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CircPTK2-miR-181c-5p-HMGB1: a new regulatory pathway for microglia activation and hippocampal neuronal apoptosis induced by sepsis

Li, Min, Hu, Junwen, Peng, Yucong, Li, Jingbo, Ren, Reng·2021·Molecular Medicine
DOI 10.1186/s10020-021-00305-3PMC PMC8101146
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Abstract

Background: Circular RNA hsa_circ_0008305 (circPTK2), miR-181c-5p and High mobility group box-1 (HMGB1) had a targeted regulatory relationship through bioinformatics analysis. This study explained the effects of these genes in microglia and sepsis mice. Methods: Lipopolysaccharide (LPS) or Cecal Ligation and Puncture (CLP) was used to induce inflammation cell model or sepsis mouse model, as needed. Gene levels were measured by enzyme linked immunosorbent assay (ELISA), quantitative real-time PCR or Western blot, as required. Apoptosis was detected by TUNEL assay, and RNase R was used to test the stability of circPTK2. Targeting relationships between genes were analyzed using bioinformatics analysis and dual luciferase assay. Morris water maze test and mitochondrial membrane potential (MMP) detection were conducted to analyze the effects of genes on cognitive dysfunction of mice. Results: Lipopolysaccharide induction triggered the release of pro-inflammatory cytokines, the upregulation of HMGB1 and circPTK2, and the downregulation of miR-181c-5p in microglia. Overexpression of HMGB1 enhanced the effect of LPS, while silencing HMGB1 partially counteracted the effect of LPS. Moreover, miR-181c-5p was a target of circPTK2 and bound to HMGB1. MiR-181c-5p mimic partially reversed the functions of LPS and HMGB1 overexpression, reduced the levels of TNF-α, IL-1β, and HMGB1, and inhibited apoptosis. CircPTK2 knockdown had the same effect as miR-181c-5p up-regulation. In vivo, sicircPTK2 improved cognitive function, restored MMP level, inhibited apoptosis, reduced the levels of inflammatory factors and apoptotic factors, and increased the survival rate of CLP-induced mice. Conclusion: Our research reveals that circPTK2 regulates microglia activation and hippocampal neuronal apoptosis induced by sepsis via miR-181c-5p-HMGB1 signaling.

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Fig. 1 HMGB1 overexpression enhanced the levels of lipopolysaccharides (LPS)-stimulated cytokines in microglia. a–c After induction with different concentrations of LPS, the contents of TNF-α, IL-1β and HMGB1 in microglia were determined by ELISA. N = 3 for each column; +P < 0.05, ++P < 0.01, +++P < 0.001 vs 0; One-way ANOVA followed by Bonferroni's post-hoc test. d QRT-PCR was used to detect the expressions of TNF-α, IL-1β, HMGB1 in microglia cells stimulated or not stimulated by LPS. N = 3 for each column; +++P < 0.001 by t test. e The expressions of HMGB1 in the Control, Negative Control (NC), HMGB1 (HMGB1 over-expression vector), siNC, and siHMGB1 groups were determined by qRT-PCR. N = 3 for each column; ***P < 0.001, t test vs. NC; ^^^P < 0.001, t test vs siNC. (F-I) The results from ELISA and qRT-PCR showed that HMGB1 overexpression promoted the secretion and mRNA expressions of TNF-α, IL-1β and HMGB1, and enhanced the effect of LPS. N = 3 for each column; ***P < 0.001 vs. NC; &&&P < 0.001 vs. Control; △△△P < 0.001 vs. HMGB1; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. LPS; One-way ANOVA followed by Bonferroni's post-hoc test. Each experiment was repeated three times independently. β-actin was used as a control. ELISA: enzyme linked immunosorbent assay; qRT-PCR: quantitative reverse transcription real time polymerase chain reaction
