Increase of Zinc Finger Protein 179 in Response to CCAAT/Enhancer Binding Protein Delta Conferring an Antiapoptotic Effect in Astrocytes of Alzheimer’s Disease

Shao Ming Wang, Yi Chao Lee, Chiung Yuan Ko, Ming-Derg Lai, Ding-Yen Lin, Ping Chieh Pao, Jhih Ying Chi, Yu Wei Hsiao, Tsung-lin Liu, Ju-Ming Wang

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Reactive astrogliosis is a cellular manifestation of neuroinflammation and occurs in response to all forms and severities of the central nervous system (CNS)’s injury and disease. Both astroglial proliferation and antiapoptotic processes are aspects of astrogliosis. However, the underlying mechanism of this response remains poorly understood. In addition, little is known about why activated astrocytes are more resistant to stress and inflammation. CCAAT/enhancer binding protein delta (CEBPD) is a transcription factor found in activated astrocytes that surround β-amyloid plaques. In this study, we found that astrocytes activation was attenuated in the cortex and hippocampus of APPswe/PS1 E9 (AppTg)/Cebpd −/− mice. Furthermore, an increase in apoptotic astrocytes was observed in AppTg/Cebpd −/− mice, suggesting that CEBPD plays a functional role in enhancing the antiapoptotic ability of astrocytes. We found that Zinc Finger Protein 179 (ZNF179) was a CEBPD-regulated gene that played an antiapoptotic, but not proliferative, role in astrocytes. The transcriptions of the proapoptotic genes, insulin-like growth factor binding protein 3 (IGFBP3) and BCL2-interacting killer (BIK), were suppressed by ZNF179 via its interaction with the promyelocytic leukemia zinc finger (PLZF) protein in astrocytes. This study provides the first evidence that ZNF179, PLZF, IGFBP3, and BIK contributed to the novel CEBPD-induced antiapoptotic feature of astrocytes.

Original languageEnglish
Pages (from-to)370-382
Number of pages13
JournalMolecular Neurobiology
Volume51
Issue number1
DOIs
Publication statusPublished - 2014 Jan 1

Fingerprint

CCAAT-Enhancer-Binding Protein-delta
Zinc Fingers
Astrocytes
Alzheimer Disease
Proteins
Insulin-Like Growth Factor Binding Protein 3
Nervous System Trauma
Aptitude
Amyloid Plaques
Nervous System Diseases
Genes
Hippocampus
Leukemia
Transcription Factors
Central Nervous System

All Science Journal Classification (ASJC) codes

  • Neuroscience (miscellaneous)
  • Neurology
  • Cellular and Molecular Neuroscience

Cite this

@article{8b7ab33dc2cf4e9992cf8a7b9a139a38,
title = "Increase of Zinc Finger Protein 179 in Response to CCAAT/Enhancer Binding Protein Delta Conferring an Antiapoptotic Effect in Astrocytes of Alzheimer’s Disease",
abstract = "Reactive astrogliosis is a cellular manifestation of neuroinflammation and occurs in response to all forms and severities of the central nervous system (CNS)’s injury and disease. Both astroglial proliferation and antiapoptotic processes are aspects of astrogliosis. However, the underlying mechanism of this response remains poorly understood. In addition, little is known about why activated astrocytes are more resistant to stress and inflammation. CCAAT/enhancer binding protein delta (CEBPD) is a transcription factor found in activated astrocytes that surround β-amyloid plaques. In this study, we found that astrocytes activation was attenuated in the cortex and hippocampus of APPswe/PS1 E9 (AppTg)/Cebpd −/− mice. Furthermore, an increase in apoptotic astrocytes was observed in AppTg/Cebpd −/− mice, suggesting that CEBPD plays a functional role in enhancing the antiapoptotic ability of astrocytes. We found that Zinc Finger Protein 179 (ZNF179) was a CEBPD-regulated gene that played an antiapoptotic, but not proliferative, role in astrocytes. The transcriptions of the proapoptotic genes, insulin-like growth factor binding protein 3 (IGFBP3) and BCL2-interacting killer (BIK), were suppressed by ZNF179 via its interaction with the promyelocytic leukemia zinc finger (PLZF) protein in astrocytes. This study provides the first evidence that ZNF179, PLZF, IGFBP3, and BIK contributed to the novel CEBPD-induced antiapoptotic feature of astrocytes.",
author = "Wang, {Shao Ming} and Lee, {Yi Chao} and Ko, {Chiung Yuan} and Ming-Derg Lai and Ding-Yen Lin and Pao, {Ping Chieh} and Chi, {Jhih Ying} and Hsiao, {Yu Wei} and Tsung-lin Liu and Ju-Ming Wang",
year = "2014",
month = "1",
day = "1",
doi = "10.1007/s12035-014-8714-9",
language = "English",
volume = "51",
pages = "370--382",
journal = "Molecular Neurobiology",
issn = "0893-7648",
publisher = "Humana Press",
number = "1",

