Neuroprotective effects of microRNA-210 against oxygen-glucose deprivation through inhibition of apoptosis in PC12 cells

Qiu, Jie; Zhou, Xiaoyu; Zhou, Xiaoguang; Cheng, Rui; Liu, Haiying; Li, Yong

doi:10.3892/mmr.2013.1431

Cited by 39 publications

(33 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study has shown that miR-210 expression is upregulated in PC12 cells following a 4-h exposure to OGD (17). Consistently, the current study also demonstrated that OGD upregulates the expression of miR-210 in both miR-210 knockdown and control cells.…”

Section: Discussionsupporting

confidence: 78%

“…However, following IH, this apoptotic component becomes detrimental, leading to excessive neuronal loss. Previous studies have revealed that miR-210 treatment within the first 4 h post-OGD prevents cell apoptosis (17). The present study showed that anti-miR210 transfection induced apoptosis in both normoxic and hypoxic conditions, which demonstrates that miR-210 modulates the cellular apoptotic response to OGD.…”

Section: Discussionsupporting

confidence: 56%

“…Furthermore, an OGD model was used to investigate the link between miR-210 and IH injury in PC12 cells through the overexpression of miR-210 (17). To further elucidate the effect of miR-210 on apoptosis in PC12 cells following exposure to OGD, the present study used anti-miRNA transfection to downregulate the expression of miR-210.…”

Section: Discussionmentioning

confidence: 99%

“…The chamber was sealed and stored in an incubator for 4 h at 37˚C. Control cells were washed with glucose-containing DMEM and incubated in a normoxic incubator for 4 h, as previously described (17).…”

Section: Oxygen Glucose Deprivation (Ogd)mentioning

confidence: 99%

“…However, following IH, this apoptotic component becomes detrimental, leading to excessive neuronal loss. Therefore, in a previous study (17), the effect of miR-210 on the IH-induced apoptosis of neurons was investigated in an ex vivo model of IH (18)(19)(20), through the use of PC12 rat pheochromocytoma cells combined with oxygen glucose deprivation (OGD). The results of the study demonstrated that miR-210 overexpression suppressed cell apoptosis by inhibiting caspase activity and regulating the balance between the expression levels of Bcl-2 and Bax.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells

Qiu

Zhou

et al. 2014

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

Abstract. It was previously demonstrated that microRNA-210 (miR-210) exhibited neuroprotective effects in a murine model of hypoxic-ischemic encephalopathy via inhibition of apoptosis. The aim of the present study was to further elucidate the effect of miR-210 on apoptosis in PC12 cells following transfection with miR-210 inhibitors and exposure to oxygen glucose depri vation (OGD). The expression levels of miR-210 were identified using reverse transcription-quantitative polymerase chain reaction analysis. Apoptosis was investigated using Annexin V-fluorescein isothiocyanate assays. Apoptosis-related protein expression levels were studied with western blot analysis. The results showed that the expression levels of miR-210 were upregulated in PC12 cells following a 4-h exposure to OGD, relative to those in normoxic control cells. miR-210 knockdown increased cell apoptosis by inducing caspase activity and regulating the balance between Bcl-2 and Bax levels. The present study demonstrated that miR-210 knockdown induced cell apoptosis using an ex vivo model of ischemic hypoxia (IH). Knockdown of miR-210 represents a potential novel therapeutic approach to combat neonatal IH.

show abstract

Section: Discussionsupporting

confidence: 78%

Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Oxygen Glucose Deprivation (Ogd)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells

Qiu

Zhou

et al. 2014

Molecular Medicine Reports

Self Cite

View full text Add to dashboard Cite

show abstract

Validation of Altered Umbilical Cord Blood MicroRNA Expression in Neonatal Hypoxic-Ischemic Encephalopathy

