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Abcam rabbit anti cc1

Effects of EA stimulation on NG2-expressing cell types in the perilesional striatum and the corpus callosum of mice at 21 days after MCAO . Photomicrographs (A) and histograms (B and C) showing labeling and quantification of NG2 (green) -, <t>CC1</t> (red) -, CD31 (red) - and CD68 (red) -positive cells in the perilesional striatum and the corpus callosum of MCAO mice. EA stimulation significantly increased the NG2 and CD68double positive cells in the perilesional striatum. n = 6. All data are shown as mean ± SEM. ## P < 0.01, vs . MCAO group; & P < 0.05, vs . MCAO + EA1 group (one-way analysis of variance with Tukey's post hoc tests). Scale bar in A: 20 μm. DAPI: 4′,6-Diamidino-2-phenylindole; EA1: electroacupuncture at 1 mA; MCAO: middle cerebral artery occlusion; NG2: neural/glial antigen 2.

Rabbit Anti Cc1, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 1183 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke"

Article Title: Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke

Journal: Neural Regeneration Research

doi: 10.4103/1673-5374.330611

Figure Legend Snippet: Effects of EA stimulation on NG2-expressing cell types in the perilesional striatum and the corpus callosum of mice at 21 days after MCAO . Photomicrographs (A) and histograms (B and C) showing labeling and quantification of NG2 (green) -, CC1 (red) -, CD31 (red) - and CD68 (red) -positive cells in the perilesional striatum and the corpus callosum of MCAO mice. EA stimulation significantly increased the NG2 and CD68double positive cells in the perilesional striatum. n = 6. All data are shown as mean ± SEM. ## P < 0.01, vs . MCAO group; & P < 0.05, vs . MCAO + EA1 group (one-way analysis of variance with Tukey's post hoc tests). Scale bar in A: 20 μm. DAPI: 4′,6-Diamidino-2-phenylindole; EA1: electroacupuncture at 1 mA; MCAO: middle cerebral artery occlusion; NG2: neural/glial antigen 2.

Techniques Used: Expressing, Labeling

Effects of EA stimulation on cellular phenotype and the expression of BDNF and GSK3β in GFP + /DAPI + NG2-expressing cells, or whole cells in ipsilateral perilesional striatum of NG2-mEGFP mice at 21 days after MCAO . Quantitative analysis of the flow cytometry data (A and C) and histograms showing the percentage of GFP + /DAPI + cells also expressing BrdU, CC1, CD31, CD68, and GSK3β, as well as the percentage of DAPI + cells also expressing BDNF (B and D, respectively). The numbers of GFP + cells that also express BrdU, CC1, CD31and GSKβ were significantly increased after EA1 stimulation. n = 5. All data are shown as mean ± SEM. # P < 0.05, ## P < 0.01, and ### P < 0.01, vs . MCAO group (independent samples t -test). BDNF: Brain-derived neurotrophic factor; BrdU: bromodeoxyuridine; DAPI: 4′,6-Diamidino-2-phenylindole; EA1: Electroacupuncture at 1 mAEA1: electroacupuncture at 1 mA; GFP: green fluorescent protein; GSK3β: glycogen synthase kinase 3 beta; MCAO: middle cerebral artery occlusion; mEGFP: mutated enhanced green fluorescent protein; NG2: neural/glial antigen 2.

Figure Legend Snippet: Effects of EA stimulation on cellular phenotype and the expression of BDNF and GSK3β in GFP + /DAPI + NG2-expressing cells, or whole cells in ipsilateral perilesional striatum of NG2-mEGFP mice at 21 days after MCAO . Quantitative analysis of the flow cytometry data (A and C) and histograms showing the percentage of GFP + /DAPI + cells also expressing BrdU, CC1, CD31, CD68, and GSK3β, as well as the percentage of DAPI + cells also expressing BDNF (B and D, respectively). The numbers of GFP + cells that also express BrdU, CC1, CD31and GSKβ were significantly increased after EA1 stimulation. n = 5. All data are shown as mean ± SEM. # P < 0.05, ## P < 0.01, and ### P < 0.01, vs . MCAO group (independent samples t -test). BDNF: Brain-derived neurotrophic factor; BrdU: bromodeoxyuridine; DAPI: 4′,6-Diamidino-2-phenylindole; EA1: Electroacupuncture at 1 mAEA1: electroacupuncture at 1 mA; GFP: green fluorescent protein; GSK3β: glycogen synthase kinase 3 beta; MCAO: middle cerebral artery occlusion; mEGFP: mutated enhanced green fluorescent protein; NG2: neural/glial antigen 2.

