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rabbit anti human ca1 antibody  (Novus Biologicals)


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    Structured Review

    Novus Biologicals rabbit anti human ca1 antibody
    Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) <t>CA1</t> protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.
    Rabbit Anti Human Ca1 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti human ca1 antibody/product/Novus Biologicals
    Average 90 stars, based on 2 article reviews
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    Images

    1) Product Images from "Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease."

    Article Title: Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease.

    Journal: Cellular and molecular gastroenterology and hepatology

    doi: 10.1016/j.jcmgh.2020.06.005

    Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) CA1 protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.
    Figure Legend Snippet: Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) CA1 protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.

    Techniques Used: Cell Differentiation, Gene Expression, Derivative Assay, Cell Culture, Expressing, Marker, Isolation, Immunohistochemistry, Comparison, MANN-WHITNEY



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    Novus Biologicals rabbit anti human ca1 antibody
    Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) <t>CA1</t> protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.
    Rabbit Anti Human Ca1 Antibody, supplied by Novus Biologicals, 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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    Servicebio Inc rabbit anti-mouse ca1 antibody
    Establishment of <t>CA1</t> KI ApoE [−/−] C57BL/6 mice via the CRISPR/Cas9 gene re-editing technique. A. Diagram of the establishment of KI mice with CA1 cDNA inserts. An expression cassette with a CAG promoter and CA1-encoding gene was inserted into intron 1 of the Rosa26 locus in the C57BL/6 mouse chromosome via the CRISPR/Cas9 system. B. Representative PCR images showing the successful establishment of CA1-overexpressing KI mice. a. PCR with primer set 1 yielded one band of 296 bp in KI mice. b. PCR with primer set 2 yielded one band of 335 bp in KI mice. c. PCR with primer set 3 yielded one band of 245 bp in the KI mice. KI: knock-in mice; WT: wild type; M: molecular size marker of DNA.
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    Cusabio rabbit polyclonal ca1
    A Light microscopy images of organoids (patient #110) cultured for 72 h in DIFF, BMP4, DBZ or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bar, 500 μm. B RT-qPCR analysis of the RNA levels of enterocytic ( KRT20 , <t>CA1</t> , KLF4 and FABP2 ) and mucosecretory ( AGR2 , TFF2 and TFF3 ) genes in organoids from patients #47, #86, #110, #130 for 48 h and #47, #110, #130, #159 for 72 h cultured in DIFF (red), BMP4 (blue), DBZ (orange) or B + D (green) media in the absence (vehicle) or presence of calcitriol (100 nM). * P < 0.05, ** P < 0.01, *** P < 0.001. C RT-qPCR analysis of the RNA levels of stemness genes in organoids from the same patients and in the same conditions as in B. D Western blot analysis and quantification of the effect of calcitriol on the expression of enterocytic (CA1) and mucosecretory (TFF2) marker proteins in organoids from four patients incubated in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM) for 48 h. The stemness PTK7 protein was used as control of differentiation and GAPDH as loading control. * P < 0.05. E Immunofluorescence analysis of the expression of enterocytic and mucosecretory protein markers in organoids (patient #158) cultured for 48 h in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bars, 30 µm. Box-plots show the quantification of fluorescence intensity (Log 2 MGV) (patients #92, #158 and #166; the number of organoids analyzed was 68 for KLF4, 104 for KRT19, 110 for AGR2 and 79 for TFF2). ** P < 0.01, *** P < 0.001. F Western blot analysis and quantification of the level of phospho(P)-SMAD1/5/8 in organoid cultures that were incubated for 24 h with calcitriol (100 nM) or vehicle before incubation in DIFF medium or BMP4 medium (50 ng/mL) during the indicated times. MGV: mean gray value.
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    Cusabio anti ca1
    A Light microscopy images of organoids (patient #110) cultured for 72 h in DIFF, BMP4, DBZ or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bar, 500 μm. B RT-qPCR analysis of the RNA levels of enterocytic ( KRT20 , <t>CA1</t> , KLF4 and FABP2 ) and mucosecretory ( AGR2 , TFF2 and TFF3 ) genes in organoids from patients #47, #86, #110, #130 for 48 h and #47, #110, #130, #159 for 72 h cultured in DIFF (red), BMP4 (blue), DBZ (orange) or B + D (green) media in the absence (vehicle) or presence of calcitriol (100 nM). * P < 0.05, ** P < 0.01, *** P < 0.001. C RT-qPCR analysis of the RNA levels of stemness genes in organoids from the same patients and in the same conditions as in B. D Western blot analysis and quantification of the effect of calcitriol on the expression of enterocytic (CA1) and mucosecretory (TFF2) marker proteins in