Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13

Jiang, Dongxiao; Sun, Xinhu; Wang, Shengwu; Man, Honghao

doi:10.1016/j.biopha.2019.108941

Cited by 44 publications

(24 citation statements)

References 33 publications

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“…Increased expression of miR-320a and miR-320b has been identified in eyes with proliferative diabetic retinopathy [ 63 ], but this is the first report of an association between miR-320d and diabetic retinopathy. MiR-874 has been found to alleviate diabetic retinopathy in a murine model by regulating the NF-κB signaling pathway [ 64 ], ameliorating renal injury in diabetic nephropathy [ 65 ], and providing neuroprotection in a stroke model [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

A Pilot Study on MicroRNA Profile in Tear Fluid to Predict Response to Anti-VEGF Treatments for Diabetic Macular Edema

Chan

Yang

Wong

et al. 2020

JCM

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(1) Background: Intravitreal anti-vascular endothelial growth factor (anti-VEGF) is an established treatment for center-involving diabetic macular edema (ci-DME). However, the clinical response is heterogeneous. This study investigated miRNAs as a biomarker to predict treatment response to anti-VEGF in DME. (2) Methods: Tear fluid, aqueous, and blood were collected from patients with treatment-naïve DME for miRNA expression profiling with quantitative polymerase chain reaction. Differentially expressed miRNAs between good and poor responders were identified from tear fluid. Bioinformatics analysis with the miEAA tool, miRTarBase Annotations, Gene Ontology categories, KEGG, and miRWalk pathways identified interactions between enriched miRNAs and biological pathways. (3) Results: Of 24 participants, 28 eyes received bevacizumab (15 eyes) or aflibercept (13 eyes). Tear fluid had the most detectable miRNA species (N = 315), followed by serum (N = 309), then aqueous humor (N = 134). MiRNAs that correlated with change in macular thickness were miR-214-3p, miR-320d, and hsa-miR-874-3p in good responders; and miR-98-5p, miR-196b-5p, and miR-454-3p in poor responders. VEGF-related pathways and the angiogenin-PRI complex were enriched in good responders, while transforming growth factor-β and insulin-like growth factor pathways were enriched in poor responders. (4) Conclusions: We reported a panel of novel miRNAs that provide insight into biological pathways in DME. Validation in larger independent cohorts is needed to determine the predictive performance of these miRNA candidate biomarkers.

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Section: Discussionmentioning

confidence: 99%

A Pilot Study on MicroRNA Profile in Tear Fluid to Predict Response to Anti-VEGF Treatments for Diabetic Macular Edema

Chan

Yang

Wong

et al. 2020

JCM

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“…Cerebral ischemia and hypoxia can cause ischemic stroke, which accounts for about 80% of strokes. 1,2 Ischemic stroke has a catastrophic impact on people's life and has an extremely high incidence and mortality rate worldwide. 3 Cognitive impairment is one of the most common complications of a stroke.…”

Section: Introductionmentioning

confidence: 99%

<p>Protective Effects of Chlorogenic Acid on Cerebral Ischemia/Reperfusion Injury Rats by Regulating Oxidative Stress-Related Nrf2 Pathway</p>