Techniques Used: Expressing, Flow Cytometry, Derivative Assay

Image Search Results

Figure 1. Recipient CC1 signaling mitigates hepatic IRI and suppresses NF-kB p65 in mouse OLT. Mouse WT livers subjected to 18 hours of cold storage were transplanted into WT or CC1KO syngeneic recipients (n ¼ 6–8/group). OLT/serum samples were analyzed 6 hours after reperfusion. The sham group (n ¼ 5) underwent the same procedures except for OLT. (A) Representative H&E and TUNEL staining. DAPI, 40,6-diamidino-2-phenylindole. Scale bars ¼ 100 mm. (B) Suzuki’s histologic grading of liver IRI and quantiﬁcation of TUNELþ cells/HPF. (C) sAST/sALT and (D) lactate dehydrogenase (LDH) levels (U/L). Quantitative reverse transcription polymerase chain reaction–assisted OLT detection of (E) IFN-gamma, IL6, IL17, and gran- zyme B/perforin 1, and (F) TLR4, IL1b, and TNF-a (n ¼ 6–7/group). Data normalized to hypoxanthine guanine phosphor- ibosyltransferase gene expression. (G) Western blot–assisted detection of phosphorylated (p)-IkBa, IkBa, p-NF-kB p65, NF-kB p65, and vinculin (VCL). The relative intensity ratio of p-IkBa/IkBa and p-NF-kB p65/NF-kB p65 (n ¼ 4/group) is shown. Data are shown as mean ± standard error of the mean *P < .05, **P < .01, Student t test.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 1. Recipient CC1 signaling mitigates hepatic IRI and suppresses NF-kB p65 in mouse OLT. Mouse WT livers subjected to 18 hours of cold storage were transplanted into WT or CC1KO syngeneic recipients (n ¼ 6–8/group). OLT/serum samples were analyzed 6 hours after reperfusion. The sham group (n ¼ 5) underwent the same procedures except for OLT. (A) Representative H&E and TUNEL staining. DAPI, 40,6-diamidino-2-phenylindole. Scale bars ¼ 100 mm. (B) Suzuki’s histologic grading of liver IRI and quantiﬁcation of TUNELþ cells/HPF. (C) sAST/sALT and (D) lactate dehydrogenase (LDH) levels (U/L). Quantitative reverse transcription polymerase chain reaction–assisted OLT detection of (E) IFN-gamma, IL6, IL17, and gran- zyme B/perforin 1, and (F) TLR4, IL1b, and TNF-a (n ¼ 6–7/group). Data normalized to hypoxanthine guanine phosphor- ibosyltransferase gene expression. (G) Western blot–assisted detection of phosphorylated (p)-IkBa, IkBa, p-NF-kB p65, NF-kB p65, and vinculin (VCL). The relative intensity ratio of p-IkBa/IkBa and p-NF-kB p65/NF-kB p65 (n ¼ 4/group) is shown. Data are shown as mean ± standard error of the mean *P < .05, **P < .01, Student t test.

Article Snippet: The following primary antibodies were used in this study: phospho-IkBa (2859/14D4), IkBa (4812/44D4), phospho-NF-kB p65 (3033/93H1), NF-kB p65 (8242/D14E12), CC1 (14771/D1P4T), vinculin (13901/E1E9V), and b-actin (4970/13E5) (all from Cell Signaling Technology.

