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miR-182-5p and miR-378a-3p regulate ferroptosis in I/R-induced renal injury

Ding, Chenguang, Ding, Xiaoming, Zheng, Jin, Wang, Bo, Li, Yang, Xiang, Heli, Dou, Meng, Qiao, Yuxi, Tian, Puxun, Xue, Wujun·2020·Cell Death & Disease
DOI 10.1038/s41419-020-03135-zPMC PMC7595188
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Abstract

Renal tubular cell death is the key factor of the pathogenesis of ischemia/reperfusion (I/R) kidney injury. Ferroptosis is a type of regulated cell death (RCD) found in various diseases. However, the underlying molecular mechanisms related to ferroptosis in renal I/R injury remain unclear. In the present study, we investigated the regulatory role of microRNAs on ferroptosis in I/R-induced renal injury. We established the I/R-induced renal injury model in rats, and H/R induced HK-2 cells injury in vitro. CCK-8 was used to measure cell viability. Fe 2+ and ROS levels were assayed to evaluate the activation of ferroptosis. We performed RNA sequencing to profile the miRNAs expression in H/R-induced injury and ferroptosis. Western blot analysis was used to detect the protein expression. qRT-PCR was used to detect the mRNA and miRNA levels in cells and tissues. We further used luciferase reporter assay to verify the direct targeting effect of miRNA. We found that ischemia/reperfusion-induced ferroptosis in rat’s kidney. We identified that miR-182-5p and miR-378a-3p were upregulated in the ferroptosis and H/R-induced injury, and correlates reversely with glutathione peroxidases 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression in renal I/R injury tissues, respectively. In vitro studies showed that miR-182-5p and miR-378a-3p induced ferroptosis in cells. We further found that miR-182-5p and miR-378a-3p regulated the expression of GPX4 and SLC7A11 negatively by directly binding to the 3′UTR of GPX4 and SLC7A11 mRNA. In vivo study showed that silencing miR-182-5p and miR-378a-3p alleviated the I/R-induced renal injury in rats. In conclusion, we demonstrated that I/R induced upregulation of miR-182-5p and miR-378a-3p, leading to activation of ferroptosis in renal injury through downregulation of GPX4 and SLC7A11.

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Figures

Fig. 1 MiR-182-5p and miR-378a-3p aberrantly expressed in the cells suffering from H/R-induced injury and ferroptosis. HK-2 cells were treated with 1 μM ferrostatin-1 (Fer-1), 10 μM erastin or not 1 h before the H/R induction. A Fer-1 inhibited the decrease of cell viability induced by H/R. Fer-1 inhibited the increase of iron level induced by H/R. C Fer-1 inhibited the increase of Lipid ROS level induced by H/R. D Fer-1 inhibited the increase of mitochondrial superoxide level induced by H/R. E Fer-1 inhibited H/R-induced cell death. F Heat map showing expression profiles for the H/R-induced and G erastin-treated cells compared with the control group. H Venn diagram showed the intersection of the aberrantly expressed miRNAs in H/R-induced and erastin-treated cells. I, J Upregulation of miR-182-5p and miR-378a-3p in the H/R-induced and erastin-treated HK-2 and TCMK-1 cells were verified by qRT-PCR. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 vs. indicated group.
