Acceleration of TDP43 and FUS/TLS protein expressions in the preconditioned hippocampus following repeated transient ischemia

Sun, Miao; Yamashita, Toru; Shang, Jingwei; Liu, Ning; Deguchi, Kentaro; Li, Wentao; Ikeda, Yoshio; Feng, Juan; Abe, Kōji

doi:10.1002/jnr.23301

Cited by 9 publications

(14 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TARDBP, also known as TDP-43, has been identified as a major constituent of proteinaceous inclusions characteristic of most forms of amyotrophic lateral sclerosis and frontotemporal lobar degeneration (22) . The 43-kDa transactivation response DNA binding protein (TDP43), FUS/TLS, heat shock protein 70, and β-amyloid have been reported to be induced and involved in cerebral ischemia, amyotrophic lateral sclerosis, and Alzheimer's disease (23) . However, their involvements in ischemic tolerance have never been examined, although they could be involved in endogenous neuroprotection under ischemic preconditioning (23) .…”

Section: Resultsmentioning

confidence: 99%

“…The 43-kDa transactivation response DNA binding protein (TDP43), FUS/TLS, heat shock protein 70, and β-amyloid have been reported to be induced and involved in cerebral ischemia, amyotrophic lateral sclerosis, and Alzheimer's disease (23) . However, their involvements in ischemic tolerance have never been examined, although they could be involved in endogenous neuroprotection under ischemic preconditioning (23) .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

et al. 2016

View full text Add to dashboard Cite

RNA polymerase II C-terminal domain phosphatases are newly emerging family of phosphatases that contain FCPH domain with Mg+2-binding DXDX(T/V) signature motif. Its subfamily includes small CTD phosphatases (SCPs). Recently, we identified several interacting partners of human SCP1 with appearance of dephosphorylation and O-GlcNAcylation. In this study, using an established cell line with inducible CTDSPL2 protein (a member of the new phosphatase family), proteomic screening was conducted to identify binding partners of CTDSPL2 in nuclear extract through immunoprecipitation of CTDSPL2 with its associated. This approach led to the identification of several interacting partners of CTDSPL2. This will provide a better understanding on CTDSPL2. [BMB Reports 2016; 49(6): 319-324]

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

et al. 2016

View full text Add to dashboard Cite

show abstract

“… 10 Dysregulation of TAR-DNA binding protein 43 (TDP43) confers to various disorders such as amyotrophic lateral sclerosis, brain ischemia, and Alzheimer’s disease. 11 Also, dysregulation of TDP43 contributes to the progression of neuroblastoma and breast cancer. 12 However, the profiling of TDP43 in glioma remains incompletely delineated.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of TDP43-Mediated SNHG12-miR-195-SOX5 Feedback Loop Impeded Malignant Biological Behaviors of Glioma Cells

Liu

Zheng

Xue

et al. 2018

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

Long non-coding RNA (lncRNA) dysregulation is involved in tumorigenesis and regulation of diverse cellular processes in gliomas. lncRNA SNHG12 is upregulated and promotes cell growth in human osteosarcoma cells. TAR-DNA binding protein 43 (TDP43) functions as an oncogene in various tumors by modulating RNA expression. Downregulation of TDP43 or SNHG12 significantly inhibited malignant biological behaviors of glioma cells. miR-195, downregulated in glioma tissues and cells, significantly impaired the malignant progression of glioma cells. TDP43 upregulated miR-195 in an SNHG12-dependent manner. We further revealed that SNHG12 and miR-195 were in an RNA-induced silencing complex (RISC). Inhibition of SNHG12 combined with restoration of miR-195 robustly reduced tumor growth in vivo. SOX5 was overexpressed in glioma tissues and cells. miR-195 targeted SOX5 3′ UTR in a sequence-specific manner. Gelsolin was activated by SOX5. More importantly, SOX5 activated SNHG12 promoter and upregulated its expression, forming a feedback loop. Dysregulation of SNHG12, miR-195, and SOX5 predicted poor prognosis of glioma patients. The present study demonstrated that SNHG12-miR-195-SOX5 feedback loop exerted a crucial role in the regulation of glioma cells’ malignant progression.

show abstract

“…Their work identified 43 kDa transactivation response DNA-binding protein (TDP43), fused in sarcoma/translocated in liposarcoma (FUS/TLS), and heat shock protein 70 kDa (HSP70) as potential mRNA targets. This group demonstrated the neuroprotective role of these proteins in a previous investigation [55]. Other corroborative work has shown that miR-132, which targets FUS/TLS, increased and peaked at post-injury day 1, but was subsequently downregulated from 7 days to 6 months after ischemia [54].…”

Section: Ischemic Preconditioningmentioning

confidence: 68%

MicroRNA Changes in Preconditioning-Induced Neuroprotection

Bell

Cho

Giffard

2017

Transl. Stroke Res.

View full text Add to dashboard Cite

Preconditioning is a paradigm in which sub-lethal stress – prior to a more injurious insult – induces protection against injury. In the central nervous system (CNS), preconditioning against ischemic stroke is induced by short durations of ischemia, brief seizures, exposure to anesthetics, and other stresses. Increasing evidence supports the contribution of microRNAs (miRNAs) to the pathogenesis of cerebral ischemia and ischemic tolerance induced by preconditioning. Studies investigating miRNA changes induced by preconditioning have to date identified 562 miRNAs that change expression levels after preconditioning, and 15% of these changes were reproduced in at least one additional study. Of miRNAs assessed as changed by preconditioning in more than one study, about 40% changed in the same direction in more than one study. Most of the studies to assess the role of specific miRNAs in the neuroprotective mechanism of preconditioning were performed in vitro, with fewer studies manipulating individual miRNAs in vivo. Thus, while many miRNAs change in response to preconditioning stimuli, the mechanisms underlying their effects are not well understood. The data does suggest that miRNAs may play significant roles in preconditioning-induced neuroprotection. This review focuses on the current state of knowledge of the possible role of miRNAs in preconditioning-induced cerebral protection.

show abstract

Acceleration of TDP43 and FUS/TLS protein expressions in the preconditioned hippocampus following repeated transient ischemia

Cited by 9 publications

References 47 publications

A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

Inhibition of TDP43-Mediated SNHG12-miR-195-SOX5 Feedback Loop Impeded Malignant Biological Behaviors of Glioma Cells

MicroRNA Changes in Preconditioning-Induced Neuroprotection

Contact Info

Product

Resources

About