Techniques: TUNEL Assay, Staining, Reverse Transcription, Polymerase Chain Reaction, Gene Expression, Western Blot

Figure 2. CC1 signaling enhances TIM-3 expression and suppresses CD4þ T-cell inﬂammatory signature. (A) Representative (n ¼ 4/group) ﬂow cytometry of CC1 and TIM-3 expression in peripheral blood lymphocytes from naive WT and CC1KO mice. TIM-3þ frequency in (B) WT CC1þ and CC1 CD4þ T cells and in (C) WT and CC1KO CD4þ and CD8þ T cells. (D) Repre- sentative (n ¼ 4/group) ﬂow cytometry of CC1 and TIM-3 expression in activated peripheral blood lymphocytes from WT and CC1KO mice subjected to hepatic IRI. TIM-3þ frequency in (E) WT CC1þ and CC1 CD4þ T cells and in (F) WT and CC1KO CD4þ and CD8þ T cells. (G) CC1þ frequency in naive vs post-IRI in WT CD4þ T cells. (H) TIM-3þ frequency in naive vs post-IRI in WT and CC1KO CD4þ T cells. (I) Quantitative reverse-transcription polymerase chain reaction–assisted detection of IFN-g, T-box protein (T-bet) expressed in T cells, IL6, IL17, IL22, and TNF-a in CD4þ T cells from WT and CC1KO mice before and after stimulation (n ¼ 6/group). White square: WT; black square: CC1KO mouse. Data shown as mean ± standard error of the mean. *P < .05, ****P < .0001, Student t test.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 2. CC1 signaling enhances TIM-3 expression and suppresses CD4þ T-cell inﬂammatory signature. (A) Representative (n ¼ 4/group) ﬂow cytometry of CC1 and TIM-3 expression in peripheral blood lymphocytes from naive WT and CC1KO mice. TIM-3þ frequency in (B) WT CC1þ and CC1 CD4þ T cells and in (C) WT and CC1KO CD4þ and CD8þ T cells. (D) Repre- sentative (n ¼ 4/group) ﬂow cytometry of CC1 and TIM-3 expression in activated peripheral blood lymphocytes from WT and CC1KO mice subjected to hepatic IRI. TIM-3þ frequency in (E) WT CC1þ and CC1 CD4þ T cells and in (F) WT and CC1KO CD4þ and CD8þ T cells. (G) CC1þ frequency in naive vs post-IRI in WT CD4þ T cells. (H) TIM-3þ frequency in naive vs post-IRI in WT and CC1KO CD4þ T cells. (I) Quantitative reverse-transcription polymerase chain reaction–assisted detection of IFN-g, T-box protein (T-bet) expressed in T cells, IL6, IL17, IL22, and TNF-a in CD4þ T cells from WT and CC1KO mice before and after stimulation (n ¼ 6/group). White square: WT; black square: CC1KO mouse. Data shown as mean ± standard error of the mean. *P < .05, ****P < .0001, Student t test.

Techniques: Expressing, Cytometry, Reverse Transcription, Polymerase Chain Reaction

