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miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2

Xiao, Xiao, Jiang, Youjing, Liang, Weibo, Wang, Yanyun, Cao, Shuqiang, Yan, He, Gao, Linbo, Zhang, Lin·2019·Molecular Brain
DOI 10.1186/s13041-019-0501-0PMC PMC6749650
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Abstract

Ferroptosis, a newly discovered form of iron-dependent regulated cell death, has been implicated in traumatic brain injury (TBI). MiR-212-5p has previously been reported to be downregulated in extracellular vesicles following TBI. To investigate whether miR-212-5p is involved in the ferroptotic neuronal death in TBI mice, we first examined the accumulation of malondialdehyde (MDA) and ferrous ion, and the expression of ferroptosis-related molecules at 6 h, 12 h, 24 h, 48 h and 72 h following controlled cortical impact (CCI) in mice. There was a significant upregulation in the expression of Gpx4 and Acsl4 at 6 h, Slc7a11 from 12 h to 72 h, and Nox2 and Sat1 from 6 h to 72 h post injury. Similarly, an upregulation in the expression of Gpx4 at 6 h, Nox2 from 6 h to 72 h, xCT from 12 h to 72 h, and Sat1 at 72 h after CCI was observed at the protein level. Interestingly, MDA and ferrous ion were increased whereas miR-212-5p was decreased in the CCI group compared to the sham group. Furthermore, we found that overexpression of miR-212-5p attenuated ferroptosis while downregulation of miR-212-5p promoted ferroptotic cell death partially by targeting prostaglandin-endoperoxide synthase-2 (Ptgs2) in HT-22 and Neuro-2a cell lines. In addition, administration of miR-212-5p in CCI mice significantly improved learning and spatial memory. Collectively, these findings indicate that miR-212-5p may protect against ferroptotic neuronal death in CCI mice partially by targeting Ptgs2.

