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MicroRNA-124 mediates the cholinergic anti-inflammatory action through inhibiting the production of pro-inflammatory cytokines

Sun, Yang, Li, Qi, Gui, Huan, Xu, Dong-Ping, Yang, Yi-Li, Su, Ding-Feng, Liu, Xia·2013·Cell Research
DOI 10.1038/cr.2013.116PMC PMC3817544
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Figure 1 The inhibitory actions of nicotine on LPS-induced IL-6 and TNF-α productions are mechanistically different. (A) ELISA and (B) q-PCR detection of IL-6 and TNF-α in RAW264.7 macrophages incubated with vehicle or the indicated amounts of nicotine for 10 min and then stimulated with vehicle or 100 ng/ml LPS for 9 h. (C) ELISA detection of IL-6 and TNF-α in the supernatant of peritoneal macrophages incubated with vehicle or the indicated concentrations of nicotine for 10 min and stimulated with vehicle or 1 ng/ml LPS for 9 h. (D) q-PCR detection of IL-6 and TNF-α mRNAs in peritoneal macrophages treated with 1 ng/ml LPS in the presence or absence of 0.1 nM nicotine. (E) RAW264.7 cells were transfected with control siRNA or siRNA against Dicer for 48 h (Dicer protein was examined with immunoblotting, left panel, representative of three independent experiments), and stimulated with LPS in the presence or absence of 5 mM nicotine. IL-6 and TNF-α were measured by ELISA. The percentages were calculated using LPS alone as 100%. Data represent mean ± SD (n = 3). *P < 0.05, **P < 0.01 by Student's t-test.
Figure 1 The inhibitory actions of nicotine on LPS-induced IL-6 and TNF-α productions are mechanistically different. (A) ELISA and (B) q-PCR detection of IL-6 and TNF-α in RAW264.7 macrophages incubated with vehicle or the indicated amounts of nicotine for 10 min and then stimulated with vehicle or 100 ng/ml LPS for 9 h. (C) ELISA detection of IL-6 and TNF-α in the supernatant of peritoneal macrophages incubated with vehicle or the indicated concentrations of nicotine for 10 min and stimulated with vehicle or 1 ng/ml LPS for 9 h. (D) q-PCR detection of IL-6 and TNF-α mRNAs in peritoneal macrophages treated with 1 ng/ml LPS in the presence or absence of 0.1 nM nicotine. (E) RAW264.7 cells were transfected with control siRNA or siRNA against Dicer for 48 h (Dicer protein was examined with immunoblotting, left panel, representative of three independent experiments), and stimulated with LPS in the presence or absence of 5 mM nicotine. IL-6 and TNF-α were measured by ELISA. The percentages were calculated using LPS alone as 100%. Data represent mean ± SD (n = 3). *P < 0.05, **P < 0.01 by Student's t-test.CC BY-NC-ND · PubMed Central
Figure 2 α7nAChR activation upregulates miR-124. (A) q-PCR of miRNAs in RAW264.7 cells stimulated with 100 ng/ml LPS in the absence or presence of 5 mM nicotine for 9 h. (B) q-PCR of miR-124 in mice peritoneal macrophages stimulated with 1 ng/ml LPS in the absence or presence of 0.1 nM nicotine for 9 h. (C) Time courses of miR-124 induction in RAW264.7 cells stimulated with 100 ng/ml LPS with or without 5 mM nicotine. IL-6 and TNF-α productions in the supernatant were determined by ELISA. (D) q-PCR of miR-124 in peritoneal macrophages of α7nAChR+/+ or α7nAChR−/− mice treated with 1 ng/ml LPS with or without 0.1 nM nicotine for 9 h. (E) q-PCR of miR-124 in RAW264.7 cells pre-incubated with vehicle, 5 mM nicotine, 5 mM nicotine in combination with 10 μM MLA and then stimulated with 100 ng/ml LPS for 9 h. (F) q-PCR of miR-124 in RAW264.7 cells pre-incubated with 5 μM PNU for 10 min and then stimulated with vehicle or 100 ng/ml LPS for 9 h. Data represent mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.