Fig. 1 MiR-182-5p and miR-378a-3p aberrantly expressed in the cells suffering from H/R-induced injury and ferroptosis. HK-2 cells were treated with 1 μM ferrostatin-1 (Fer-1), 10 μM erastin or not 1 h before the H/R induction. A Fer-1 inhibited the decrease of cell viability induced by H/R. Fer-1 inhibited the increase of iron level induced by H/R. C Fer-1 inhibited the increase of Lipid ROS level induced by H/R. D Fer-1 inhibited the increase of mitochondrial superoxide level induced by H/R. E Fer-1 inhibited H/R-induced cell death. F Heat map showing expression profiles for the H/R-induced and G erastin-treated cells compared with the control group. H Venn diagram showed the intersection of the aberrantly expressed miRNAs in H/R-induced and erastin-treated cells. I, J Upregulation of miR-182-5p and miR-378a-3p in the H/R-induced and erastin-treated HK-2 and TCMK-1 cells were verified by qRT-PCR. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 vs. indicated group.CC BY · PubMed Central
Fig. 2 MiR-182-5p and miR-378-3p promotes ferroptosis in the renal epithelial cells. HK-2 and TCMK-1 cells were treated with miR-182-5p mimics (10 pmol) or inhibitor (40 pmol), or miR-378a-3p mimics (10 pmol) or inhibitor (40 pmol) for 36 h, then the cells were subjected to various detection. A The efficacy of the miRNAs mimics and inhibitors in TCMK-1 and HK-2 cells was verified by qRT-PCR. B Cell viability of TCMK-1 and HK-2 cells were reduced by miR-182-5p and miR-378a-3p mimics, and enhanced by miR-182-5p and miR-378a-3p inhibitors. C Iron level and D lip ROS level of TCMK-1 and HK-2 cells were elevated by miR-182-5p and miR-378a-3p mimics, and decreased by miR-182-5p and miR-378a-3p inhibitors. E miR-182-5p and miR-378a-3p mimics induced increasing of cell death of TCMK-1 and HK-2 cells, while miR-182-5p and miR-378a-3p inhibitors decreased the cell death, as indicated by TUNEL staining (green), Bar = 100 μm. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. indicated group.
Fig. 2 MiR-182-5p and miR-378-3p promotes ferroptosis in the renal epithelial cells. HK-2 and TCMK-1 cells were treated with miR-182-5p mimics (10 pmol) or inhibitor (40 pmol), or miR-378a-3p mimics (10 pmol) or inhibitor (40 pmol) for 36 h, then the cells were subjected to various detection. A The efficacy of the miRNAs mimics and inhibitors in TCMK-1 and HK-2 cells was verified by qRT-PCR. B Cell viability of TCMK-1 and HK-2 cells were reduced by miR-182-5p and miR-378a-3p mimics, and enhanced by miR-182-5p and miR-378a-3p inhibitors. C Iron level and D lip ROS level of TCMK-1 and HK-2 cells were elevated by miR-182-5p and miR-378a-3p mimics, and decreased by miR-182-5p and miR-378a-3p inhibitors. E miR-182-5p and miR-378a-3p mimics induced increasing of cell death of TCMK-1 and HK-2 cells, while miR-182-5p and miR-378a-3p inhibitors decreased the cell death, as indicated by TUNEL staining (green), Bar = 100 μm. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. indicated group.CC BY · PubMed Central
Fig. 3 Ferroptosis is enhanced in the kidney of I/R injured rats. Rats renal artery was clamped with non-traumatic clamps for 45 min, followed by restoring of the renal blood flow. Control rats underwent sham surgery (sham group) without ischemia-reperfusion injury (IRI). Blood samples and renal tissues were collected 48 h after the injury. A Serum creatinine and B blood urea nitrogen levels were significantly higher in the I/R group than in the sham group. C Kidney tissue sections were subjected to histological examination by hematoxylin and eosin staining (H&E) and TUNEL assay to evaluate renal tubule injury. D Increased iron level and E ROS level in I/R renal tissues indicates the increase of ferroptosis. F Western blot was used to detect the indicated protein expression. The protein intensity was analyzed by using ImageJ. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. ***P < 0.001 vs. the sham group.
Fig. 3 Ferroptosis is enhanced in the kidney of I/R injured rats. Rats renal artery was clamped with non-traumatic clamps for 45 min, followed by restoring of the renal blood flow. Control rats underwent sham surgery (sham group) without ischemia-reperfusion injury (IRI). Blood samples and renal tissues were collected 48 h after the injury. A Serum creatinine and B blood urea nitrogen levels were significantly higher in the I/R group than in the sham group. C Kidney tissue sections were subjected to histological examination by hematoxylin and eosin staining (H&E) and TUNEL assay to evaluate renal tubule injury. D Increased iron level and E ROS level in I/R renal tissues indicates the increase of ferroptosis. F Western blot was used to detect the indicated protein expression. The protein intensity was analyzed by using ImageJ. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. ***P < 0.001 vs. the sham group.CC BY · PubMed Central
Fig. 4 MiR-182-5p and miR-378a-3p negatively correlates with the GPX4 and SLC7A11 expression, respectively. A The representative photograph showing fluorescence in situ hybridization in renal tissues, green represented biotin-labeled probe against miR-182-5p and miR-378a-3p and blue represents DAPI staining of the nucleus. B miR-182-5p and miR-378a-3p expression increased in the I/R renal injury rats. C Western blot was used to detect the GPX4 and SLC7A11 protein expression in the renal tissues. The protein intensity was analyzed by using ImageJ. D Pearson analysis showed the negative correlation of miR-182-5p and miR-378a-3p with GPX4 and SLC7A11 protein expression. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. ***P < 0.001 vs. the sham group.
