Plasmid pLXSN-Mediated Adrenomedullin Gene Therapy for Cerebral Vasospasm Following Subarachnoid Hemorrhage in Rats

Li, Xin; Xia, Xiaoshuang

doi:10.12659/msm.901914

Cited by 2 publications

(2 citation statements)

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“…In cerebral vasospasm, there are increases in endothelin and superoxides, and decreases in endothelial nitric oxide synthase levels. Gene therapy to increase endothelial nitric oxide synthase and heme oxygenase-1 and decrease superoxide dismutase for the prevention of vasospasm has shown positive results in preclinical studies 23. However, the same results will be difficult to replicate in humans because modes of transfer, inflammation associated with viruses, and viral cytotoxicity are major concerns for the clinical translation of gene therapy.…”

Section: Resultsmentioning

confidence: 99%

“…Gene therapy to increase endothelial nitric oxide synthase and heme oxygenase-1 and decrease superoxide dismutase for the prevention of vasospasm has shown positive results in preclinical studies. 23 However, the same results will be difficult to replicate in humans because modes of transfer, inflammation associated with viruses, and viral cytotoxicity are major concerns for the clinical translation of gene therapy. However, the potential for gene therapy is enormous, particularly if rapid onset and robust delivery methods with good risk-benefit profiles, such as nonviral delivery of RNA/DNA to the central nervous system, are used.…”

Section: Gene Therapymentioning

confidence: 99%

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Precision Medicine in Acute Brain Injury: A Narrative Review

Mahajan

Kapoor²,

Prabhakar³

2020

Journal of Neurosurgical Anesthesiology

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Over the past few years, the concept of personalized medicine has percolated into the management of different neurological conditions. Improving outcomes after acute brain injury (ABI) continues to be a major challenge. Unrecognized individual multiomic variations in addition to multiple interacting processes may explain why we fail to observe comprehensive improvements in ABI outcomes even when applied treatments appear to be beneficial logically. The provision of clinical care based on a multiomic approach may revolutionize the management of traumatic brain injury, delayed cerebral ischemia after subarachnoid hemorrhage, acute ischemic stroke, and several other neurological diseases. The challenge is to incorporate all the information obtained from genomic studies, other omic data, and individual variability into a practical tool that can be used to assist clinical decision-making. The effective execution of such strategies, which is still far away, requires the development of protocols on the basis of these complex interactions and strict adherence to management protocols. In this review, we will discuss various omics and physiological targets to guide individualized patient management after ABI.

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Section: Resultsmentioning

confidence: 99%

Section: Gene Therapymentioning

confidence: 99%

Precision Medicine in Acute Brain Injury: A Narrative Review

Mahajan

Kapoor²,

Prabhakar³

2020

Journal of Neurosurgical Anesthesiology

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Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)

Song

Chen

et al. 2018

Med Sci Monit

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BackgroundA mouse model of subarachnoid hemorrhage (SAH) investigated the effects of melatonin treatment on the generation of reactive oxygen species (ROS) and the activation of the SIRT3 gene in early brain injury (EBI).Material/MethodsMale C57BL/6J mice were assigned to three groups: the SAH group; the sham group; and the SAH + melatonin-treated group (intraperitoneal dose, 150 mg/kg). TUNEL was used to study apoptosis of neuronal cells, Western-blot and immunohistochemistry detected expression of Sirt3, Bcl-2, superoxide dismutase 2 (SOD2), Bax, and cleaved caspase-3. Real-time polymerase chain reaction (PCR) and a luciferase reporter assay evaluated the effects of melatonin on SIRT3 gene expression. Malondialdehyde (MDA) and the reactive oxygen species (ROS) scavenger, reduced glutathione (GSH), and its ratio with oxidized glutathione (GSSG) was measured.ResultsThe increase in neurological score and increase in cerebral edema following SAH were reduced in the SAH + melatonin-treated group. Neuronal apoptosis following SAH was reduced in the SAH + melatonin-treated group. Increased levels of SOD2, Bax, and cleaved caspase-3 following SAH were reduced in the SAH + melatonin-treated group; reduced levels of Sirt3 and Bcl-2 following SAH were increased in the SAH + melatonin-treated group. The GSH: GSSG ratio was increased, and the MDA level was decreased when melatonin treatment was used following SAH. Melatonin upregulated SIRT3 expression by increasing the transcription efficiency of the SIRT3 promoter in human glioma cell lines U87 and U251.ConclusionsMelatonin provided protection from the effects of EBI following SAH by regulating the expression of murine SIRT3.

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Plasmid pLXSN-Mediated Adrenomedullin Gene Therapy for Cerebral Vasospasm Following Subarachnoid Hemorrhage in Rats

Cited by 2 publications

References 29 publications

Precision Medicine in Acute Brain Injury: A Narrative Review

Precision Medicine in Acute Brain Injury: A Narrative Review

Melatonin Treatment Regulates SIRT3 Expression in Early Brain Injury (EBI) Due to Reactive Oxygen Species (ROS) in a Mouse Model of Subarachnoid Hemorrhage (SAH)

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