Figure 2 α7nAChR activation upregulates miR-124. (A) q-PCR of miRNAs in RAW264.7 cells stimulated with 100 ng/ml LPS in the absence or presence of 5 mM nicotine for 9 h. (B) q-PCR of miR-124 in mice peritoneal macrophages stimulated with 1 ng/ml LPS in the absence or presence of 0.1 nM nicotine for 9 h. (C) Time courses of miR-124 induction in RAW264.7 cells stimulated with 100 ng/ml LPS with or without 5 mM nicotine. IL-6 and TNF-α productions in the supernatant were determined by ELISA. (D) q-PCR of miR-124 in peritoneal macrophages of α7nAChR+/+ or α7nAChR−/− mice treated with 1 ng/ml LPS with or without 0.1 nM nicotine for 9 h. (E) q-PCR of miR-124 in RAW264.7 cells pre-incubated with vehicle, 5 mM nicotine, 5 mM nicotine in combination with 10 μM MLA and then stimulated with 100 ng/ml LPS for 9 h. (F) q-PCR of miR-124 in RAW264.7 cells pre-incubated with 5 μM PNU for 10 min and then stimulated with vehicle or 100 ng/ml LPS for 9 h. Data represent mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.CC BY-NC-ND · PubMed Central
Figure 3 miR-124 mediates the cholinergic inhibitory actions on IL-6 and TNF-α production. For A and B, RAW264.7 cells were transfected with the indicated amounts of miR-124 mimic or negative control for 36 h and then stimulated with 100 ng/ml LPS for 9 h. (A) IL-6 (left panel) and TNF-α (right panel) in the supernatants were measured by ELISA. (B) IL-6 mRNA (left panel) and TNF-α mRNA (right panel) levels were quantitated with q-PCR. For C and D, RAW264.7 cells were transfected with 100 nM miR-124 inhibitor or negative control for 36 h and then stimulated with 100 ng/ml LPS with or without 5 mM nicotine for 9 h. (C) IL-6 (left panel) and TNF-α (right panel) in the supernatants were determined by ELISA. (D) IL-6 mRNA (left panel) and TNF-α mRNA (right panel) levels were measured by q-PCR. Results are mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.
Figure 3 miR-124 mediates the cholinergic inhibitory actions on IL-6 and TNF-α production. For A and B, RAW264.7 cells were transfected with the indicated amounts of miR-124 mimic or negative control for 36 h and then stimulated with 100 ng/ml LPS for 9 h. (A) IL-6 (left panel) and TNF-α (right panel) in the supernatants were measured by ELISA. (B) IL-6 mRNA (left panel) and TNF-α mRNA (right panel) levels were quantitated with q-PCR. For C and D, RAW264.7 cells were transfected with 100 nM miR-124 inhibitor or negative control for 36 h and then stimulated with 100 ng/ml LPS with or without 5 mM nicotine for 9 h. (C) IL-6 (left panel) and TNF-α (right panel) in the supernatants were determined by ELISA. (D) IL-6 mRNA (left panel) and TNF-α mRNA (right panel) levels were measured by q-PCR. Results are mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.CC BY-NC-ND · PubMed Central
Figure 4 miR-124 is essential for the anti-inflammatory effect of the cholinergic pathway in LPS-induced septic mice. (A) q-PCR of miR-124 in various tissues obtained from BALB/c mice injected intraperitoneally with 30 mg/kg LPS with or without 2 mg/kg nicotine for 3 h. Data represent mean ± SD (n = 6). (B) q-PCR of miR-124 in spleen obtained from BALB/c mice injected intraperitoneally with 30 mg/kg LPS in the presence or absence of 3 mg/kg PNU. Data represent mean ± SD (n = 6). (C) BALB/c mice were injected via the tail vein daily with 100 nmol/kg miR-124 agomir or matched control for 3 days. A lethal dose of LPS (30 mg/kg) was then administered. The survival rate was recorded every 2 h (n = 14). (D) ELISA detection of serum IL-6 and TNF-α obtained from BALB/c mice 6 h after treatment as described in C. Results are mean ± SD (n = 6). (E) BALB/c mice were injected via the tail vein daily with 12.5 mg/kg morpholino-conjugated miR-124 antisense (vivo-MO) or matched control for 3 days. They were then given intraperitoneally 30 mg/kg LPS together with 2 mg/kg nicotine. The survival rate was recorded every 2 h (n = 14). (F) ELISA detection of serum IL-6 and TNF-α obtained from BALB/c mice 6 h after treatment as described in E. Results are mean ± SD (n = 6). *P < 0.05 and **P < 0.01 (Student's t-test in A, B, D and F, log-rank test in C and E).