Figure 4. Enhanced T cell–speciﬁc TIM-3 alleviates IRI-OLT and suppresses Kupffer cell NF-kB p65 in CC1-deﬁcient re- cipients. WT livers after 18 hours of cold storage were transplanted into WT, CC1KO, T cell–speciﬁc TIM-3Tg/CC1KO, and TIM-3Tg/CC1KO þ anti–TIM-3 antibody (n ¼ 6–8/group). OLT/serum samples were analyzed at 6 hours. (A) Representative H&E and TUNEL staining. DAPI, 40,6-diamidino-2-phenylindole. Scale bars ¼ 100 mm. (B) Suzuki’s histologic grading of liver IRI and quantiﬁcation of TUNELþ cells/HPF. (C) sAST/sALT (U/L). Quantitative reverse-transcription polymerase chain reaction–assisted detection of (D) IFN-gamma, IL6, and IL17, and (E) TLR4, IL-1b, and TNF-a in OLT (n ¼ 6/group). Data in D and E were normalized to hypoxanthine guanine phosphoribosyltransferase gene expression. (F) Western blot-assisted detection of CC1, phosphorylated (p)-NF-kB p65, NF-kB p65, and vinculin (VCL). The relative intensity ratio of p-NF-kB p65/NF-kB p65 (n ¼ 3–4/group) is shown. (G) Representative NF-kB staining in OLT. Arrows indicate nuclear NF-kB locali- zation in nonparenchymal cells. Scale bars ¼ 100 mm. (H) Representative C-type lectin domain family 4 member F (CLEC4F; Kupffer cell) and p-NF-kB p65 staining. Arrowheads indicate Kupffer cells augmenting p-NF-kB p65. Scale bars ¼ 100 mm (left panels) and 20 mm (enlarged images). Data are shown as mean ±standard error of the mean. *P < .05, **P < .01, ***P < .01, Student t test.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 4. Enhanced T cell–speciﬁc TIM-3 alleviates IRI-OLT and suppresses Kupffer cell NF-kB p65 in CC1-deﬁcient re- cipients. WT livers after 18 hours of cold storage were transplanted into WT, CC1KO, T cell–speciﬁc TIM-3Tg/CC1KO, and TIM-3Tg/CC1KO þ anti–TIM-3 antibody (n ¼ 6–8/group). OLT/serum samples were analyzed at 6 hours. (A) Representative H&E and TUNEL staining. DAPI, 40,6-diamidino-2-phenylindole. Scale bars ¼ 100 mm. (B) Suzuki’s histologic grading of liver IRI and quantiﬁcation of TUNELþ cells/HPF. (C) sAST/sALT (U/L). Quantitative reverse-transcription polymerase chain reaction–assisted detection of (D) IFN-gamma, IL6, and IL17, and (E) TLR4, IL-1b, and TNF-a in OLT (n ¼ 6/group). Data in D and E were normalized to hypoxanthine guanine phosphoribosyltransferase gene expression. (F) Western blot-assisted detection of CC1, phosphorylated (p)-NF-kB p65, NF-kB p65, and vinculin (VCL). The relative intensity ratio of p-NF-kB p65/NF-kB p65 (n ¼ 3–4/group) is shown. (G) Representative NF-kB staining in OLT. Arrows indicate nuclear NF-kB locali- zation in nonparenchymal cells. Scale bars ¼ 100 mm. (H) Representative C-type lectin domain family 4 member F (CLEC4F; Kupffer cell) and p-NF-kB p65 staining. Arrowheads indicate Kupffer cells augmenting p-NF-kB p65. Scale bars ¼ 100 mm (left panels) and 20 mm (enlarged images). Data are shown as mean ±standard error of the mean. *P < .05, **P < .01, ***P < .01, Student t test.

Techniques: TUNEL Assay, Staining, Reverse Transcription, Polymerase Chain Reaction, Gene Expression, Western Blot

Figure 5. Donor liver CC1 deﬁciency compromises T cell–speciﬁc TIM-3 regulation in CC1-deﬁcient recipients. (A) CC1KO livers after 18 hours of cold storage were transplanted into CC1KO or TIM-3Tg/CC1KO mice. OLT/serum samples were analyzed at 6 hours (n ¼ 6/group). The sham group (n ¼ 5) underwent the same procedures, except for OLT. (B) Representative H&E staining. Scale bars ¼ 100 mm. (C) Suzuki’s histologic grading of liver IRI and sAST/sALT (U/L). (D) Representative C-type lectin domain family 4 member F (CLEC4F; Kupffer cells) and phosphorylated (p)-NF-kB p65 staining in OLT. DAPI, 40,6- diamidino-2-phenylindole. Arrowheads indicate p-NF-kB p65þ cells. Scale bars ¼ 100 mm. Quantative reverse-transcription polymerase chain reaction–assisted detection of (E) IFN-gamma, IL6, and IL17 (n ¼ 6/group), and (F) TLR4, IL-1b, and TNF-a (n ¼ 6/group) in OLT. Data were normalized to hypoxanthine guanine phosphoribosyltransferase (HPRT) gene expression. (G) Western blot–assisted detection of CC1, p-NF-kB p65, NF-kB p65, and b-actin. The relative intensity ratio of p- NF-kB p65/NF-kB p65 (n ¼ 3/group) is shown. Data are shown as mean ± standard error of the mean. ***P < .001, Student t test.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 5. Donor liver CC1 deﬁciency compromises T cell–speciﬁc TIM-3 regulation in CC1-deﬁcient recipients. (A) CC1KO livers after 18 hours of cold storage were transplanted into CC1KO or TIM-3Tg/CC1KO mice. OLT/serum samples were analyzed at 6 hours (n ¼ 6/group). The sham group (n ¼ 5) underwent the same procedures, except for OLT. (B) Representative H&E staining. Scale bars ¼ 100 mm. (C) Suzuki’s histologic grading of liver IRI and sAST/sALT (U/L). (D) Representative C-type lectin domain family 4 member F (CLEC4F; Kupffer cells) and phosphorylated (p)-NF-kB p65 staining in OLT. DAPI, 40,6- diamidino-2-phenylindole. Arrowheads indicate p-NF-kB p65þ cells. Scale bars ¼ 100 mm. Quantative reverse-transcription polymerase chain reaction–assisted detection of (E) IFN-gamma, IL6, and IL17 (n ¼ 6/group), and (F) TLR4, IL-1b, and TNF-a (n ¼ 6/group) in OLT. Data were normalized to hypoxanthine guanine phosphoribosyltransferase (HPRT) gene expression. (G) Western blot–assisted detection of CC1, p-NF-kB p65, NF-kB p65, and b-actin. The relative intensity ratio of p- NF-kB p65/NF-kB p65 (n ¼ 3/group) is shown. Data are shown as mean ± standard error of the mean. ***P < .001, Student t test.