organoids from four patients incubated in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM) for 48 h. The stemness PTK7 protein was used as control of differentiation and GAPDH as loading control. * P < 0.05. E Immunofluorescence analysis of the expression of enterocytic and mucosecretory protein markers in organoids (patient #158) cultured for 48 h in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bars, 30 µm. Box-plots show the quantification of fluorescence intensity (Log 2 MGV) (patients #92, #158 and #166; the number of organoids analyzed was 68 for KLF4, 104 for KRT19, 110 for AGR2 and 79 for TFF2). ** P < 0.01, *** P < 0.001. F Western blot analysis and quantification of the level of phospho(P)-SMAD1/5/8 in organoid cultures that were incubated for 24 h with calcitriol (100 nM) or vehicle before incubation in DIFF medium or BMP4 medium (50 ng/mL) during the indicated times. MGV: mean gray value.
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    Proteintech rabbit anti car1
    A Light microscopy images of organoids (patient #110) cultured for 72 h in DIFF, BMP4, DBZ or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bar, 500 μm. B RT-qPCR analysis of the RNA levels of enterocytic ( KRT20 , <t>CA1</t> , KLF4 and FABP2 ) and mucosecretory ( AGR2 , TFF2 and TFF3 ) genes in organoids from patients #47, #86, #110, #130 for 48 h and #47, #110, #130, #159 for 72 h cultured in DIFF (red), BMP4 (blue), DBZ (orange) or B + D (green) media in the absence (vehicle) or presence of calcitriol (100 nM). * P < 0.05, ** P < 0.01, *** P < 0.001. C RT-qPCR analysis of the RNA levels of stemness genes in organoids from the same patients and in the same conditions as in B. D Western blot analysis and quantification of the effect of calcitriol on the expression of enterocytic (CA1) and mucosecretory (TFF2) marker proteins in organoids from four patients incubated in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM) for 48 h. The stemness PTK7 protein was used as control of differentiation and GAPDH as loading control. * P < 0.05. E Immunofluorescence analysis of the expression of enterocytic and mucosecretory protein markers in organoids (patient #158) cultured for 48 h in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bars, 30 µm. Box-plots show the quantification of fluorescence intensity (Log 2 MGV) (patients #92, #158 and #166; the number of organoids analyzed was 68 for KLF4, 104 for KRT19, 110 for AGR2 and 79 for TFF2). ** P < 0.01, *** P < 0.001. F Western blot analysis and quantification of the level of phospho(P)-SMAD1/5/8 in organoid cultures that were incubated for 24 h with calcitriol (100 nM) or vehicle before incubation in DIFF medium or BMP4 medium (50 ng/mL) during the indicated times. MGV: mean gray value.
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    Novus Biologicals rabbit ca1
    ( A, B, C ) Activation of biological processes at different stages of the disease assessed by Ingenuity Pathway Analysis (IPA). Heat maps represent activation z-score change over the course of disease progression and indicate pathways that are activated at 6M ( A ), 12M ( B ) and 18M ( C ). Data were obtained from four biological replicates per group for each time point. Z-score is calculated based on experimental protein expression data (log 2 AD/control ratio) and the theoretical information stored in the IPA Knowledge Base. Positive value of z-score indicates an activation of biological pathway or function. Distribution of the quantified proteins at 2M ( D ), 6M ( E ), 12M ( F ) and 18M ( G ) based on log 2 ratio AD/Control and p-value (t-test) by time point. The pie charts represent the number of quantified non-regulated proteins (grey), significantly different proteins between 3×Tg-AD and control samples, t-test p-value 0.05 (pink) and significantly regulated proteins with more than 50% expression change in comparison to the control (red). ( H–I ) Dynamics of protein expression over the course of AD progression for a selection of the most regulated proteins based on their function. Proteins involved in mRNA processing and transport ( H ) that are upregulated over time and serine protease inhibitors ( I ) that are downregulated. ( J–M ) Putative presymptomatic protein markers of the disease. ( J ) Top 10 significantly up- and downregulated proteins in 3×Tg-AD mice at presymptomatic time point (2M). ( K ) Immunoblot analysis of most regulated hits. Soluble fractions of brain proteins were analyzed from four 2-month-old control and 3×Tg-AD mice animals, respectively. Hebp1 and Glo1 levels were consistently elevated in the transgenic animals as compared to wild type controls. <t>Ca1</t> levels were reduced in transgenic animals. Presymptomatic markers that remain up- ( L ) or downregulated ( M ) across the AD progression. 10.7554/eLife.47498.007 Figure 2—source data 1. Full list of quantified proteins in the soluble brain fraction of 3×Tg-AD and wild-type mice.
    Rabbit Ca1, supplied by Novus Biologicals, 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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    Image Search Results


    Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) CA1 protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.