Liu¹,

Wang²,

Zhang³

et al. 2020

DDDT

142

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Introduction: Cerebral ischemia-reperfusion (CI/R) injury is caused by blood flow recovery after ischemic stroke. Chlorogenic acid (CGA, 5-O-caffeoylquinic acid) is a major polyphenol component of Coffea canephora, Coffea arabica L. and Mate (Ilex paraguariensis A. StHil.). Previous studies have shown that CGA has a significant neuroprotective effect and can improve global CI/R injury. However, the underlying molecular mechanism of CGA in CI/R injury has not been fully revealed. Materials: In this study, CI/R rat model was constructed. The rats were randomly divided into nine groups with ten in each group: Control, CGA (500 mg•kg-1), CI/R, CI/R + CGA (20 mg•kg-1), CI/R + CGA (100 mg•kg-1), CI/R + CGA (500 mg•kg-1), ML385 (30 mg•kg-1), CI/R + ML385 (30 mg•kg-1), CI/R + CGA + ML385. Cerebral infarction volume was detected by TTC staining. Brain pathological damage was detected by H&E staining. Apoptosis of cortical cells was detected by TUNEL staining. The expression of related proteins was detected by RT-qPCR and Western blotting. Results: Step-down test and Y maze test showed that CGA dose-dependently mitigated CI/ R-induced brain damage and enhanced learning and spatial memory. Besides, CGA promoted the expression of BDNF and NGF in a dose-dependent manner and alleviated CI/R-induced nerve injury. Moreover, CGA increased the activity of SOD and the level of GSH, as well as decreased production of ROS and LDH and the accumulation of MDA. Notably, CGA attenuated oxidative stress-induced brain injury and apoptosis and inhibited the expression of apoptosis-related proteins (cleaved caspase 3 and caspase 9). Additionally, CGA reversed CI/R induced inactivation of Nrf2 pathway and promoted Nrf2, NQO-1 and HO-1 expression. Nrf2 pathway inhibitor ML385 destroyed this promotion. Discussion: All the data indicated that CGA had a neuroprotective effect on the CI/R rats by regulating oxidative stress-related Nrf2 pathway.

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“…OGD/R model. PC12 cells that have been exposed to OGD/R have been widely used to simulate cerebral I/R injury in vitro (16,17). Cells were maintained in a glucose-deprivation buffer (Gibco; Thermo Fisher Scientific, Inc.) and incubated in an anaerobic chamber in an atmosphere of 95% N 2 /5% CO 2 for 2, 4, 6, 8 or 10 h, followed by fresh DMEM (containing 10% fetal bovine serum) under normoxic conditions with 95% air/5% CO 2 for 24 h.…”

Section: Methodsmentioning

confidence: 99%

FABP4 alleviates endoplasmic reticulum stress‑mediated ischemia‑reperfusion injury in PC12 cells via regulation of PPARγ

Yang

Dong

2021

Exp Ther Med

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Ischemic stroke is a life-threatening complication with a high rate of morbidity. Circulating fatty acid binding protein 4 (FABP4) has been reported to be associated with the outcome of acute ischemic stroke. The present study aimed to illustrate the function of FABP4 in ischemic stroke. PC12 cells exposed to oxygen glucose deprivation/reoxygenation (OGD/R) were used to mimic ischemia-reperfusion (I/R) injury in ischemic stroke. Cell viability was estimated using a Cell Counting Kit-8 assay. The expression of FABP4 in PC12 cells under OGD/R was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). PC12 cells were transfected with FABP4 small interfering RNA (siRNA), inflammatory cytokines and reactive oxygen species (ROS) were determined via RT-qPCR and ROS assay kit. Western blotting was performed to detect endoplasmic reticulum stress (ERS)-related proteins and peroxisome proliferator-activated receptor γ (PPARγ). Flow cytometry was used to evaluate the cell apoptotic rate. The expression of FABP4 increased gradually with the prolongation of reoxygenation within 8 h. FABP4-knockdown inhibited the transcription of inflammatory cytokines, the production of ROS and decreased cell apoptosis. Furthermore, decreased ERS-related proteins and increased PPARγ were estimated in PC12 cells transfected with FABP4 siRNA. PPARγ inhibitor GW9662 weakened the anti-apoptotic effect of FABP4-knockdown. Taken together, these results indicated that FABP4-knockdown suppressed cell apoptosis via relieving ERS; this effect was reversed by treatment of GW9662.

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Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13

Cited by 44 publications

References 33 publications

A Pilot Study on MicroRNA Profile in Tear Fluid to Predict Response to Anti-VEGF Treatments for Diabetic Macular Edema

A Pilot Study on MicroRNA Profile in Tear Fluid to Predict Response to Anti-VEGF Treatments for Diabetic Macular Edema

<p>Protective Effects of Chlorogenic Acid on Cerebral Ischemia/Reperfusion Injury Rats by Regulating Oxidative Stress-Related Nrf2 Pathway</p>

FABP4 alleviates endoplasmic reticulum stress‑mediated ischemia‑reperfusion injury in PC12 cells via regulation of PPARγ

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