Fig. 1 HMGB1 overexpression enhanced the levels of lipopolysaccharides (LPS)-stimulated cytokines in microglia. a–c After induction with different concentrations of LPS, the contents of TNF-α, IL-1β and HMGB1 in microglia were determined by ELISA. N = 3 for each column; +P < 0.05, ++P < 0.01, +++P < 0.001 vs 0; One-way ANOVA followed by Bonferroni's post-hoc test. d QRT-PCR was used to detect the expressions of TNF-α, IL-1β, HMGB1 in microglia cells stimulated or not stimulated by LPS. N = 3 for each column; +++P < 0.001 by t test. e The expressions of HMGB1 in the Control, Negative Control (NC), HMGB1 (HMGB1 over-expression vector), siNC, and siHMGB1 groups were determined by qRT-PCR. N = 3 for each column; ***P < 0.001, t test vs. NC; ^^^P < 0.001, t test vs siNC. (F-I) The results from ELISA and qRT-PCR showed that HMGB1 overexpression promoted the secretion and mRNA expressions of TNF-α, IL-1β and HMGB1, and enhanced the effect of LPS. N = 3 for each column; ***P < 0.001 vs. NC; &&&P < 0.001 vs. Control; △△△P < 0.001 vs. HMGB1; #P < 0.05, ##P < 0.01, ###P < 0.001 vs. LPS; One-way ANOVA followed by Bonferroni's post-hoc test. Each experiment was repeated three times independently. β-actin was used as a control. ELISA: enzyme linked immunosorbent assay; qRT-PCR: quantitative reverse transcription real time polymerase chain reactionCC BY · PubMed Central
Fig. 2 Silencing HMGB1 partially reversed the levels of TNF-α, IL-1β, HMGB1 in LPS-induced microglia. a–c The contents of TNF-α, IL-1β, and HMGB1 in the Control, siNC, siHMGB1, LPS, LPS + siHMGB1 groups were determined by ELISA. N = 3 for each column; ^P < 0.05, ^^^P < 0.001 vs siNC; &&&P < 0.001 vs Control; ###P < 0.001 LPS; One-way ANOVA followed by Bonferroni's post-hoc test. d QRT-PCR was used to detect the changes in the mRNA expressions of TNF-α, IL-1β, and HMGB1 in microglia in each group. β-actin was used as a control. N = 3 for each column; ^P < 0.05, ^^P < 0.01 vs siNC; &&&P < 0.001 vs Control; ###P < 0.001 vs LPS; One-way ANOVA followed by Bonferroni's post-hoc test. Each experiment was repeated three times independently. ELISA enzyme linked immunosorbent assay, qRT-PCR quantitative reverse transcription real time polymerase chain reaction
Fig. 2 Silencing HMGB1 partially reversed the levels of TNF-α, IL-1β, HMGB1 in LPS-induced microglia. a–c The contents of TNF-α, IL-1β, and HMGB1 in the Control, siNC, siHMGB1, LPS, LPS + siHMGB1 groups were determined by ELISA. N = 3 for each column; ^P < 0.05, ^^^P < 0.001 vs siNC; &&&P < 0.001 vs Control; ###P < 0.001 LPS; One-way ANOVA followed by Bonferroni's post-hoc test. d QRT-PCR was used to detect the changes in the mRNA expressions of TNF-α, IL-1β, and HMGB1 in microglia in each group. β-actin was used as a control. N = 3 for each column; ^P < 0.05, ^^P < 0.01 vs siNC; &&&P < 0.001 vs Control; ###P < 0.001 vs LPS; One-way ANOVA followed by Bonferroni's post-hoc test. Each experiment was repeated three times independently. ELISA enzyme linked immunosorbent assay, qRT-PCR quantitative reverse transcription real time polymerase chain reactionCC BY · PubMed Central
Fig. 3 MiR-181c-5p bound to HMGB1 and may have a negative correlation with HMGB1 in LPS-induced microglia. a TargetScan v7.2 (http://www.targetscan.org/vert_72/) and b dual luciferase assay were used to predict and verify the binding relationship between miR-181c-5p and HMGB1, respectively. HMGB1-WT was the group with wild-type sequence of HMGB1 inserted into a luciferase reporter plasmid. HMGB1-MUT was the group with mutant sequence of HMGB1 inserted into a luciferase reporter plasmid. N = 3 for each column; ‡‡‡P < 0.001 t test vs MC. c After induction with different concentrations of LPS (25, 50, 100, 200 ng/mL), qRT-PCR was used to detect the expressions of miR-181c-5p and HMGB1 in microglia. β-actin or U6 was used as a control. M miR-181c-5p mimic, MC miR-181c-5p mimic control, ELISA enzyme linked immunosorbent assay, qRT-PCR quantitative reverse transcription real time polymerase chain reaction