Techniques: Staining, Reverse Transcription, Polymerase Chain Reaction, Gene Expression, Western Blot

Figure 6. Perioperative increase of CC1 promotes anti-inﬂammatory phenotype in human OLT. (A) Pretransplant (after cold storage) and posttransplant (2 hours after reperfusion) hepatic biopsy specimens were collected from OLT patients. Post-/pre- CC1 ratios were analyzed at the gene (n ¼ 27) and protein (n ¼ 50) levels. Relationship between post-/pre-CC1 gene ratio and (B) CD154, CD28, IFN-gamma, and IL-17, (C) TLR2, TLR4, TLR9, and CD68, and (D) cathepsin G and HO-1 gene expression with b-actin normalization (n ¼ 27), *P < .05, **P < .01; nonparametric Spearman’s method.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 6. Perioperative increase of CC1 promotes anti-inﬂammatory phenotype in human OLT. (A) Pretransplant (after cold storage) and posttransplant (2 hours after reperfusion) hepatic biopsy specimens were collected from OLT patients. Post-/pre- CC1 ratios were analyzed at the gene (n ¼ 27) and protein (n ¼ 50) levels. Relationship between post-/pre-CC1 gene ratio and (B) CD154, CD28, IFN-gamma, and IL-17, (C) TLR2, TLR4, TLR9, and CD68, and (D) cathepsin G and HO-1 gene expression with b-actin normalization (n ¼ 27), *P < .05, **P < .01; nonparametric Spearman’s method.

Techniques: Gene Expression

Figure 7. Perioperative increase of CC1 attenuates hepatocellular injury and improves rejection-free human OLT survival. Post-/pre- CC1 ratios were assessed by Western blots with b-actin normalization. (A) OLT patients were divided into low (n ¼ 25) and high (n ¼ 25) post-/pre-CC1 ratio groups, based on the median value of the CC1 ratio (cutoff ¼ 1.05). (B) Representative Western blots and case patient-related clinical parameters (case patients 1 and 2: low post-/pre-CC1 ratio, case patients 3 and 4: high post-/pre-CC1 ratio). (C) sAST/sALT at POD 17. (D) Representative CD4/CC1 staining in OLT. Arrows: CC1-negative CD4þ T cells; arrowheads: CC1-positive CD4þ T cells. Scale bars ¼ 100 mm. DAPI, 40,6-diamidino-2-phenylindole. (E) Incidence of EAD. (F) The cumulative rejection rate (Kaplan-Meier method). The solid line indicates high and dotted line low post-/pre-CC1 ratio in human OLT. Data shown as mean ± standard error of the mean. *P < .05, Mann-Whitney U test in C, Fisher’s exact test in E, and log-rank test in F.