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Fig. 1 The concentration of MDA and Fe2+ and the mRNA levels of ferroptosis-related molecules following CCI. MDA (a) and Fe2+ (b) levels in the ipsilateral cortex at 6 h, 12 h, 24 h, 48 h, and 72 h after CCI (n = 6 for each group). Quantitative RT-PCR showing the relative expression levels of Gpx4 (c), Acsl4 (d), Slc7a11 (e), Nox2 (f), Sat1 (g) in the cortex at the indicated times after injury (n = 9 for each group). Data are expressed as mean ± SEM. Data were analyzed using the student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. MDA, malondialdehyde; CCI, controlled cortical impact; Fe2+, ferrous ion
Fig. 1 The concentration of MDA and Fe2+ and the mRNA levels of ferroptosis-related molecules following CCI. MDA (a) and Fe2+ (b) levels in the ipsilateral cortex at 6 h, 12 h, 24 h, 48 h, and 72 h after CCI (n = 6 for each group). Quantitative RT-PCR showing the relative expression levels of Gpx4 (c), Acsl4 (d), Slc7a11 (e), Nox2 (f), Sat1 (g) in the cortex at the indicated times after injury (n = 9 for each group). Data are expressed as mean ± SEM. Data were analyzed using the student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. MDA, malondialdehyde; CCI, controlled cortical impact; Fe2+, ferrous ionCC BY · PubMed Central
Fig. 2 The protein levels of ferroptosis-related molecules at the indicated times after CCI. Cortical expression of Gpx4, Acsl4, Nox2, xCT and Sat1 were measured in CCI and sham groups at 6 h (a), 12 h (b), 24 h (c), 48 h (d), 72 h (e). Data are expressed as mean ± SEM and analyzed with the student’s t-test, n = 5 per group, *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impact
Fig. 2 The protein levels of ferroptosis-related molecules at the indicated times after CCI. Cortical expression of Gpx4, Acsl4, Nox2, xCT and Sat1 were measured in CCI and sham groups at 6 h (a), 12 h (b), 24 h (c), 48 h (d), 72 h (e). Data are expressed as mean ± SEM and analyzed with the student’s t-test, n = 5 per group, *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impactCC BY · PubMed Central
Fig. 3 miR-212-5p was constantly downregulated after CCI and negatively regulated ferroptosis in neuronal cell lines. a Quantitative RT-PCR showing the relative expression levels of miR-212-5p in the cortex at 6 h, 12 h, 1d, 2d, 3d after injury (n = 9 for each group). b The HT-22 and Neuro-2a cells were treated with Rsl3 (3 μM) with or without a cell death inhibitor (ferrostatin-1, 1 μM; zVAD-fmk, 10 μM; necrosulfonamide, 0.5 μM) for 24 h. Data were analyzed using analysis of variance (ANOVA) with Tukey’s post hoc test. c Overexpression of miR-212-5p suppressed Rsl3-induced cell death in HT-22 and Neuro-2a cells. d Inhibition of endogenous miR-212-5p enhanced Rsl3-induced cell death in HT-22 and Neuro-2a cells. Indicated cells were treated with Rsl3 (3 μM) for 24 h. The transfection efficacy of overexpression (e) or inhibition (f) was confirmed by qRT-PCR analysis. Cell death was assayed using the Cytotoxicity Detection kit. Data shown represent mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impact
Fig. 3 miR-212-5p was constantly downregulated after CCI and negatively regulated ferroptosis in neuronal cell lines. a Quantitative RT-PCR showing the relative expression levels of miR-212-5p in the cortex at 6 h, 12 h, 1d, 2d, 3d after injury (n = 9 for each group). b The HT-22 and Neuro-2a cells were treated with Rsl3 (3 μM) with or without a cell death inhibitor (ferrostatin-1, 1 μM; zVAD-fmk, 10 μM; necrosulfonamide, 0.5 μM) for 24 h. Data were analyzed using analysis of variance (ANOVA) with Tukey’s post hoc test. c Overexpression of miR-212-5p suppressed Rsl3-induced cell death in HT-22 and Neuro-2a cells. d Inhibition of endogenous miR-212-5p enhanced Rsl3-induced cell death in HT-22 and Neuro-2a cells. Indicated cells were treated with Rsl3 (3 μM) for 24 h. The transfection efficacy of overexpression (e) or inhibition (f) was confirmed by qRT-PCR analysis. Cell death was assayed using the Cytotoxicity Detection kit. Data shown represent mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impactCC BY · PubMed Central
Fig. 4 miR-212-5p directly targets Ptgs2 in HT22 and Neuro-2a cell lines. Schematic diagram of strategy to discover the target gene of miR-212-5p is shown in (a). b The expression of Ptgs2 was significantly increased at all indicated time points after CCI. c Sequence alignment of miR-212-5p and the 3′-UTR of Ptgs2. The seed sequence of miR-212-5p and the binding sites in 3′-UTR are marked with underscores. d miR-212-5p overexpression inhibited the expression of 3′-UTR-luciferase reporter of Ptgs2 in HT-22 and Neuro-2a cells, but the mutant construct was immune to miR-212-5p. The 3′-UTR mutants containing mismatched nucleotides are shown at the bottom. In HT-22 (e) or Neuro-2a (f) cells, miR-212-5p overexpression inhibited the expression of Ptgs2, while inhibition of miR-212-5p caused the downregulation of Ptgs2. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001
Fig. 4 miR-212-5p directly targets Ptgs2 in HT22 and Neuro-2a cell lines. Schematic diagram of strategy to discover the target gene of miR-212-5p is shown in (a). b The expression of Ptgs2 was significantly increased at all indicated time points after CCI. c Sequence alignment of miR-212-5p and the 3′-UTR of Ptgs2. The seed sequence of miR-212-5p and the binding sites in 3′-UTR are marked with underscores. d miR-212-5p overexpression inhibited the expression of 3′-UTR-luciferase reporter of Ptgs2 in HT-22 and Neuro-2a cells, but the mutant construct was immune to miR-212-5p. The 3′-UTR mutants containing mismatched nucleotides are shown at the bottom. In HT-22 (e) or Neuro-2a (f) cells, miR-212-5p overexpression inhibited the expression of Ptgs2, while inhibition of miR-212-5p caused the downregulation of Ptgs2. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001CC BY · PubMed Central
Fig. 5 miR-212-5p improved water maze performance after CCI in mice. a Intracerebroventricular (i.c.v.) injection site brain schematic diagram. b time course of the experiments. c in MWM test, mean escape latency for each group was plotted during the 7th to 13th day. Data of escape latency are performed using two-way analysis of variance (ANOVA) for repeated measures. d The frequency of crossing the platform was recorded on the 15th day. The speed of each mouse in the spatial probe test was recorded and shown in (e). These Data are presented as mean ± SEM (n = 13 for each group) and analyzed with the student’s t-test. *p < 0.05, **p < 0.01. CCI, controlled cortical impact; MWM, Morris Water Maze
Fig. 5 miR-212-5p improved water maze performance after CCI in mice. a Intracerebroventricular (i.c.v.) injection site brain schematic diagram. b time course of the experiments. c in MWM test, mean escape latency for each group was plotted during the 7th to 13th day. Data of escape latency are performed using two-way analysis of variance (ANOVA) for repeated measures. d The frequency of crossing the platform was recorded on the 15th day. The speed of each mouse in the spatial probe test was recorded and shown in (e). These Data are presented as mean ± SEM (n = 13 for each group) and analyzed with the student’s t-test. *p < 0.05, **p < 0.01. CCI, controlled cortical impact; MWM, Morris Water MazeCC BY · PubMed Central

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Metadata

Authors
Xiao, X., Jiang, Y., Liang, W., Wang, Y., Cao, S., Yan, H., Gao, L., & Zhang, L.
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2019-09-18
Volume
12
Issue
1
ISSN
1756-6606
DOI
10.1186/s13041-019-0501-0
PMC
PMC6749650
Cited by
163
References
6
Language
en
Licence
Funders
  • Fundamental Research Funds for the Central Universities (No. 2018SCUH0053)
  • Science and Technology Major Projects of Sichuan Province of China (No.2017SZDZX0013)
  • Science and Technology Support Program of Sichuan Province of China (No.2016SZ0013)

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