RETRACTED: MicroRNA-376b-5p targets SOX7 to alleviate ischemic brain injury in a mouse model through activating Wnt/β-catenin signaling pathway

Zhao, Bin; Wang, Peng; Yu, Jing; Zhang, Yizhi

doi:10.1016/j.lfs.2021.119072

Cited by 4 publications

(4 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other miRNAs (Fig. 1 ) that are involved and exhibit regulatory functions on BBB permeability or integrity after ischemic stroke including miR-29b [ 53 ], miR-34a [ 67 – 69 ], miR-150 [ 70 ], miR-122 [ 71 ], miR-210 [ 72 ], miR-21 [ 73 ], miR-539 [ 74 ], miR-155 [ 75 , 76 ], miR-149-5p [ 77 ], miR-1 [ 78 ], miR-132 [ 79 ], let-7g*[ 80 , 81 ], miR-98 [ 80 ], miR-126-3p/5p [ 82 ], miR-98 [ 83 ], miR-668 [ 84 ], miR-182 [ 85 ], miR-503 [ 54 ], let-7f [ 86 ], miR-30a [ 87 ], miR-376b-5p [ 88 ], miR-149-5p [ 89 ], miR-92b [ 90 ], and miR-141-3p [ 91 ].…”

Section: Non-coding Rnas Regulate Bbb/bscb Functions In Cns Disordersmentioning

confidence: 99%

Non-coding RNAs in the regulation of blood–brain barrier functions in central nervous system disorders

Sun

Hamblin

Yin

2022

Fluids Barriers CNS

View full text Add to dashboard Cite

The blood–brain barrier (BBB) is an essential component of the neurovascular unit that controls the exchanges of various biological substances between the blood and the brain. BBB damage is a common feature of different central nervous systems (CNS) disorders and plays a vital role in the pathogenesis of the diseases. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNA (lncRNAs), and circular RNAs (circRNAs), are important regulatory RNA molecules that are involved in almost all cellular processes in normal development and various diseases, including CNS diseases. Cumulative evidences have demonstrated ncRNA regulation of BBB functions in different CNS diseases. In this review, we have summarized the miRNAs, lncRNAs, and circRNAs that can be served as diagnostic and prognostic biomarkers for BBB injuries, and demonstrated the involvement and underlying mechanisms of ncRNAs in modulating BBB structure and function in various CNS diseases, including ischemic stroke, hemorrhagic stroke, traumatic brain injury (TBI), spinal cord injury (SCI), multiple sclerosis (MS), Alzheimer's disease (AD), vascular cognitive impairment and dementia (VCID), brain tumors, brain infections, diabetes, sepsis-associated encephalopathy (SAE), and others. We have also discussed the pharmaceutical drugs that can regulate BBB functions via ncRNAs-related signaling cascades in CNS disorders, along with the challenges, perspective, and therapeutic potential of ncRNA regulation of BBB functions in CNS diseases.

show abstract

Section: Non-coding Rnas Regulate Bbb/bscb Functions In Cns Disordersmentioning

confidence: 99%

Non-coding RNAs in the regulation of blood–brain barrier functions in central nervous system disorders

Sun

Hamblin

Yin

2022

Fluids Barriers CNS

View full text Add to dashboard Cite

show abstract

“…This inhibition leads to detrimental processes including apoptosis, ferroptosis, inflammation, inhibition of nerve regeneration and angiogenesis, and disruption of BBB. 174 – 176 , 178 , 198 , 214 , 215 , 233 , 244 , 247 , 253 , 348 , 400 These pathological events contribute to organ damage promotion. In summary, the activation of the canonical Wnt/β-catenin pathway during ischemia serves as a protective mechanism, while its inhibition during reperfusion contributes to organ damage.…”

Section: Discussion and Perspectivesmentioning

confidence: 99%

“…Additionally, this treatment promoted the polarization of reactive microglia toward the M2 phenotype; increased the number of A2 phenotype astrocytes with neuroprotective effects; reduced the number of neurotoxic A1 phenotype astrocytes; initiated the anti-inflammatory and neuroprotective effects of microglia and astrocytes; reduced the neuroinflammation following cerebral ischemia, which may be attributed to the Wnt3a-mediated activation of the Wnt/β-catenin signaling pathway. 215 Finally, treatment with curcumin has shown efficacy in reversing the inflammatory response caused by Wnt/PCP signaling activation in neuronal cells subjected to H/R. 216 …”

