RBM5 and p53 expression after rat spinal cord injury: Implications for neuronal apoptosis

Zhang, Jinlong; Cui, Zhiming; Feng, Guoliang; Bao, Guofeng; Xu, Guanhua; Sun, Yuyu; Wang, Lingling; Chen, Jiajia; Jin, Huricha; Liu, Jian; Yang, Longfei; Li, Weidong

doi:10.1016/j.biocel.2014.12.020

Cited by 43 publications

(32 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pifithrin‐ μ is reported to attenuate the translocation of p53 to mitochondria and inhibit cellular apoptosis . Translocation of p53 to the mitochondria induces mitochondrial cytochrome C (CyC) release, and activation of a caspase cascade, which leads to programmed cell death . Peak activation of caspase levels was reported at 24 hours following SCI in rats .…”

Section: Resultsmentioning

confidence: 99%

Pifithrin‐μ modulates microglial activation and promotes histological recovery following spinal cord injury

et al. 2018

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Pifithrin‐μ modulates microglial activation and promotes histological recovery following spinal cord injury

et al. 2018

View full text Add to dashboard Cite

show abstract

“…~2-fold) may be insufficient to alter gene expression. Furthermore, RBM5 protein appears to be considerably higher (~3–4 fold above sham) after SCI in vivo or H 2 O 2 injury to PC12 cells in vitro (Zhang et al, 2015). Thus viral dose-response studies are needed to test the effect of increasing RBM5 levels (by overexpression) on gene changes as measured by microarray or RNA-seq.…”

Section: Discussionmentioning

confidence: 99%

“…We reported that RBM5 protein levels increase after hippocampal/cortical injury in a mouse model of traumatic brain injury (TBI) (Jackson et al, 2015). RBM5 protein levels also increase after spinal cord trauma (Zhang et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

Whole-transcriptome microarray analysis reveals regulation of Rab4 by RBM5 in neurons

2017

View full text Add to dashboard Cite

RNA binding motif 5 (RBM5) is a nuclear protein that modulates gene transcription and mRNA splicing in cancer cells. The brain is among the highest RBM5 expressing organ in the body but its mRNA target(s) or functions in the CNS have not been elucidated. Here we knocked down (KO) RBM5 in primary rat cortical neurons and analyzed total RNA extracts by gene microarray vs. neurons transduced with lentivirus to deliver control (non-targeting) shRNA. The mRNA levels of Sec23A (involved in ER-Golgi transport) and the small GTPase Rab4a (involved in endocytosis/protein trafficking) were increased in RBM5 KO neurons relative to controls. At the protein level, only Rab4a was significantly increased in RBM5 KO extracts. Also, elevated Rab4a levels in KO neurons were associated with decreased membrane levels of oligomeric serotonin transporters (SERT). Finally, RBM5 KO was associated with increased uptake of membrane-derived monomeric SERT. Significance: Rab4a is involved in the regulation of endocytosis and protein trafficking in cells. In the CNS it regulates diverse neurobiological functions including (but not limited to) trafficking of transmembrane proteins involved in neurotransmission (e.g. SERT), maintaining dendritic spine size, promoting axonal growth, and modulates cognition. Our findings suggest that RBM5 regulates Rab4a in rat neurons.

show abstract

“…SCI negatively affects a patient's quality of life and causes significant economic burden to society. Significant efforts have been made to search for new drug candidates that will promote functional recovery after SCI (Li et al, ; Zhang et al, ). In our study, systemic administration of melatonin immediately after SCI in female rats reduced spinal cavity volume and improved functional recovery.…”

Section: Discussionmentioning

confidence: 99%

Melatonin improves functional recovery in female rats after acute spinal cord injury by modulating polarization of spinal microglial/macrophages

Zhang

Liu

Zhang

et al. 2019

J of Neuroscience Research

View full text Add to dashboard Cite

Spinal cord injury (SCI) is a devastating neurological disorder, but few drugs have proven to be effective for its treatment. Neuroinflammation exaggerates the secondary injury subsequent to trauma. Emerging evidence suggests that melatonin may help protect neural tissue against secondary injury after SCI, but the underlying mechanisms remain elusive. Microglial/macrophages polarization plays an important role in regulating immune responses. To examine whether melatonin exerts neuroprotective effects after acute SCI by regulating microglial/macrophages polarization in the spinal cord, we administered intraperitoneal injections of melatonin (50 mg/kg) in female rats immediately after SCI and then daily for seven consecutive days (n = 6). Compared with the vehicle‐treated group (n = 6), the melatonin‐treated group exhibited a greater Basso, Beattie, and Bresnahan locomotor rating score, smaller spinal cavity, and less cleaved caspase 3 immunofluorescence staining in the injured spinal segments. Real‐time PCR data revealed decreases in the expression levels of M1 microglia phenotypic markers and increases in M2 markers in the spinal cord of melatonin‐treated SCI rats, as compared to levels in the vehicle‐treated group. Melatonin increased the number of CD206+ and Arg1+ cells, decreased the number of CD16+ and iNOS+ cells and reduced the levels of pro‐inflammatory cytokines (TNF‐α, IL‐6, and IL‐1β) in the spinal cord tissue of female SCI rats. Current findings suggest that melatonin may inhibit pro‐inflammatory responses and promote M2 polarization of microglial/macrophages in the spinal cord in the early stage of SCI, facilitating functional recovery. Accordingly, melatonin may represent a promising therapeutic candidate for acute SCI.

show abstract

RBM5 and p53 expression after rat spinal cord injury: Implications for neuronal apoptosis

Cited by 43 publications

References 55 publications

Pifithrin‐μ modulates microglial activation and promotes histological recovery following spinal cord injury

Pifithrin‐μ modulates microglial activation and promotes histological recovery following spinal cord injury

Whole-transcriptome microarray analysis reveals regulation of Rab4 by RBM5 in neurons

Melatonin improves functional recovery in female rats after acute spinal cord injury by modulating polarization of spinal microglial/macrophages

Contact Info

Product

Resources

About