Journal: Gastroenterology

Article Title: T Cell CEACAM1-TIM-3 Crosstalk Alleviates Liver Transplant Injury in Mice and Humans.

doi: 10.1053/j.gastro.2023.07.004

Figure Lengend Snippet: Figure 7. Perioperative increase of CC1 attenuates hepatocellular injury and improves rejection-free human OLT survival. Post-/pre- CC1 ratios were assessed by Western blots with b-actin normalization. (A) OLT patients were divided into low (n ¼ 25) and high (n ¼ 25) post-/pre-CC1 ratio groups, based on the median value of the CC1 ratio (cutoff ¼ 1.05). (B) Representative Western blots and case patient-related clinical parameters (case patients 1 and 2: low post-/pre-CC1 ratio, case patients 3 and 4: high post-/pre-CC1 ratio). (C) sAST/sALT at POD 17. (D) Representative CD4/CC1 staining in OLT. Arrows: CC1-negative CD4þ T cells; arrowheads: CC1-positive CD4þ T cells. Scale bars ¼ 100 mm. DAPI, 40,6-diamidino-2-phenylindole. (E) Incidence of EAD. (F) The cumulative rejection rate (Kaplan-Meier method). The solid line indicates high and dotted line low post-/pre-CC1 ratio in human OLT. Data shown as mean ± standard error of the mean. *P < .05, Mann-Whitney U test in C, Fisher’s exact test in E, and log-rank test in F.

Techniques: Western Blot, Staining, MANN-WHITNEY

Journal: Neural Regeneration Research

Article Title: Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke

doi: 10.4103/1673-5374.330611

Figure Lengend Snippet: Effects of EA stimulation on NG2-expressing cell types in the perilesional striatum and the corpus callosum of mice at 21 days after MCAO . Photomicrographs (A) and histograms (B and C) showing labeling and quantification of NG2 (green) -, CC1 (red) -, CD31 (red) - and CD68 (red) -positive cells in the perilesional striatum and the corpus callosum of MCAO mice. EA stimulation significantly increased the NG2 and CD68double positive cells in the perilesional striatum. n = 6. All data are shown as mean ± SEM. ## P < 0.01, vs . MCAO group; & P < 0.05, vs . MCAO + EA1 group (one-way analysis of variance with Tukey's post hoc tests). Scale bar in A: 20 μm. DAPI: 4′,6-Diamidino-2-phenylindole; EA1: electroacupuncture at 1 mA; MCAO: middle cerebral artery occlusion; NG2: neural/glial antigen 2.

Article Snippet: The samples were then incubated with following primary antibodies: mouse anti-green fluorescent protein (GFP; 1:100, Cat# 2955, Cell Signaling), rabbit anti-GFP (1:100, Cat# G10362, Invitrogen), rat anti-BrdU (1:100, Cat# ab6326, Abcam), rabbit anti-CC1 (1:100, Cat# ab40778, Abcam), rat anti-CD31 (1:100, Cat# 550274, BD Biosciences, San Jose, CA, USA), mouse anti-CD68 (1:100, Cat# MCA1957, AbD Serotec), rabbit anti-BDNF (1:100, Cat# ab108319, Abcam), or mouse anti-GSK3β (1:100, Cat# ab93926, Abcam), and counterstained with 4′,6-diamidino-2-phenylindole (DAPI, H3570, Invitrogen) to label cell nuclei.

Techniques: Expressing, Labeling

Journal: Neural Regeneration Research

Article Title: Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke

doi: 10.4103/1673-5374.330611

Figure Lengend Snippet: Effects of EA stimulation on cellular phenotype and the expression of BDNF and GSK3β in GFP + /DAPI + NG2-expressing cells, or whole cells in ipsilateral perilesional striatum of NG2-mEGFP mice at 21 days after MCAO . Quantitative analysis of the flow cytometry data (A and C) and histograms showing the percentage of GFP + /DAPI + cells also expressing BrdU, CC1, CD31, CD68, and GSK3β, as well as the percentage of DAPI + cells also expressing BDNF (B and D, respectively). The numbers of GFP + cells that also express BrdU, CC1, CD31and GSKβ were significantly increased after EA1 stimulation. n = 5. All data are shown as mean ± SEM. # P < 0.05, ## P < 0.01, and ### P < 0.01, vs . MCAO group (independent samples t -test). BDNF: Brain-derived neurotrophic factor; BrdU: bromodeoxyuridine; DAPI: 4′,6-Diamidino-2-phenylindole; EA1: Electroacupuncture at 1 mAEA1: electroacupuncture at 1 mA; GFP: green fluorescent protein; GSK3β: glycogen synthase kinase 3 beta; MCAO: middle cerebral artery occlusion; mEGFP: mutated enhanced green fluorescent protein; NG2: neural/glial antigen 2.