Fig. 4 MiR-182-5p and miR-378a-3p negatively correlates with the GPX4 and SLC7A11 expression, respectively. A The representative photograph showing fluorescence in situ hybridization in renal tissues, green represented biotin-labeled probe against miR-182-5p and miR-378a-3p and blue represents DAPI staining of the nucleus. B miR-182-5p and miR-378a-3p expression increased in the I/R renal injury rats. C Western blot was used to detect the GPX4 and SLC7A11 protein expression in the renal tissues. The protein intensity was analyzed by using ImageJ. D Pearson analysis showed the negative correlation of miR-182-5p and miR-378a-3p with GPX4 and SLC7A11 protein expression. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. ***P < 0.001 vs. the sham group.CC BY · PubMed Central
Fig. 5 MiR-182-5p targets GPX4 and miR-378a-3p targets SLC7A11, respectively, in the renal epithelial cells. A The predicted binding site between 3′UTR of GPX4 mRNA and miR-182-5p, and the predicted binding site between 3′UTR of SLC7A11 mRNA and miR-378a-3p. B HK-2 cells were co‑transfected with luciferase constructs containing the GPX4 WT or MUT 3′‑UTRs and miR‑182-5p mimics or mimics NC, or co‑transfected with luciferase constructs containing the SLC7A11 WT or MUT 3′‑UTRs and miR‑378a-3p mimics or mimics NC. Luciferase activity was measured. C RIP assay followed by qRT-PCR to assay miR-182-5p and miR-378a-3p endogenously associated with GPX4 and SLC7A11, respectively. D miR-182-5p and miR-378a-3p scarcely influence the GPX4 and SLC7A11 mRNA levels. E The GPX4 and SLC7A11 expression levels were downregulated after treated with miR-182-5p and miR-378a-3p mimics and upregulated with the treatment with miRNAs inhibitors in HK-2 and TCMK-1 cells. The protein intensity was analyzed by using ImageJ. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. indicated group.
Fig. 5 MiR-182-5p targets GPX4 and miR-378a-3p targets SLC7A11, respectively, in the renal epithelial cells. A The predicted binding site between 3′UTR of GPX4 mRNA and miR-182-5p, and the predicted binding site between 3′UTR of SLC7A11 mRNA and miR-378a-3p. B HK-2 cells were co‑transfected with luciferase constructs containing the GPX4 WT or MUT 3′‑UTRs and miR‑182-5p mimics or mimics NC, or co‑transfected with luciferase constructs containing the SLC7A11 WT or MUT 3′‑UTRs and miR‑378a-3p mimics or mimics NC. Luciferase activity was measured. C RIP assay followed by qRT-PCR to assay miR-182-5p and miR-378a-3p endogenously associated with GPX4 and SLC7A11, respectively. D miR-182-5p and miR-378a-3p scarcely influence the GPX4 and SLC7A11 mRNA levels. E The GPX4 and SLC7A11 expression levels were downregulated after treated with miR-182-5p and miR-378a-3p mimics and upregulated with the treatment with miRNAs inhibitors in HK-2 and TCMK-1 cells. The protein intensity was analyzed by using ImageJ. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs. indicated group.CC BY · PubMed Central
Fig. 6 MiR-182-5p and miR-378a-3p regulates ferroptosis in the renal epithelial cells by targeting GPX4 and SLC7A11, respectively. The HK-2 cells were treated with indicated miRNA mimic (10 pmol) and GPX4 overexpression lentivirus (MOI = 50) with a final concentration of 5 μg/mL polybrene for, or co-treated with the miRNA mimic and lentivirus for 36 h, then the cells were subjected to various detection. nc, control mimic; cv, control lentivirus. A miR-182-5p and miR-378a-3p inhibited the GPX4 and SLC7A11 protein expression which were upregulated by the lentivirus treatment. B Overexpression of GPX4 and SLC7A11 inhibited the reduction of cell viability induced by miRNA mimic. C Overexpression of GPX4 and SLC7A11 inhibited the increase of cell iron level, ROS level (D), and mitosox intensity (E) induced by miRNA mimic. F Overexpression of GPX4 and SLC7A11 inhibited the miRNA mimic-induced cell death of HK-2 cells. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 vs. indicated group.
