Cited by 104Histone Deacetylase Inhibitors ResearchCell death mechanisms and regulationGenomics and Chromatin Dynamics

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Neuroprotection by Histone Deacetylase-Related Protein

Morrison, Brad E., Majdzadeh, Nazanin, Zhang, Xiaoguang, Lyles, Aaron, Bassel-Duby, Rhonda, Olson, Eric N., D'Mello, Santosh R.·2006·Molecular and Cellular Biology

DOI 10.1128/mcb.26.9.3550-3564.2006

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Abstract

The expression of histone deacetylase-related protein (HDRP) is reduced in neurons undergoing apoptosis. Forced reduction of HDRP expression in healthy neurons by treatment with antisense oligonucleotides also induces cell death. Likewise, neurons cultured from mice lacking HDRP are more vulnerable to cell death. Adenovirally mediated expression of HDRP prevents neuronal death, showing that HDRP is a neuroprotective protein. Neuroprotection by forced expression of HDRP is not accompanied by activation of the phosphatidylinositol 3-kinase-Akt or Raf-MEK-ERK signaling pathway, and treatment with pharmacological inhibitors of these pathways fails to inhibit the neuroprotection by HDRP. Stimulation of c-Jun phosphorylation and expression, an essential feature of neuronal death, is prevented by HDRP. We found that HDRP associates with c-Jun N-terminal kinase (JNK) and inhibits its activity, thus explaining the inhibition of c-Jun phosphorylation by HDRP. HDRP also interacts with histone deacetylase 1 (HDAC1) and recruits it to the c-Jun gene promoter, resulting in an inhibition of histone H3 acetylation at the c-Jun promoter. Although HDRP lacks intrinsic deacetylase activity, treatment with pharmacological inhibitors of histone deacetylases induces apoptosis even in the presence of ectopically expressed HDRP, underscoring the importance of c-Jun promoter deacetylation by HDRP-HDAC1 in HDRP-mediated neuroprotection. Our results suggest that neuroprotection by HDRP is mediated by the inhibition of c-Jun through its interaction with JNK and HDAC1.

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Authors: Morrison, B. E., Majdzadeh, N., Zhang, X., Lyles, A., Bassel-Duby, R., Olson, E. N., & D'Mello, S. R.
Affiliations: The University of Texas at Dallas (US)
Department of Molecular Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390
The University of Texas Southwestern Medical Center (US)
Department of Molecular and Cell Biology, University of Texas at Dallas, 2601 N. Floyd Rd., Richardson, Texas 75083
ORCID: Morrison, Brad E.
Zhang, Xiaoguang
Olson, Eric N.
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 2006-05-01
Volume: 26
Issue: 9
Pages: 3550-3564
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.26.9.3550-3564.2006
OpenAlex: W2024126284
Cited by: 100
References: 51
Citations by year: 2026: 2 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 6 · 2018: 5 · 2017: 2 · 2016: 2 · 2015: 8 · 2014: 6 · 2013: 7 · 2012: 7
FWCI: 3.53
Type: journal article
Language: en
Open access: closed
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Defense
National Institutes of Health
National Institute of Neurological Disorders and Stroke (NS047201, R01NS040408, NS40408, R01NS047201)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: neuroprotection, neuronal apoptosis, c-Jun phosphorylation, c-Jun N-terminal kinase, HDAC1, histone H3 acetylation, c-jun promoter, phosphatidylinositol 3-kinase/Akt signaling, MAPK/ERK pathway, antisense oligonucleotides, adenoviral gene expression, histone deacetylase inhibitors
MeSH terms: Phosphoinositide-3 Kinase Inhibitors, Animals, Cell Nucleus, Enzyme Inhibitors, Histone Deacetylases, Neurons, Phosphorylation, RNA, Messenger, Transcription, Genetic, Proto-Oncogene Proteins c-jun, Apoptosis, Phosphatidylinositol 3-Kinases, JNK Mitogen-Activated Protein Kinases, Extracellular Signal-Regulated MAP Kinases, Mice, Rats, Histone Deacetylase Inhibitors

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Neuroprotection by Histone Deacetylase-Related Protein

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