Techniques: Expressing, Flow Cytometry, Derivative Assay

Matrilin-2 and Inhibin A immunofluorescence in white matter stroke. a, Matrilin-2 (Matn2) and Inhibinα (InhA) immunofluorescence in control white matter, colocalized with makers of OPCs (PDGFRα), astrocytes (GFAP), and mature OLs (CC1). Matn2 and InhA levels are low in control white matter. b, Matn2 staining is prominent 5 d after stroke and colocalizes extensively with PDGFRα. InhA staining remains low in 5 d after white matter stroke. c, Matn2 staining is decreased to levels near control white matter at 15 d after stroke. InhA staining is increased and localizes with GFAP+ cellular elements.

Journal: The Journal of Neuroscience

Article Title: White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery

doi: 10.1523/JNEUROSCI.0103-19.2019

Figure Lengend Snippet: Matrilin-2 and Inhibin A immunofluorescence in white matter stroke. a, Matrilin-2 (Matn2) and Inhibinα (InhA) immunofluorescence in control white matter, colocalized with makers of OPCs (PDGFRα), astrocytes (GFAP), and mature OLs (CC1). Matn2 and InhA levels are low in control white matter. b, Matn2 staining is prominent 5 d after stroke and colocalizes extensively with PDGFRα. InhA staining remains low in 5 d after white matter stroke. c, Matn2 staining is decreased to levels near control white matter at 15 d after stroke. InhA staining is increased and localizes with GFAP+ cellular elements.

Article Snippet: Primary antibodies were as follows (in alphabetical order): rabbit anti-6xHis antibody (Abcam, 1:1000), rabbit anti-Activin Receptor type IIA (ActRIIA, Abcam, 1:200), rabbit anti-Aldh1 (1:1000, Abcam), mouse anti-βIV-spectrin (1:200, Neuromab), rabbit anti-Caspr (1:500, Abcam), mouse anti-CC1 (1:200, Abcam), rabbit anti CC1 (1:100, EMD Millipore), chicken anti-GFP (1:1000, Abcam), goat anti-GFP (1:5000, gift from Dr. Nathaniel Heintz, Rockefeller University), mouse anti-glutamine synthetase (Millipore, 1:500), rabbit and goat anti-GSTπ (both 1:500, Abcam), rabbit anti-Iba1 (1:1000, Wako Chemicals), mouse anti-human Inhibinα (1:100, Abcam), rabbit anti-mouse Inhibinα (1:500, Abcam), rabbit anti-Matrilin-2 (1:200, Abcam; and 1:100, Santa Cruz Biotechnology), chicken anti-mCherry (Novus Biologicals, 1:500), rat anti-myelin basic protein (MBP, 1:1000, EMD Millipore), rabbit anti-NG2 (1:200, EMD Millipore), mouse anti-Olig1 (EMD Millipore), rat anti-Olig1 (gift from Dr. Bennett Novitch, UCLA), and rabbit anti-Olig2 (1:500, EMD Millipore).

Techniques: Immunofluorescence, Staining

Analysis of stroke OPC transcriptome. a, Molecular pathway analysis of differentially regulated genes in 5 d, 15 d, 15 d versus 5 d stroke OPC transcriptomes. All genes are FDR ≤ 0.1. Red represents upregulation. Green represents downregulation. The fold change (log2) for each gene is indicated below the gene symbol. Several genes are hubs in their links within these networks, such as RXRa and PTEN in day 5, CSF2, and IGF1 in day 15, and Fyn and PKC in day 15 versus day 5. Dotted lines indicate indirect relationship, in which an association is reported in the literature but not a mechanistic role. b, Confirmatory qPCR analysis of select differentially regulated genes from RNAseq dataset of 5 and 15 d stroke OPC transcriptomes; 5 and 15 d qPCR columns show fold change relative to expression of that gene in control (nonstroke) subcortical white matter OPCs. p value columns are two-tailed t test comparisons between 5 or 15 d versus control. c, Immunohistochemical staining for Cox2 (PTGS1), UBN1, and CSF2 15 d after stroke. Cox2 colocalization with markers of OL-lineage cells (Olig2) and mature OLs (CC1) and Cox2 colocalization with a marker of mature astrocytes (glutamine synthetase). UBN1 colocalization with Olig2. CSF2/Olig 2 and overlap in the same microscopic field. The box in the overlap image is enlarged in the rightmost panel. Scale bar, 20 μm. d, List of most significantly associated upstream regulators that are predicted to induce genes in the day 5 and day 15 OPC stroke transcriptomes, and that would induce genes that are significantly different in day 5 to day 15. p value is Fisher's exact test and indicates that a given upstream regulators has a significant predicted interaction with the transcriptome. The activation score indicates the strength of the induction or inhibition of a set of downstream genes from a particular upstream regulator.