Fig. 3 MiR-181c-5p bound to HMGB1 and may have a negative correlation with HMGB1 in LPS-induced microglia. a TargetScan v7.2 (http://www.targetscan.org/vert_72/) and b dual luciferase assay were used to predict and verify the binding relationship between miR-181c-5p and HMGB1, respectively. HMGB1-WT was the group with wild-type sequence of HMGB1 inserted into a luciferase reporter plasmid. HMGB1-MUT was the group with mutant sequence of HMGB1 inserted into a luciferase reporter plasmid. N = 3 for each column; ‡‡‡P < 0.001 t test vs MC. c After induction with different concentrations of LPS (25, 50, 100, 200 ng/mL), qRT-PCR was used to detect the expressions of miR-181c-5p and HMGB1 in microglia. β-actin or U6 was used as a control. M miR-181c-5p mimic, MC miR-181c-5p mimic control, ELISA enzyme linked immunosorbent assay, qRT-PCR quantitative reverse transcription real time polymerase chain reactionCC BY · PubMed Central
Fig. 4 The effect of miR-181c-5p on cytokines and apoptosis in microglia. a–d The contents and mRNA levels of TNF-α, IL-1β, and HMGB1 in the Control, MC, M, LPS, LPS + M, LPS + M + HMGB1 groups were determined by ELISA and qRT-PCR, respectively. N = 3 for each column; ***P < 0.001 vs Control; ^^P < 0.01, ^^^P < 0.001 vs MC; &&P < 0.01, &&&P < 0.001 vs M; ###P < 0.001 vs LPS; §§§P < 0.001 vs LPS + M; One-way ANOVA followed by Bonferroni's post-hoc test. e QRT-PCR was used to determine the level of miR-181c-5p in each group. U6 was served as a control. N = 3 for each column; ***P < 0.001 vs Control; ^^P < 0.01, ^^^P < 0.001 vs MC; &&P < 0.01, &&&P < 0.001 vs M; ###P < 0.001 vs LPS; §§§P < 0.001 vs LPS + M; One-way ANOVA followed by Bonferroni's post-hoc test. f The apoptosis of microglia in each group was detected by TUNEL. N = 3. Each experiment was repeated three times independently. M miR-181c-5p mimic; MC miR-181c-5p mimic control; ELISA enzyme linked immunosorbent assay; qRT-PCR quantitative reverse transcription real time polymerase chain reaction
Fig. 4 The effect of miR-181c-5p on cytokines and apoptosis in microglia. a–d The contents and mRNA levels of TNF-α, IL-1β, and HMGB1 in the Control, MC, M, LPS, LPS + M, LPS + M + HMGB1 groups were determined by ELISA and qRT-PCR, respectively. N = 3 for each column; ***P < 0.001 vs Control; ^^P < 0.01, ^^^P < 0.001 vs MC; &&P < 0.01, &&&P < 0.001 vs M; ###P < 0.001 vs LPS; §§§P < 0.001 vs LPS + M; One-way ANOVA followed by Bonferroni's post-hoc test. e QRT-PCR was used to determine the level of miR-181c-5p in each group. U6 was served as a control. N = 3 for each column; ***P < 0.001 vs Control; ^^P < 0.01, ^^^P < 0.001 vs MC; &&P < 0.01, &&&P < 0.001 vs M; ###P < 0.001 vs LPS; §§§P < 0.001 vs LPS + M; One-way ANOVA followed by Bonferroni's post-hoc test. f The apoptosis of microglia in each group was detected by TUNEL. N = 3. Each experiment was repeated three times independently. M miR-181c-5p mimic; MC miR-181c-5p mimic control; ELISA enzyme linked immunosorbent assay; qRT-PCR quantitative reverse transcription real time polymerase chain reactionCC BY · PubMed Central
Fig. 5 CircPTK2 directly targeted miR-181c-5p and was negatively correlated with miR-181c-5p in LPS-induced microglia. a After treatment with RNase R, PTK2 level decreased significantly, while CircPTK2 level remained unchanged. N = 3 for each column; △△△P < 0.001 t test vs Rnase R-. b The results from starBase v2.0 (http://starbase.sysu.edu.cn/starbase2/) and c dual luciferase assay showed that circPTK2 could target miR-181c-5p. N = 3 for each column; ‡‡‡P < 0.001 t test vs MC. d After induction with different doses of LPS, qRT-PCR was used to detect the expressions of miR-181c-5p and circPTK2 in microglia. β-actin or U6 was used as a control. N = 3. Each experiment was repeated three times independently. M miR-181c-5p mimic; MC miR-181c-5p mimic control; qRT-PCR quantitative reverse transcription real time polymerase chain reaction