Figure 4 miR-124 is essential for the anti-inflammatory effect of the cholinergic pathway in LPS-induced septic mice. (A) q-PCR of miR-124 in various tissues obtained from BALB/c mice injected intraperitoneally with 30 mg/kg LPS with or without 2 mg/kg nicotine for 3 h. Data represent mean ± SD (n = 6). (B) q-PCR of miR-124 in spleen obtained from BALB/c mice injected intraperitoneally with 30 mg/kg LPS in the presence or absence of 3 mg/kg PNU. Data represent mean ± SD (n = 6). (C) BALB/c mice were injected via the tail vein daily with 100 nmol/kg miR-124 agomir or matched control for 3 days. A lethal dose of LPS (30 mg/kg) was then administered. The survival rate was recorded every 2 h (n = 14). (D) ELISA detection of serum IL-6 and TNF-α obtained from BALB/c mice 6 h after treatment as described in C. Results are mean ± SD (n = 6). (E) BALB/c mice were injected via the tail vein daily with 12.5 mg/kg morpholino-conjugated miR-124 antisense (vivo-MO) or matched control for 3 days. They were then given intraperitoneally 30 mg/kg LPS together with 2 mg/kg nicotine. The survival rate was recorded every 2 h (n = 14). (F) ELISA detection of serum IL-6 and TNF-α obtained from BALB/c mice 6 h after treatment as described in E. Results are mean ± SD (n = 6). *P < 0.05 and **P < 0.01 (Student's t-test in A, B, D and F, log-rank test in C and E).CC BY-NC-ND · PubMed Central
Figure 5 miR-124 targets STAT3 to inhibit IL-6 production. (A) Luciferase activity of HEK293 cells 24 h after transfection with the reporter containing 3′-UTR of STAT3, IL-6 or TNF-α mRNA and miR-124 mimic. (B) Western blotting of STAT3 protein in RAW264.7 cells transfected with miR-124 mimic or inhibitor and their corresponding controls for 36 h. (C) Western blotting of STAT3 and Y705-phosphorylated STAT3 in RAW264.7 cells transfected with the miR-124 mimic or negative control for 36 h, and then stimulated with vehicle or 100 ng/ml LPS for 9 h. (D) ELISA and q-PCR detection of IL-6 or TNF-α in RAW264.7 cells transfected with STAT3 siRNA or control siRNA for 48 h and then treated with 100 ng/ml LPS for 9 h. (E) ELISA detection of IL-6 or TNF-α in the supernatants of RAW264.7 cells transfected with STAT3 siRNA and miR-124 mimic for 36 h and then treated with 100 ng/ml LPS for 9 h. (F) ELISA and q-PCR detection of IL-6 in STAT3+/+ or STAT3−/− MEFs stimulated with 1 μg/ml LPS for 9 h. For B and C, data are representative of three independent experiments. For A and D-F, data represent mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.