Fig. 6 MiR-182-5p and miR-378a-3p regulates ferroptosis in the renal epithelial cells by targeting GPX4 and SLC7A11, respectively. The HK-2 cells were treated with indicated miRNA mimic (10 pmol) and GPX4 overexpression lentivirus (MOI = 50) with a final concentration of 5 μg/mL polybrene for, or co-treated with the miRNA mimic and lentivirus for 36 h, then the cells were subjected to various detection. nc, control mimic; cv, control lentivirus. A miR-182-5p and miR-378a-3p inhibited the GPX4 and SLC7A11 protein expression which were upregulated by the lentivirus treatment. B Overexpression of GPX4 and SLC7A11 inhibited the reduction of cell viability induced by miRNA mimic. C Overexpression of GPX4 and SLC7A11 inhibited the increase of cell iron level, ROS level (D), and mitosox intensity (E) induced by miRNA mimic. F Overexpression of GPX4 and SLC7A11 inhibited the miRNA mimic-induced cell death of HK-2 cells. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 vs. indicated group.CC BY · PubMed Central
Fig. 7 Inhibition of miR-182-5p and miR-378a-3p attenuates I/R-induced kidney injury in vivo. The rats were divided into seven groups: Sham group, I/R model group, I/R + nc-antagomir group (I/R + inc), I/R + miR-182-5p antagomir group (I/R + i-miR-182-5p), I/R + miR-378a-3p antagomir group (I/R + i-miR-378a-3p), I/R + saline group (I/R + saline), and I/R + Ferostatin-1 group (I/R + Fer-1), with 10 rats in each group. Antagomir was administrated by tail injection at the dosage of 80 mg/kg and Fer-1 was served as the ferroptosis inhibitor in AKI model by intraperitoneal injection at the concentration of 5 mg/kg. A Serum creatinine and B blood urea nitrogen levels were significantly decreased in the antagomir and Fer-1 administrated group than in the I/R group. C Iron level and D ROS level decreased in the antagomir and Fer-1 administrated group than in the I/R group. E H&E and TUNEL assay showed reduced renal tubule injury in the antagomir and Fer-1 administrated group than in the I/R group. n = 10. Data are presented as the mean ± s.e.m. **P < 0.01, ***P < 0.001 vs. indicated group.
Fig. 7 Inhibition of miR-182-5p and miR-378a-3p attenuates I/R-induced kidney injury in vivo. The rats were divided into seven groups: Sham group, I/R model group, I/R + nc-antagomir group (I/R + inc), I/R + miR-182-5p antagomir group (I/R + i-miR-182-5p), I/R + miR-378a-3p antagomir group (I/R + i-miR-378a-3p), I/R + saline group (I/R + saline), and I/R + Ferostatin-1 group (I/R + Fer-1), with 10 rats in each group. Antagomir was administrated by tail injection at the dosage of 80 mg/kg and Fer-1 was served as the ferroptosis inhibitor in AKI model by intraperitoneal injection at the concentration of 5 mg/kg. A Serum creatinine and B blood urea nitrogen levels were significantly decreased in the antagomir and Fer-1 administrated group than in the I/R group. C Iron level and D ROS level decreased in the antagomir and Fer-1 administrated group than in the I/R group. E H&E and TUNEL assay showed reduced renal tubule injury in the antagomir and Fer-1 administrated group than in the I/R group. n = 10. Data are presented as the mean ± s.e.m. **P < 0.01, ***P < 0.001 vs. indicated group.CC BY · PubMed Central

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Metadata

Authors
Ding, C., Ding, X., Zheng, J., Wang, B., Li, Y., Xiang, H., Dou, M., Qiao, Y., Tian, P., & Xue, W.
ORCID
Qiao, Yuxi
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2020-10-28
Volume
11
Issue
10
ISSN
2041-4889
DOI
10.1038/s41419-020-03135-z
PMC
PMC7595188
Cited by
197
References
7
Language
en
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Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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