Journal: The Journal of Neuroscience

Article Title: White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery

doi: 10.1523/JNEUROSCI.0103-19.2019

Figure Lengend Snippet: Analysis of stroke OPC transcriptome. a, Molecular pathway analysis of differentially regulated genes in 5 d, 15 d, 15 d versus 5 d stroke OPC transcriptomes. All genes are FDR ≤ 0.1. Red represents upregulation. Green represents downregulation. The fold change (log2) for each gene is indicated below the gene symbol. Several genes are hubs in their links within these networks, such as RXRa and PTEN in day 5, CSF2, and IGF1 in day 15, and Fyn and PKC in day 15 versus day 5. Dotted lines indicate indirect relationship, in which an association is reported in the literature but not a mechanistic role. b, Confirmatory qPCR analysis of select differentially regulated genes from RNAseq dataset of 5 and 15 d stroke OPC transcriptomes; 5 and 15 d qPCR columns show fold change relative to expression of that gene in control (nonstroke) subcortical white matter OPCs. p value columns are two-tailed t test comparisons between 5 or 15 d versus control. c, Immunohistochemical staining for Cox2 (PTGS1), UBN1, and CSF2 15 d after stroke. Cox2 colocalization with markers of OL-lineage cells (Olig2) and mature OLs (CC1) and Cox2 colocalization with a marker of mature astrocytes (glutamine synthetase). UBN1 colocalization with Olig2. CSF2/Olig 2 and overlap in the same microscopic field. The box in the overlap image is enlarged in the rightmost panel. Scale bar, 20 μm. d, List of most significantly associated upstream regulators that are predicted to induce genes in the day 5 and day 15 OPC stroke transcriptomes, and that would induce genes that are significantly different in day 5 to day 15. p value is Fisher's exact test and indicates that a given upstream regulators has a significant predicted interaction with the transcriptome. The activation score indicates the strength of the induction or inhibition of a set of downstream genes from a particular upstream regulator.

Techniques: Expressing, Two Tailed Test, Immunohistochemical staining, Staining, Marker, Activation Assay, Inhibition

Colocalization of candidate Inhibin A receptors to OPCs or OLs. a, OPC reporter mouse (NG2-CreERT2/R26 YFP) (Sozmen et al., 2016) and activin receptor IIa immunostaining. b, Colocalization of the mature OL protein CC1 and Ig superfamily member 1 (IGSF1)/inhibin binding protein/p120. All photomicrographs taken at 7 d after stroke. Scale bar, 100 μm. c, d, Quantification of percent immunopositive staining for ActRIIa and IGSF-1 in Olig2+ cells in control and after stroke. There is no statistically significant difference across conditions.

Journal: The Journal of Neuroscience

Article Title: White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery

doi: 10.1523/JNEUROSCI.0103-19.2019

Figure Lengend Snippet: Colocalization of candidate Inhibin A receptors to OPCs or OLs. a, OPC reporter mouse (NG2-CreERT2/R26 YFP) (Sozmen et al., 2016) and activin receptor IIa immunostaining. b, Colocalization of the mature OL protein CC1 and Ig superfamily member 1 (IGSF1)/inhibin binding protein/p120. All photomicrographs taken at 7 d after stroke. Scale bar, 100 μm. c, d, Quantification of percent immunopositive staining for ActRIIa and IGSF-1 in Olig2+ cells in control and after stroke. There is no statistically significant difference across conditions.

Techniques: Immunostaining, Binding Assay, Staining

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1) Product Images from "Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke"

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