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HDAC3 and <t>p300</t> play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of <t>CTB</t> treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.
P300 Activator Ctb, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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HDAC3 and <t>p300</t> play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of <t>CTB</t> treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.
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HDAC3 and <t>p300</t> play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of <t>CTB</t> treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.
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HDAC3 and <t>p300</t> play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of <t>CTB</t> treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.
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HDAC3 and <t>p300</t> play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of <t>CTB</t> treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.
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HDAC3 and p300 play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of CTB treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.

Journal: Advanced Science

Article Title: MeCP2 Lactylation Protects against Ischemic Brain Injury by Transcriptionally Regulating Neuronal Apoptosis

doi: 10.1002/advs.202415309

Figure Lengend Snippet: HDAC3 and p300 play roles in regulating of MeCP2 lactylation in ischemic stroke. A) Western blot analysis of MeCP2 lactylation at K210 and K249 in cortical samples from MCAO mice treated with saline or RGFP966. B) Quantification of GVI PLA2 and PDCD4 expression levels in the saline or RGFP966‐treated MCAO mice ( n = 6 per group). C) Representative images of TTC staining showing RGFP966 reduced infarct volume of MCAO mice. D) Quantification of brain infarct volume in mice treated with saline and RGFP966 at 1 d and 3 d post‐MCAO ( n = 5–7 per group). E) Evaluation of grip strength, F) mNSS scores, and G) fault step ratio in stroke mice treated with saline and RGFP966 ( n = 6–7 per group). H) Western blot analysis showing the effect of CTB treatment on MeCP2 lactylation at K210 and K249 compared to saline. I) Quantification of GVI PLA2 and PDCD4 expression levels in mice treated with saline or CTB ( n = 3 per group). J) Representative images of brain sections stained for infarction from mice treated with saline or CTB. K) Quantification of brain infarct volume in mice treated with saline or CTB ( n = 5–7 per group). L) Grip strength test, M) mNSS scores, and N) fault step ratio for mice treated with saline or CTB ( n = 9–10 per group). Modified Neurological Severity Scores (F, M) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant.

Article Snippet: [ ] Additionally, 30 μmol kg −1 of the p300 activator CTB (Cat. E1107, Selleck, USA) or 10 mg kg −1 RGFP966 (Cat. S7229, Selleck, USA) was intraperitoneally injected 12 h post‐MCAO.

Techniques: Western Blot, Saline, Expressing, Staining, Modification