}

Increase of Zinc Finger Protein 179 in Response to CCAAT/Enhancer Binding Protein Delta Conferring an Antiapoptotic Effect in Astrocytes of Alzheimer’s Disease. / Wang, Shao Ming; Lee, Yi Chao; Ko, Chiung Yuan; Lai, Ming-Derg; Lin, Ding-Yen; Pao, Ping Chieh; Chi, Jhih Ying; Hsiao, Yu Wei; Liu, Tsung-lin; Wang, Ju-Ming.

In: Molecular Neurobiology, Vol. 51, No. 1, 01.01.2014, p. 370-382.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Increase of Zinc Finger Protein 179 in Response to CCAAT/Enhancer Binding Protein Delta Conferring an Antiapoptotic Effect in Astrocytes of Alzheimer’s Disease

AU - Wang, Shao Ming

AU - Lee, Yi Chao

AU - Ko, Chiung Yuan

AU - Lai, Ming-Derg

AU - Lin, Ding-Yen

AU - Pao, Ping Chieh

AU - Chi, Jhih Ying

AU - Hsiao, Yu Wei

AU - Liu, Tsung-lin

AU - Wang, Ju-Ming

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Reactive astrogliosis is a cellular manifestation of neuroinflammation and occurs in response to all forms and severities of the central nervous system (CNS)’s injury and disease. Both astroglial proliferation and antiapoptotic processes are aspects of astrogliosis. However, the underlying mechanism of this response remains poorly understood. In addition, little is known about why activated astrocytes are more resistant to stress and inflammation. CCAAT/enhancer binding protein delta (CEBPD) is a transcription factor found in activated astrocytes that surround β-amyloid plaques. In this study, we found that astrocytes activation was attenuated in the cortex and hippocampus of APPswe/PS1 E9 (AppTg)/Cebpd −/− mice. Furthermore, an increase in apoptotic astrocytes was observed in AppTg/Cebpd −/− mice, suggesting that CEBPD plays a functional role in enhancing the antiapoptotic ability of astrocytes. We found that Zinc Finger Protein 179 (ZNF179) was a CEBPD-regulated gene that played an antiapoptotic, but not proliferative, role in astrocytes. The transcriptions of the proapoptotic genes, insulin-like growth factor binding protein 3 (IGFBP3) and BCL2-interacting killer (BIK), were suppressed by ZNF179 via its interaction with the promyelocytic leukemia zinc finger (PLZF) protein in astrocytes. This study provides the first evidence that ZNF179, PLZF, IGFBP3, and BIK contributed to the novel CEBPD-induced antiapoptotic feature of astrocytes.

AB - Reactive astrogliosis is a cellular manifestation of neuroinflammation and occurs in response to all forms and severities of the central nervous system (CNS)’s injury and disease. Both astroglial proliferation and antiapoptotic processes are aspects of astrogliosis. However, the underlying mechanism of this response remains poorly understood. In addition, little is known about why activated astrocytes are more resistant to stress and inflammation. CCAAT/enhancer binding protein delta (CEBPD) is a transcription factor found in activated astrocytes that surround β-amyloid plaques. In this study, we found that astrocytes activation was attenuated in the cortex and hippocampus of APPswe/PS1 E9 (AppTg)/Cebpd −/− mice. Furthermore, an increase in apoptotic astrocytes was observed in AppTg/Cebpd −/− mice, suggesting that CEBPD plays a functional role in enhancing the antiapoptotic ability of astrocytes. We found that Zinc Finger Protein 179 (ZNF179) was a CEBPD-regulated gene that played an antiapoptotic, but not proliferative, role in astrocytes. The transcriptions of the proapoptotic genes, insulin-like growth factor binding protein 3 (IGFBP3) and BCL2-interacting killer (BIK), were suppressed by ZNF179 via its interaction with the promyelocytic leukemia zinc finger (PLZF) protein in astrocytes. This study provides the first evidence that ZNF179, PLZF, IGFBP3, and BIK contributed to the novel CEBPD-induced antiapoptotic feature of astrocytes.

UR - http://www.scopus.com/inward/record.url?scp=84939890944&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84939890944&partnerID=8YFLogxK

U2 - 10.1007/s12035-014-8714-9

DO - 10.1007/s12035-014-8714-9

M3 - Article

VL - 51

SP - 370

EP - 382

JO - Molecular Neurobiology

JF - Molecular Neurobiology

SN - 0893-7648

IS - 1

ER -