Downregulation of Homer1b/c in SOD1 G93A Models of ALS: A Novel Mechanism of Neuroprotective Effect of Lithium and Valproic Acid

Background: Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in n...

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Published inInternational journal of molecular sciences Vol. 17; no. 12; p. 2129
Main Authors Jiang, Hai-Zhi, Wang, Shu-Yu, Yin, Xiang, Jiang, Hong-Quan, Wang, Xu-Dong, Wang, Jing, Wang, Tian-Hang, Qi, Yan, Yang, Yue-Qing, Wang, Ying, Zhang, Chun-Ting, Feng, Hong-Lin
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 17.12.2016
MDPI
Subjects
Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - genetics
Amyotrophic Lateral Sclerosis - pathology
Amyotrophic Lateral Sclerosis - therapy
Animals
Apoptosis - genetics
Cell Line
Genetic Predisposition to Disease
Homer Scaffolding Proteins - antagonists & inhibitors
Homer Scaffolding Proteins - biosynthesis
Homer Scaffolding Proteins - genetics
Humans
Lithium
Lithium - therapeutic use
Mice
Mice, Transgenic
Mutation
Proto-Oncogene Proteins c-bcl-2 - metabolism
RNA Interference
RNA, Small Interfering - genetics
Superoxide Dismutase - genetics
Valproic Acid - therapeutic use
Homer1b/c
SOD1 G93A
lithium
valproic acid (VPA)
amyotrophic lateral sclerosis
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Abstract Background: Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS. Results: In vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice. Conclusion: The suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.
AbstractList Background: Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS. Results: In vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice. Conclusion: The suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.
Mutations in the Cu/Zn superoxide dismutase ( ) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS. In vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice. The suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.
Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS.BACKGROUNDMutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS.In vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice.RESULTSIn vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice.The suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.CONCLUSIONThe suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.
Background: Mutations in the Cu/Zn superoxide dismutase ( SOD1 ) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been elucidated yet. Homer family protein Homer1b/c is expressed widely in the central nervous system and plays important roles in neurological diseases. In this study, we explored whether Homer1b/c was involved in SOD1 mutation-linked ALS. Results: In vitro studies showed that the SOD1 G93A mutation induced an increase of Homer1b/c expression at both the mRNA and protein levels in NSC34 cells. Knockdown of Homer1b/c expression using its short interfering RNA (siRNA) (si-Homer1) protected SOD1 G93A NSC34 cells from apoptosis. The expressions of Homer1b/c and apoptosis-related protein Bax were also suppressed, while Bcl-2 was increased by lithium and valproic acid (VPA) in SOD1 G93A NSC34 cells. In vivo, both the mRNA and protein levels of Homer1b/c were increased significantly in the lumbar spinal cord in SOD1 G93A transgenic mice compared with wild type (WT) mice. Moreover, lithium and VPA treatment suppressed the expression of Homer1b/c in SOD1 G93A mice. Conclusion: The suppression of SOD1 G93A mutation-induced Homer1b/c upregulation protected ALS against neuronal apoptosis, which is a novel mechanism of the neuroprotective effect of lithium and VPA. This study provides new insights into pathogenesis and treatment of ALS.
Author Yin, Xiang
Zhang, Chun-Ting
Jiang, Hong-Quan
Jiang, Hai-Zhi
Yang, Yue-Qing
Wang, Ying
Wang, Shu-Yu
Wang, Xu-Dong
Qi, Yan
Feng, Hong-Lin
Wang, Jing
Wang, Tian-Hang
AuthorAffiliation Department of Neurology, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, China; jianghz@hrbmu.edu.cn (H.-Z.J.); WangS319@hotmail.com (S.-Y.W.); YinXiang15@hotmail.com (X.Y.); jianghongquan321@hotmail.com (H.-Q.J.); wangxudonghlj@hotmail.com (X.-D.W.); hebgdwangjing@163.com (J.W.); libu979@126.com (T.-H.W.); qiswallow21@sohu.com (Y.Q.); yangyueqing714@sina.com (Y.-Q.Y.); try101_80@163.com (Y.W.); hoat77@sina.com (C.-T.Z.)
AuthorAffiliation_xml – name: Department of Neurology, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, China; jianghz@hrbmu.edu.cn (H.-Z.J.); WangS319@hotmail.com (S.-Y.W.); YinXiang15@hotmail.com (X.Y.); jianghongquan321@hotmail.com (H.-Q.J.); wangxudonghlj@hotmail.com (X.-D.W.); hebgdwangjing@163.com (J.W.); libu979@126.com (T.-H.W.); qiswallow21@sohu.com (Y.Q.); yangyueqing714@sina.com (Y.-Q.Y.); try101_80@163.com (Y.W.); hoat77@sina.com (C.-T.Z.)
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27999308$$D View this record in MEDLINE/PubMed
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Keywords Homer1b/c
SOD1 G93A
lithium
valproic acid (VPA)
amyotrophic lateral sclerosis
Language English
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Snippet Background: Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms...
Mutations in the Cu/Zn superoxide dismutase ( ) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not been...
Mutations in the Cu/Zn superoxide dismutase (SOD1) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular mechanisms have not...
Background: Mutations in the Cu/Zn superoxide dismutase ( SOD1 ) gene have been linked to amyotrophic lateral sclerosis (ALS). However, the molecular...
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StartPage 2129
SubjectTerms Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - genetics
Amyotrophic Lateral Sclerosis - pathology
Amyotrophic Lateral Sclerosis - therapy
Animals
Apoptosis - genetics
Cell Line
Genetic Predisposition to Disease
Homer Scaffolding Proteins - antagonists & inhibitors
Homer Scaffolding Proteins - biosynthesis
Homer Scaffolding Proteins - genetics
Humans
Lithium
Lithium - therapeutic use
Mice
Mice, Transgenic
Mutation
Proto-Oncogene Proteins c-bcl-2 - metabolism
RNA Interference
RNA, Small Interfering - genetics
Superoxide Dismutase - genetics
Valproic Acid - therapeutic use
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Title Downregulation of Homer1b/c in SOD1 G93A Models of ALS: A Novel Mechanism of Neuroprotective Effect of Lithium and Valproic Acid
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