et al. 2019

View full text Add to dashboard Cite

IMPORTANCE Neonatal hypoxic-ischemic encephalopathy (HIE) remains a significant cause of neurologic disability. Identifying infants suitable for therapeutic hypothermia (TH) within a narrow therapeutic time is difficult. No single robust biochemical marker is available to clinicians. OBJECTIVE To assess the ability of a panel of candidate microRNA (miRNA) to evaluate the development and severity of encephalopathy following perinatal asphyxia (PA). DESIGN, SETTING, AND PARTICIPANTS This validation study included 2 cohorts. For the discovery cohort, full-term infants with PA were enrolled at birth to the Biomarkers in Hypoxic-Ischemic Encephalopathy (BiHiVE1) study (2009-2011) in Cork, Ireland. Encephalopathy grade was defined using early electroencephalogram and Sarnat score (n = 68). The BiHiVE1 cohort also enrolled healthy control infants (n = 22). For the validation cohort, the BiHiVE2 multicenter study (2013-2015), based in Cork, Ireland (7500 live births per annum), and Karolinska Huddinge, Sweden (4400 live births per annum), recruited infants with PA along with healthy control infants to validate findings from BiHiVE1 using identical recruitment criteria (n = 80). The experimental design was formulated prior to recruitment, and analysis was conducted from June 2016 to March 2017. MAIN OUTCOMES AND MEASURES Alterations in umbilical cord whole-blood miRNA expression. RESULTS From 170 neonates, 160 were included in the final analysis. The BiHiVE1 cohort included 87 infants (21 control infants, 39 infants with PA, and 27 infants with HIE), and BiHiVE2 included 73 infants (control [n = 22], PA [n = 26], and HIE [n = 25]). The BiHiVE1 and BiHiVE2 had a median age of 40 weeks (interquartile range [IQR], 39-41 weeks) and 40 weeks (IQR, 39-41 weeks), respectively, and included 56 boys and 31 girls and 45 boys and 28 girls, respectively. In BiHiVE1, 12 candidate miRNAs were identified, and 7 of these miRNAs were chosen for validation in BiHiVE2. The BiHiVE2 cohort showed consistent alteration of 3 miRNAs; miR-374a-5p was decreased in infants diagnosed as having HIE compared with healthy control infants (median relative quantification, 0.38; IQR, 0.17-0.77 vs 0.95; IQR, 0.68-1.19; P = .009), miR-376c-3p was decreased in infants with PA compared with healthy control infants (median, 0.42; IQR, 0.21-0.61 vs 0.90; IQR, 0.70-1.30; P = .004), and mir-181b-5p was decreased in infants eligible for TH (median, 0.27; IQR, 0.14-1.41) vs 1.18; IQR, 0.70-2.05; P = .02). CONCLUSIONS AND RELEVANCE Altered miRNA expression was detected in umbilical cord blood of neonates with PA and HIE. These miRNA could assist diagnostic markers for early detection of HIE and PA at birth.

show abstract

Neuroprotective effect of licochalcone A against oxygen‐glucose deprivation/reperfusion in rat primary cortical neurons by attenuating oxidative stress injury and inflammatory response via the SIRT1/Nrf2 pathway

Liu

Xiaodi

et al. 2017

J of Cellular Biochemistry

View full text Add to dashboard Cite

Perinatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of neonatal death and neurological disability. Oxidative stress and neuroinflammation are typical pathogenic factors of HIE. Licochalcone A (LCA) exerts various biological properties, including anti-inflammatory and antioxidant activities. However, no data have been reported to elucidate the role of LCA in the development of HIE. In the present study, primary cultured rat cortical neurons were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro to simulate the in vivo situation of neonatal HIE. Interestingly, LCA significantly antagonized cell injury under OGD/R by increasing cell survival, inhibiting lactate dehydrogenase (LDH) release and cell apoptosis. Furthermore, treatment with LCA suppressed oxidative stress by decreasing reactive oxygen species (ROS) production and malondialdehyde (MDA) content, and increasing superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in primary rat cortical neurons after OGD/R. LCA stimulation also restrained OGD/R-triggered increase in pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production. Importantly, LCA treatment effectively counteracts OGD/R-mediated downregulation of silent information regulator 1 (SIRT1), nuclear factor erythroid2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1), and upregulation of nuclear factor kappa B p65 (NF-κB p65). Moreover, administration with SIRT1 inhibitor EX527 partly abolished LCA-induced neuroprotective effects on rat cortical neurons exposed to OGD/R. In conclusion, our study indicates that LCA exerts a neuroprotective effect against OGD/R-induced neuronal injury in rat primary cortical neurons, suggesting that LCA might act as a candidate therapeutic target drug used for HIE and related diseases.

show abstract

Neuroprotective effects of microRNA-210 against oxygen-glucose deprivation through inhibition of apoptosis in PC12 cells

Cited by 39 publications

References 52 publications

MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells

MicroRNA-210 knockdown contributes to apoptosis caused by oxygen glucose deprivation in PC12 cells

Validation of Altered Umbilical Cord Blood MicroRNA Expression in Neonatal Hypoxic-Ischemic Encephalopathy

Neuroprotective effect of licochalcone A against oxygen‐glucose deprivation/reperfusion in rat primary cortical neurons by attenuating oxidative stress injury and inflammatory response via the SIRT1/Nrf2 pathway

Contact Info

Product

Resources

About