    Journal: Cellular and molecular gastroenterology and hepatology

    Article Title: Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Epithelial Barrier Integrity in Patients With Crohn's Disease.

    doi: 10.1016/j.jcmgh.2020.06.005

    Figure Lengend Snippet: Figure 5. BMP9–ALK1 signaling is associated with epithelial cell differentiation toward colonocytes. (A) Lineage-specific gene expression in NIBD patient-derived colonic epithelial cell monolayers. Expanded cells were cultured in expansion media in the presence or absence of BMP9 and ALK1–Fc chimera protein. Each gene expression was normalized to RPLP0 (N ¼ 6 per group). (B) CA1 protein expression in NIBD patient-derived colonic epithelial monolayers (N ¼ 4 per group). (C) Colonocyte marker expression in colonic epithelial cells isolated from CD patients (N ¼ 15) and NIBD controls (N ¼ 12). Each gene expression was normalized to GAPDH. (D) CA1 expression by immunohistochemistry in the colonic mucosa of NIBD controls (left) and CD patients (right). (E) CA1 protein expression in the colonic mucosa of NIBD controls and CD patients (N ¼ 5 per group). *P < .05, **P < .01, ***P < .001, and ****P < .0001. P values were determined by the (A and B) Friedman test followed by the Dunn multiple comparison test, or the (C and E) Mann–Whitney test.

    Article Snippet: Rabbit anti-human CA1 antibody was obtained from Novus Biologicals (NBP1-88191).

    Techniques: Cell Differentiation, Gene Expression, Derivative Assay, Cell Culture, Expressing, Marker, Isolation, Immunohistochemistry, Comparison, MANN-WHITNEY

    Establishment of CA1 KI ApoE [−/−] C57BL/6 mice via the CRISPR/Cas9 gene re-editing technique. A. Diagram of the establishment of KI mice with CA1 cDNA inserts. An expression cassette with a CAG promoter and CA1-encoding gene was inserted into intron 1 of the Rosa26 locus in the C57BL/6 mouse chromosome via the CRISPR/Cas9 system. B. Representative PCR images showing the successful establishment of CA1-overexpressing KI mice. a. PCR with primer set 1 yielded one band of 296 bp in KI mice. b. PCR with primer set 2 yielded one band of 335 bp in KI mice. c. PCR with primer set 3 yielded one band of 245 bp in the KI mice. KI: knock-in mice; WT: wild type; M: molecular size marker of DNA.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Establishment of CA1 KI ApoE [−/−] C57BL/6 mice via the CRISPR/Cas9 gene re-editing technique. A. Diagram of the establishment of KI mice with CA1 cDNA inserts. An expression cassette with a CAG promoter and CA1-encoding gene was inserted into intron 1 of the Rosa26 locus in the C57BL/6 mouse chromosome via the CRISPR/Cas9 system. B. Representative PCR images showing the successful establishment of CA1-overexpressing KI mice. a. PCR with primer set 1 yielded one band of 296 bp in KI mice. b. PCR with primer set 2 yielded one band of 335 bp in KI mice. c. PCR with primer set 3 yielded one band of 245 bp in the KI mice. KI: knock-in mice; WT: wild type; M: molecular size marker of DNA.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: CRISPR, Expressing, Knock-In, Marker

    Changes in the body weights of the AS model mice. CA1-overexpressing ApoE [−/−] mice and ordinary ApoE [−/−] mice were induced to AS with high-fat food. These patients were divided into the following groups: normal, AS model, AS model with MTZ treatment and AS model with MTZ preventive-treatment. Each group included 15 mice. Mice with CA1 overexpression generally had greater body weights than did those without CA1 overexpression. The weight of the mice with AS was generally greater than that of the mice without AS, and the weight of the mice with AS was reduced following MTZ treatment and MTZ-preventive treatment.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Changes in the body weights of the AS model mice. CA1-overexpressing ApoE [−/−] mice and ordinary ApoE [−/−] mice were induced to AS with high-fat food. These patients were divided into the following groups: normal, AS model, AS model with MTZ treatment and AS model with MTZ preventive-treatment. Each group included 15 mice. Mice with CA1 overexpression generally had greater body weights than did those without CA1 overexpression. The weight of the mice with AS was generally greater than that of the mice without AS, and the weight of the mice with AS was reduced following MTZ treatment and MTZ-preventive treatment.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Over Expression