Section: Wnt Pathways and Organ I/r Injurymentioning

confidence: 99%

Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets

Zhang,

Liu,

Meng

et al. 2024

Sig Transduct Target Ther

View full text Add to dashboard Cite

Ischemia-reperfusion (I/R) injury paradoxically occurs during reperfusion following ischemia, exacerbating the initial tissue damage. The limited understanding of the intricate mechanisms underlying I/R injury hinders the development of effective therapeutic interventions. The Wnt signaling pathway exhibits extensive crosstalk with various other pathways, forming a network system of signaling pathways involved in I/R injury. This review article elucidates the underlying mechanisms involved in Wnt signaling, as well as the complex interplay between Wnt and other pathways, including Notch, phosphatidylinositol 3-kinase/protein kinase B, transforming growth factor-β, nuclear factor kappa, bone morphogenetic protein, N-methyl-D-aspartic acid receptor-Ca2+-Activin A, Hippo-Yes-associated protein, toll-like receptor 4/toll-interleukine-1 receptor domain-containing adapter-inducing interferon-β, and hepatocyte growth factor/mesenchymal-epithelial transition factor. In particular, we delve into their respective contributions to key pathological processes, including apoptosis, the inflammatory response, oxidative stress, extracellular matrix remodeling, angiogenesis, cell hypertrophy, fibrosis, ferroptosis, neurogenesis, and blood-brain barrier damage during I/R injury. Our comprehensive analysis of the mechanisms involved in Wnt signaling during I/R reveals that activation of the canonical Wnt pathway promotes organ recovery, while activation of the non-canonical Wnt pathways exacerbates injury. Moreover, we explore novel therapeutic approaches based on these mechanistic findings, incorporating evidence from animal experiments, current standards, and clinical trials. The objective of this review is to provide deeper insights into the roles of Wnt and its crosstalk signaling pathways in I/R-mediated processes and organ dysfunction, to facilitate the development of innovative therapeutic agents for I/R injury.

show abstract

“…Previous studies have shown that SIRT1, as an activator of the Wnt/ β -catenin signaling pathway, can increase the transcriptional activity of Wnt1 and β -catenin by affecting the stability of c-myc, promote the nuclear transfer of β -catenin, and activates the Wnt/ β -catenin signaling pathway [ 32 , 34 ]. Moreover, we also observed that the Wnt/ β -catenin signaling pathway participates in the development process of neurological diseases [ 35 , 36 ]. In this study, we found that glutamate treatment downregulated the expression of SIRT1, Wnt1, β -catenin, and cyclin D1.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of NGR1 against Glutamate-Induced Cytotoxicity in HT22 Hippocampal Neuronal Cells by Upregulating the SIRT1/Wnt/β-Catenin Pathway

Wang¹,

Gao

Yang³

et al. 2021

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Notoginsenoside R1 (NGR1) is an active compound isolated from Panax notoginseng. Despite the NGR1 having been used as a traditional medicine, little is known about the neuroprotective effects. In this study, we investigate the protective effects of NGR1 against glutamate-induced cytotoxicity in HT22 cells and its possible molecular mechanism. We assessed the toxicity of NGR1 and the protective activity by MTT assay. The levels of oxidative stress indices superoxide dismutase (SOD), glutathione (GSH), and mitochondrial membrane potential (MMP) were measured by the kits. The levels of reactive oxygen species (ROS) and Ca2+ concentration were measured by flow cytometry. Furthermore, we determined the expression of mitochondrial dysfunction related protein PINK1, Parkin, silent mating type information regulation 2 homolog-1 (sirtuin 1; SIRT1), and Wnt/β-catenin by Western blotting. Here, we discovered that glutamate treatment led to cell viability loss, apoptosis facilitation, Ca2+ upregulation, MMP fluorescence intensity downregulation, and ROS generation of HT22 cells. In parallel, expression of Parkin was declined by glutamate. While, NGR1 treatment alleviated all the above phenomena. We further clarified that NGR1 alleviated glutamate-induced oxidative stress, apoptosis, and mitochondrial dysfunction by upregulating SIRT1 to activate Wnt/β-catenin pathways. These findings demonstrate that NGR1 alleviated glutamate-induced cell damage, and NGR1 may play a protective role in neurological complications.

show abstract

RETRACTED: MicroRNA-376b-5p targets SOX7 to alleviate ischemic brain injury in a mouse model through activating Wnt/β-catenin signaling pathway

Cited by 4 publications

References 28 publications

Non-coding RNAs in the regulation of blood–brain barrier functions in central nervous system disorders

Non-coding RNAs in the regulation of blood–brain barrier functions in central nervous system disorders

Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets

Protective Effect of NGR1 against Glutamate-Induced Cytotoxicity in HT22 Hippocampal Neuronal Cells by Upregulating the SIRT1/Wnt/β-Catenin Pathway

Contact Info

Product

Resources

About