Fig. 5 CircPTK2 directly targeted miR-181c-5p and was negatively correlated with miR-181c-5p in LPS-induced microglia. a After treatment with RNase R, PTK2 level decreased significantly, while CircPTK2 level remained unchanged. N = 3 for each column; △△△P < 0.001 t test vs Rnase R-. b The results from starBase v2.0 (http://starbase.sysu.edu.cn/starbase2/) and c dual luciferase assay showed that circPTK2 could target miR-181c-5p. N = 3 for each column; ‡‡‡P < 0.001 t test vs MC. d After induction with different doses of LPS, qRT-PCR was used to detect the expressions of miR-181c-5p and circPTK2 in microglia. β-actin or U6 was used as a control. N = 3. Each experiment was repeated three times independently. M miR-181c-5p mimic; MC miR-181c-5p mimic control; qRT-PCR quantitative reverse transcription real time polymerase chain reactionCC BY · PubMed Central
Fig. 6 CircPTK2 partially offset the effect of miR-181c-5p on cytokines and apoptosis in microglia. a–d The contents and mRNA levels of TNF-α, IL-1β, and HMGB1 in the Control, siNC, sicirc, LPS, LPS + sicirc, LPS + sicirc + I groups were detected by ELISA and qRT-PCR. N = 3 for each column; ***P < 0.001 vs. Control; ^^P < 0.01, ^^^P < 0.001 vs. siNC; &&&P < 0.001 vs. siCirc; ###P < 0.001 vs. LPS; §§§P < 0.001 vs. LPS + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e QRT-PCR was used to determine the level of miR-181c-5p in each group. N = 3 for each column; ***P < 0.001 vs. Control; ^^P < 0.01, ^^^P < 0.001 vs. siNC; &&&P < 0.001 vs. siCirc; ###P < 0.001 vs. LPS; §§P < 0.01 vs. LPS + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. f The apoptosis of microglia in each group was detected by TUNEL. Sicirc sicircPTK2; ELISA enzyme linked immunosorbent assay; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin or U6 were used as control
Fig. 6 CircPTK2 partially offset the effect of miR-181c-5p on cytokines and apoptosis in microglia. a–d The contents and mRNA levels of TNF-α, IL-1β, and HMGB1 in the Control, siNC, sicirc, LPS, LPS + sicirc, LPS + sicirc + I groups were detected by ELISA and qRT-PCR. N = 3 for each column; ***P < 0.001 vs. Control; ^^P < 0.01, ^^^P < 0.001 vs. siNC; &&&P < 0.001 vs. siCirc; ###P < 0.001 vs. LPS; §§§P < 0.001 vs. LPS + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e QRT-PCR was used to determine the level of miR-181c-5p in each group. N = 3 for each column; ***P < 0.001 vs. Control; ^^P < 0.01, ^^^P < 0.001 vs. siNC; &&&P < 0.001 vs. siCirc; ###P < 0.001 vs. LPS; §§P < 0.01 vs. LPS + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. f The apoptosis of microglia in each group was detected by TUNEL. Sicirc sicircPTK2; ELISA enzyme linked immunosorbent assay; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin or U6 were used as controlCC BY · PubMed Central
Fig. 7 Effects of circPTK2 and miR-181c-5p on learning and memory functions, mitochondrial function, hippocampal cell apoptosis and inflammation in CLP-induced mice. a and b Morris water maze test was used to measure the latency period and all quadrant residence time of mice in the Sham, CLP, CLP + siNC, CLP + sicirc, CLP + sicirc + antagomir groups. N = 6 per group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. Sham; ^P < 0.05, ^^P < 0.01 vs. CLP + siNC; #P < 0.05, ##P < 0.01 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. c CircPTK2 knockdown partially restored mitochondrial membrane potential in CLP-induced mice, and miR-181c-5p antagomir again reversed the effect of sicircPTK2. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. d The effects of circPTK2 and miR-181c-5p on hippocampal cell apoptosis was determined by TUNEL. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e–g The expressions of IL-1β, TNF-α and Caspase-3 in the hippocampus of mice in each group were detected by qRT-PCR and Western blot. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. CLP Cecal Ligation and Puncture; Sicirc sicircPTK2; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin were used as control