    Sudan IV staining of mouse cardiac aorta tissues. The number and extent of accumulated lipids in the aorta were semiquantitatively analyzed by calculating lipid accumulation in the whole aorta. The lipid accumulation in the CA1-overexpressing mice was much greater than that in the mice without CA1 overexpression. MTZ treatment significantly decreased the quantity and volume of lipid accumulation. ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001, and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Sudan IV staining of mouse cardiac aorta tissues. The number and extent of accumulated lipids in the aorta were semiquantitatively analyzed by calculating lipid accumulation in the whole aorta. The lipid accumulation in the CA1-overexpressing mice was much greater than that in the mice without CA1 overexpression. MTZ treatment significantly decreased the quantity and volume of lipid accumulation. ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001, and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Staining, Over Expression

    HE staining of mouse cardiac aorta tissues. The extent and composition of the aortic lesions were semiquantified by calculating the surface plaque area across the entire aortic area. The number of aortic plaques and wall thickness in CA1-overexpressing mice were greater than those in mice without CA1 overexpression. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: HE staining of mouse cardiac aorta tissues. The extent and composition of the aortic lesions were semiquantified by calculating the surface plaque area across the entire aortic area. The number of aortic plaques and wall thickness in CA1-overexpressing mice were greater than those in mice without CA1 overexpression. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Staining, Over Expression

    Oil Red O staining of mouse cardiac aorta tissues. The number and size of fat deposits were semiquantitatively analyzed. Fat deposition in cardiac aorta tissues was greater in CA1-overexpressing mice with AS than in mice with AS without CA1 overexpression. MTZ treatment significantly decreased the volume and number of fat deposits. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Oil Red O staining of mouse cardiac aorta tissues. The number and size of fat deposits were semiquantitatively analyzed. Fat deposition in cardiac aorta tissues was greater in CA1-overexpressing mice with AS than in mice with AS without CA1 overexpression. MTZ treatment significantly decreased the volume and number of fat deposits. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Staining, Over Expression

    Biochemical examination of mouse peripheral blood. Compared with those in healthy controls, HDL levels were significantly lower, and AI, LDL, TC and TG levels were elevated in AS mice. The levels of these indices were restored after MTZ treatment. Moreover, the HDL level was significantly lower and the levels of AI, LDL, TC and TG were greater in CA1-overexpressing mice than in ApoE [−/−] mice with normal CA1 expression, regardless of whether these mice were induced to develop AS or treated with MTZ. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Biochemical examination of mouse peripheral blood. Compared with those in healthy controls, HDL levels were significantly lower, and AI, LDL, TC and TG levels were elevated in AS mice. The levels of these indices were restored after MTZ treatment. Moreover, the HDL level was significantly lower and the levels of AI, LDL, TC and TG were greater in CA1-overexpressing mice than in ApoE [−/−] mice with normal CA1 expression, regardless of whether these mice were induced to develop AS or treated with MTZ. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Expressing

    Immunostaining of CA1 expression in mouse aortic tissues. Immunohistochemistry revealed CA1 expression (brown) in the aortic plaques of the animals with AS (↓). CA1 was also weakly expressed in aortic VSMCs (↓↓). Immunofluorescent immunohistochemistry revealed that CA1 levels were increased in the cardiac aorta tissues of CA1-overexpressing ApoE [−/−] mice, regardless of whether the KI mice had induced AS, compared with those of ordinary ApoE [−/−] mice. The quantified signal is normalized to the total cellularized area. ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Immunostaining of CA1 expression in mouse aortic tissues. Immunohistochemistry revealed CA1 expression (brown) in the aortic plaques of the animals with AS (↓). CA1 was also weakly expressed in aortic VSMCs (↓↓). Immunofluorescent immunohistochemistry revealed that CA1 levels were increased in the cardiac aorta tissues of CA1-overexpressing ApoE [−/−] mice, regardless of whether the KI mice had induced AS, compared with those of ordinary ApoE [−/−] mice. The quantified signal is normalized to the total cellularized area. ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Immunostaining, Expressing, Immunohistochemistry

