Differential response of miRNA-21 and its targets after traumatic brain injury in aging mice

Sandhir, Rajat; Gregory, Eugene; Berman, Nancy E.J.

doi:10.1016/j.neuint.2014.09.009

Cited by 41 publications

(28 citation statements)

References 41 publications

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“…Several studies have reported miR-221/222 could target TIMP3 in cancers [37-39]. Besides, miR-21, miR-181, miR-373 and miR-206 could regulate TIMP3 [41-44]. It is well known that each microRNA usually has multiple target genes, and the same gene can be targeted by multiple microRNAs.…”

Section: Discussionmentioning

confidence: 99%

MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Wen

Han

et al. 2018

Cell Physiol Biochem

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Background/Aims: MiRNAs are involved in phenotype modulation of neural cells after peripheral nerve injury. However, the roles of miRNAs on the survival of dorsal root ganglion (DRG) neurons have not yet been fully understood. Methods: In this study, the expression of miR-142-3p was measured in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection by microarray profiling and quantitative PCR. The functional assays including the cell viability, colony formation, cell cycle and apoptosis assays were performed in miR-142-3p mimic or inhibitor transfected cell lines. Results: MiR-142-3p was identified to be siginificantly upregulated in rat DRGs (L4-L6) during the initial 24 hours post sciatic nerve transection. MiR-142-3p mimic enhanced cell viability by promoting cell cycle and inhibiting cell apoptosis in cultured DRG neurons. In addition, cyclin-dependent kinase inhibitor 1B (CDKN1B, also known as p27/Kip1) and tissue inhibitor of metalloproteinase 3 (TIMP3) were identified as targets of miR-142-3p. Furthermore, knockdown of CDKN1B or TIMP3 by specific siRNAs could reverse the effect of miR-142-3p. Conclusions: In the conclusion, the results showed that miR-142-3p could promote neuronal cell cycle and inhibit apoptosis at least partially through suppressing CDKN1B and TIMP3 after peripheral nerve injury.

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Section: Discussionmentioning

confidence: 99%

MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Wen

Han

et al. 2018

Cell Physiol Biochem

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“…Instead of brain remodeling and functional recovery by cell replacement effects, evidence suggests that the major effects of neurorestoration were due to the paracrine effects of secretion-based factors such as MSCs-derived exosomes that may reduce neuroinflammation, promote neurogenesis and angiogenesis, rescue pattern separation and spatial learning impairments, and improve functional recovery after TBI in animal models [107,176,178,191,204,205,215,216,[235][236][237]. In addition, as exosomes contain various miRNAs, which play a key role in modifying the phenotype and/or the physiology and modulating the cellular processes of the recipient cell, and miRNAs such as miR-21 could be potential therapeutic targets for interventions after TBI, the combination of miRNAs and MSC-derived exosomes might be a novel approach for the treatment of TBI [238]. That is, MSCs-derived exosomes that carry and transfer their cargo such as miRNAs to parenchymal cells may mediate brain plasticity and improve functional recovery after TBI [204].…”

Section: Extracellular Vesicles and Exosomesmentioning

confidence: 99%

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Understanding the pathophysiology of TBI is crucial for the development of more effective therapeutic strategies. At the moment of the traumatic impact, transfer of kinetic forces causes neurologic damage; this primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, called secondary neural injury. These areas of ongoing secondary injury, or areas of "traumatic penumbra," represent crucial targets for therapeutic interventions. This chapter is focused on the interplay between progression of parenchymal injury and the neuroprotective and neurorestorative processes that are emerging and developing subsequently to traumatic impact. Thus, we emphasized the role of traumatic penumbra in TBI pathogenesis and suggested a crucial contribution of the neurovascular units (NVUs) and paracrine effects of exosomes and miRNAs in promoting neurological recovery.

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“…More importantly, miRNAs are potential therapeutic targets in TBI. For example, miR-21, a strong prosurvival miRNA, was up-regulated in adult rat brains after TBI but down-regulated in aged rat brains after TBI [172]. A recent study manipulated the expression level of miR-21 in brain using intracerebroventricular infusion of miR-21 agomir or antagomir to evaluate the potential effect of miR-21 on neurological function in the fluid percussion injury rat model of TBI [173].…”

Section: Investigational Drugs Under Preclinical Studiesmentioning

confidence: 99%

Investigational agents for treatment of traumatic brain injury

Xiong

Zhang

Mahmood

et al. 2015

Expert Opinion on Investigational Drugs

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Introduction Traumatic brain injury (TBI) is a major cause of death and disability worldwide. To date, there are no pharmacologic agents proven to improve outcomes from TBI because all the Phase III clinical trials in TBI have failed. Thus, there is a compelling need to develop treatments for TBI. Areas covered The aim of this review is to provide an overview of select cell-based and pharmacological therapies under early development for the treatment of TBI, which seek to enhance cognitive and neurological functional recovery through neuroprotective and neurorestorative strategies. Expert’s opinion TBI elicits both complex degenerative and regenerative tissue responses in the brain. TBI can lead to cognitive, behavioral, and motor deficits. Although numerous promising neuroprotective treatment options have emerged from preclinical studies that mainly target the lesion, translation of preclinical effective neuroprotective drugs to clinical trials has proven challenging. Accumulating evidence indicates that the mammalian brain has a significant, albeit limited, capacity for both structural and functional plasticity as well as regeneration essential for spontaneous functional recovery after injury. A new therapeutic approach is to stimulate neurovascular remodeling by enhancing angiogenesis, neurogenesis, oligodendrogenesis, and axonal sprouting, which in concert, may improve neurological functional recovery after TBI.

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Differential response of miRNA-21 and its targets after traumatic brain injury in aging mice

Cited by 41 publications

References 41 publications

MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Investigational agents for treatment of traumatic brain injury

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