Figure 5 miR-124 targets STAT3 to inhibit IL-6 production. (A) Luciferase activity of HEK293 cells 24 h after transfection with the reporter containing 3′-UTR of STAT3, IL-6 or TNF-α mRNA and miR-124 mimic. (B) Western blotting of STAT3 protein in RAW264.7 cells transfected with miR-124 mimic or inhibitor and their corresponding controls for 36 h. (C) Western blotting of STAT3 and Y705-phosphorylated STAT3 in RAW264.7 cells transfected with the miR-124 mimic or negative control for 36 h, and then stimulated with vehicle or 100 ng/ml LPS for 9 h. (D) ELISA and q-PCR detection of IL-6 or TNF-α in RAW264.7 cells transfected with STAT3 siRNA or control siRNA for 48 h and then treated with 100 ng/ml LPS for 9 h. (E) ELISA detection of IL-6 or TNF-α in the supernatants of RAW264.7 cells transfected with STAT3 siRNA and miR-124 mimic for 36 h and then treated with 100 ng/ml LPS for 9 h. (F) ELISA and q-PCR detection of IL-6 in STAT3+/+ or STAT3−/− MEFs stimulated with 1 μg/ml LPS for 9 h. For B and C, data are representative of three independent experiments. For A and D-F, data represent mean ± SD (n = 3). NS, not significant (P > 0.05); **P < 0.01 by Student's t-test.CC BY-NC-ND · PubMed Central
Figure 6 miR-124 targets TACE to inhibit TNF-α production. (A) Western blotting of pro-TNF-α and TNF-α proteins in RAW264.7 cells incubated with 5 mM nicotine for 10 min or transfected with miR-124 mimic for 36 h, and then stimulated with 100 ng/ml LPS for 9 h. (B) Luciferase activity of HEK293 cells co-transfected with the miR-124 mimic or inhibitor and the luciferase reporter of TACE 3′-UTR wild type (WT) or Mutant (Mut) for 24 h. (C) Western blotting of TACE protein in RAW264.7 cells treated as described in A. The two bands detected may represent processing or glycosylation of TACE as indicated by the Ab manufacturer. (D) ELISA detection of TNF-α in the supernatants of RAW264.7 cells transfected with TACE siRNA and miR-124 mimic for 36 h and then treated with 100 ng/ml LPS for 9 h. For A and C, data are representative of three independent experiments. For B and D, data represent mean ± SD (n = 3). NS, not significant; **P < 0.01 by Student's t-test.
Figure 6 miR-124 targets TACE to inhibit TNF-α production. (A) Western blotting of pro-TNF-α and TNF-α proteins in RAW264.7 cells incubated with 5 mM nicotine for 10 min or transfected with miR-124 mimic for 36 h, and then stimulated with 100 ng/ml LPS for 9 h. (B) Luciferase activity of HEK293 cells co-transfected with the miR-124 mimic or inhibitor and the luciferase reporter of TACE 3′-UTR wild type (WT) or Mutant (Mut) for 24 h. (C) Western blotting of TACE protein in RAW264.7 cells treated as described in A. The two bands detected may represent processing or glycosylation of TACE as indicated by the Ab manufacturer. (D) ELISA detection of TNF-α in the supernatants of RAW264.7 cells transfected with TACE siRNA and miR-124 mimic for 36 h and then treated with 100 ng/ml LPS for 9 h. For A and C, data are representative of three independent experiments. For B and D, data represent mean ± SD (n = 3). NS, not significant; **P < 0.01 by Student's t-test.CC BY-NC-ND · PubMed Central
Figure 7 miR-124 mediates the cholinergic anti-inflammatory action through targeting STAT3 and TACE. Nicotine upregulates miR-124 expression through activating α7nAChR in LPS-stimulated macrophages. STAT3 is critical for IL-6 production in response to LPS. Its activation leads to increased transcription and production of IL-6, which in turn induces STAT3 phosphorylation via IL-6 receptor and further increases IL-6 transcription, forming a positive feedback loop. miR-124 targets STAT3, and decreases STAT3 and its phosphorylation, resulting in the reduction of IL-6 at the transcription level. In addition, miR-124 targets TACE to modulate TNF-α maturation.
Figure 7 miR-124 mediates the cholinergic anti-inflammatory action through targeting STAT3 and TACE. Nicotine upregulates miR-124 expression through activating α7nAChR in LPS-stimulated macrophages. STAT3 is critical for IL-6 production in response to LPS. Its activation leads to increased transcription and production of IL-6, which in turn induces STAT3 phosphorylation via IL-6 receptor and further increases IL-6 transcription, forming a positive feedback loop. miR-124 targets STAT3, and decreases STAT3 and its phosphorylation, resulting in the reduction of IL-6 at the transcription level. In addition, miR-124 targets TACE to modulate TNF-α maturation.CC BY-NC-ND · PubMed Central

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Metadata

Authors
Sun, Y., Li, Q., Gui, H., Xu, D.-P., Yang, Y.-L., Su, D.-F., & Liu, X.
Venue
Cell Research
Publisher
Springer Science and Business Media LLC
Published
2013-08-27
Volume
23
Issue
11
Pages
1270-1283
ISSN
  • 1001-0602
  • 1748-7838
DOI
10.1038/cr.2013.116
PMC
PMC3817544
Cited by
230
References
9
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/3.0 (tdm)

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