Fig. 7 Effects of circPTK2 and miR-181c-5p on learning and memory functions, mitochondrial function, hippocampal cell apoptosis and inflammation in CLP-induced mice. a and b Morris water maze test was used to measure the latency period and all quadrant residence time of mice in the Sham, CLP, CLP + siNC, CLP + sicirc, CLP + sicirc + antagomir groups. N = 6 per group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. Sham; ^P < 0.05, ^^P < 0.01 vs. CLP + siNC; #P < 0.05, ##P < 0.01 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. c CircPTK2 knockdown partially restored mitochondrial membrane potential in CLP-induced mice, and miR-181c-5p antagomir again reversed the effect of sicircPTK2. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. d The effects of circPTK2 and miR-181c-5p on hippocampal cell apoptosis was determined by TUNEL. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e–g The expressions of IL-1β, TNF-α and Caspase-3 in the hippocampus of mice in each group were detected by qRT-PCR and Western blot. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. CLP Cecal Ligation and Puncture; Sicirc sicircPTK2; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin were used as controlCC BY · PubMed Central
Fig. 8 The relationship between circPTK2, miR-181c-5p and HMGB1 in CLP-induced mice. a–d The expressions of circPTK2, miR-181c-5p and HMGB1 in the hippocampus tissues of mice in the Sham, CLP, CLP + siNC, CLP + sicirc, CLP + sicirc + antagomir groups were detected by qRT-PCR and Western blot. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e Kaplan–Meier curve was used to calculate the survival rate of mice in each group. N = 15. CLP Cecal Ligation and Puncture; Sicirc sicircPTK2; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin or U6 were used as control
Fig. 8 The relationship between circPTK2, miR-181c-5p and HMGB1 in CLP-induced mice. a–d The expressions of circPTK2, miR-181c-5p and HMGB1 in the hippocampus tissues of mice in the Sham, CLP, CLP + siNC, CLP + sicirc, CLP + sicirc + antagomir groups were detected by qRT-PCR and Western blot. N = 3 for each column; ***P < 0.001 vs. Sham; ^^^P < 0.001 vs. CLP + siNC; ###P < 0.001 vs. CLP + siCirc; One-way ANOVA followed by Bonferroni's post-hoc test. e Kaplan–Meier curve was used to calculate the survival rate of mice in each group. N = 15. CLP Cecal Ligation and Puncture; Sicirc sicircPTK2; qRT-PCR quantitative reverse transcription real time polymerase chain reaction. β-actin or U6 were used as controlCC BY · PubMed Central

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Metadata

Authors
Li, M., Hu, J., Peng, Y., Li, J., & Ren, R.
ORCID
Li, Min
Venue
Molecular Medicine
Publisher
Springer Science and Business Media LLC
Published
2021-05-05
Volume
27
Issue
1
ISSN
  • 1076-1551
  • 1528-3658
DOI
10.1186/s10020-021-00305-3
PMC
PMC8101146
Cited by
36
References
38
Language
en
Licence
Funders
Natural Science Foundation of Zhejiang Province (LY19H090028)

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Li, M., Hu, J., Peng, Y., Li, J., & Ren, R. (2021). CircPTK2-miR-181c-5p-HMGB1: a new regulatory pathway for microglia activation and hippocampal neuronal apoptosis induced by sepsis. Molecular Medicine. https://doi.org/10.1186/s10020-021-00305-3

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