MicroRNA-532-5p protects against cerebral ischemia-reperfusion injury by directly targeting CXCL1

Shi, Yuanyuan; Yi, ZhongQuan; Zhao, PanWen; Xu, Yun; Pan, PingLei

doi:10.18632/aging.202846

Cited by 24 publications

(14 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is not only in cancers that the regulation of CXCL1 expression by miRNAs occurs. During cerebral ischemia–reperfusion injury, there is a downregulation of miR-429 in brain microvascular endothelial cells [ 128 ] and miR-532-5p in brain tissues [ 129 ]. At least for miR-532-5p, this was shown to be related to the promoter of this miRNA: hypermethylation.…”

Section: Cxcl1 Mrna Stability As a Methods To Regulate Cxcl1 Expressionmentioning

confidence: 99%

CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space

Korbecki

Barczak

Gutowska

et al. 2022

IJMS

View full text Add to dashboard Cite

CXCL1 is one of the most important chemokines, part of a group of chemotactic cytokines involved in the development of many inflammatory diseases. It activates CXCR2 and, at high levels, CXCR1. The expression of CXCL1 is elevated in inflammatory reactions and also has important functions in physiology, including the induction of angiogenesis and recruitment of neutrophils. Due to a lack of reviews that precisely describe the regulation of CXCL1 expression and function, in this paper, we present the mechanisms of CXCL1 expression regulation with a special focus on cancer. We concentrate on the regulation of CXCL1 expression through the regulation of CXCL1 transcription and mRNA stability, including the involvement of NF-κB, p53, the effect of miRNAs and cytokines such as IFN-γ, IL-1β, IL-17, TGF-β and TNF-α. We also describe the mechanisms regulating CXCL1 activity in the extracellular space, including proteolytic processing, CXCL1 dimerization and the influence of the ACKR1/DARC receptor on CXCL1 localization. Finally, we explain the role of CXCL1 in cancer and possible therapeutic approaches directed against this chemokine.

show abstract

Section: Cxcl1 Mrna Stability As a Methods To Regulate Cxcl1 Expressionmentioning

confidence: 99%

CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space

Korbecki

Barczak

Gutowska

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…In order to simulate cerebral I/R injury in vitro , an OGD/R model was established as described previously ( 21 – 24 ). Briefly, SH-SY5Y cells were seeded in plates pre-coated with poly-L-lysine (cat.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‑126 protects SH‑SY5Y cells from ischemia/reperfusion injury‑induced apoptosis by inhibiting RAB3IP

et al. 2021

View full text Add to dashboard Cite

MicroRNA (miR)-126 is known to inhibit inflammatory responses in various inflammatory-related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR-126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH-SY5Y was cultured in an oxygen-glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR-126 expression and cell viability. SH-SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH-SY5Y cells were transfected with a miR-126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH-SY5Y cells were co-transfected with RAB3IP overexpression or NC plasmid together with mimic-NC or mimic-miR, and then maintained in an OGD/R environment to evaluate miR-126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR-126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic-miR, cell viability increased compared with the mimic-NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic-miR group compared with the mimic-NC group. RAB3IP expression was reduced following mimic-miR transfection. In rescue experiments, miR-126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR-126. In addition, RAB3IP overexpression attenuated the protective effect of miR-126 on OGD/R-induced apoptosis. These findings suggest that miR-126 protects against cerebral I/R injury by targeting RAB3IP.

show abstract

“…Indeed, miR-326 inhibits neuronal apoptosis and attenuates mitochondrial damage ( He et al, 2020 ; Huang et al, 2021 ). miR-532-5p showed a neuroprotective effect reducing apoptosis, ROS production, and inflammation in cerebral ischemia-reperfusion injury ( Shi et al, 2021b ), and ischemic stroke ( Mu et al, 2020 ), while mir-92a-3p, belonging to the miR-17–92 family, is a synaptic-related miRNA ( Siedlecki-Wullich et al, 2021 ), involved in neural cells proliferation, differentiation, and maturation ( Zhang et al, 2013 ; Xia et al, 2020 ).…”

Section: Clinical Cellular and Molecular Mechanisms Of Frailty: The Potential Role Of Mirnasmentioning

confidence: 99%

“…Mature miR-532-5p derived from pre-miR-532 which is localized on chromosome X in the human genome. miR-532-5p showed a neuroprotective effect reducing apoptosis, ROS production, and inflammation in cerebral ischemia-reperfusion injury ( Shi et al, 2021b ), and ischemic stroke ( Mu et al, 2020 ). Moreover it has been implicated in inflammation ( Yan et al, 2020 ), osteoporosis ( Guo et al, 2020 ), as well as in tumor progression ( Kim et al, 2021 ; Yu et al, 2021 ).…”

Section: Cognitive Frailty: the Potential Role Of Mirnasmentioning

confidence: 99%

The Potential Role of miRNAs in Cognitive Frailty

Carini

Musazzi

Bolzetta³

et al. 2021

Front. Aging Neurosci.

View full text Add to dashboard Cite

Frailty is an aging related condition, which has been defined as a state of enhanced vulnerability to stressors, leading to a limited capacity to meet homeostatic demands. Cognitive impairment is also frequent in older people, often accompanying frailty. Age is the main independent risk factor for both frailty and cognitive impairment, and compelling evidence suggests that similar age-associated mechanisms could underlie both clinical conditions. Accordingly, it has been suggested that frailty and cognitive impairment share common pathways, and some authors proposed “cognitive frailty” as a single complex phenotype. Nevertheless, so far, no clear common underlying pathways have been discovered for both conditions. microRNAs (miRNAs) have emerged as key fine-tuning regulators in most physiological processes, as well as pathological conditions. Importantly, miRNAs have been proposed as both peripheral biomarkers and potential molecular factors involved in physiological and pathological aging. In this review, we discuss the evidence linking changes of selected miRNAs expression with frailty and cognitive impairment. Overall, miR-92a-5p and miR-532-5p, as well as other miRNAs implicated in pathological aging, should be investigated as potential biomarkers (and putative molecular effectors) of cognitive frailty.

show abstract

MicroRNA-532-5p protects against cerebral ischemia-reperfusion injury by directly targeting CXCL1

Cited by 24 publications

References 36 publications

CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space

CXCL1: Gene, Promoter, Regulation of Expression, mRNA Stability, Regulation of Activity in the Intercellular Space

MicroRNA‑126 protects SH‑SY5Y cells from ischemia/reperfusion injury‑induced apoptosis by inhibiting RAB3IP

The Potential Role of miRNAs in Cognitive Frailty

Contact Info

Product

Resources

About