    Calcification of mouse cardiac aorta tissues via Von Kossa staining. Extensive calcium deposition was detected in cardiac aorta tissues from CA1-overexpressing AS and AS mice following MTZ treatment. Little calcification was observed in the aortic tissues of ordinary ApoE [−/−] mice with induced AS.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Calcification of mouse cardiac aorta tissues via Von Kossa staining. Extensive calcium deposition was detected in cardiac aorta tissues from CA1-overexpressing AS and AS mice following MTZ treatment. Little calcification was observed in the aortic tissues of ordinary ApoE [−/−] mice with induced AS.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Staining

    Immunofluorescence analysis of macrophages in mouse cardiac aorta tissues. The aortic tissues were stained with DAPI (blue). CD86 (green) represents the M1 macrophage subtype, and CD163 (yellow) represents the M2 macrophage subtype. The expression levels of CD86 were semiquantitatively analyzed. Higher CD86 expression was detected in the aortic tissues of CA1-overexpressing mice than in those of ordinary Apoe [−/−] mice. Increased CD86 expression was detected in the aortic tissues of both CA1-overexpressing mice and ordinary ApoE [−/−] mice when they were induced to AS. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Journal: Atherosclerosis Plus

    Article Title: ApoE [−/−] CA1-overexpressing knock-in mice aggravated atherosclerosis by increasing M1 macrophages

    doi: 10.1016/j.athplu.2025.03.003

    Figure Lengend Snippet: Immunofluorescence analysis of macrophages in mouse cardiac aorta tissues. The aortic tissues were stained with DAPI (blue). CD86 (green) represents the M1 macrophage subtype, and CD163 (yellow) represents the M2 macrophage subtype. The expression levels of CD86 were semiquantitatively analyzed. Higher CD86 expression was detected in the aortic tissues of CA1-overexpressing mice than in those of ordinary Apoe [−/−] mice. Increased CD86 expression was detected in the aortic tissues of both CA1-overexpressing mice and ordinary ApoE [−/−] mice when they were induced to AS. ∗ indicates P < 0.05, ∗∗ indicates P < 0.01, ∗∗∗ indicates P < 0.001 and ∗∗∗∗ indicates P < 0.0001.

    Article Snippet: Rabbit anti-mouse CA1 antibody was obtained from Servicebio (China).

    Techniques: Immunofluorescence, Staining, Expressing

    A Light microscopy images of organoids (patient #110) cultured for 72 h in DIFF, BMP4, DBZ or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bar, 500 μm. B RT-qPCR analysis of the RNA levels of enterocytic ( KRT20 , CA1 , KLF4 and FABP2 ) and mucosecretory ( AGR2 , TFF2 and TFF3 ) genes in organoids from patients #47, #86, #110, #130 for 48 h and #47, #110, #130, #159 for 72 h cultured in DIFF (red), BMP4 (blue), DBZ (orange) or B + D (green) media in the absence (vehicle) or presence of calcitriol (100 nM). * P < 0.05, ** P < 0.01, *** P < 0.001. C RT-qPCR analysis of the RNA levels of stemness genes in organoids from the same patients and in the same conditions as in B. D Western blot analysis and quantification of the effect of calcitriol on the expression of enterocytic (CA1) and mucosecretory (TFF2) marker proteins in organoids from four patients incubated in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM) for 48 h. The stemness PTK7 protein was used as control of differentiation and GAPDH as loading control. * P < 0.05. E Immunofluorescence analysis of the expression of enterocytic and mucosecretory protein markers in organoids (patient #158) cultured for 48 h in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bars, 30 µm. Box-plots show the quantification of fluorescence intensity (Log 2 MGV) (patients #92, #158 and #166; the number of organoids analyzed was 68 for KLF4, 104 for KRT19, 110 for AGR2 and 79 for TFF2). ** P < 0.01, *** P < 0.001. F Western blot analysis and quantification of the level of phospho(P)-SMAD1/5/8 in organoid cultures that were incubated for 24 h with calcitriol (100 nM) or vehicle before incubation in DIFF medium or BMP4 medium (50 ng/mL) during the indicated times. MGV: mean gray value.

    Journal: Cell Death & Disease

    Article Title: Vitamin D opposes multilineage cell differentiation induced by Notch inhibition and BMP4 pathway activation in human colon organoids

    doi: 10.1038/s41419-024-06680-z

    Figure Lengend Snippet: A Light microscopy images of organoids (patient #110) cultured for 72 h in DIFF, BMP4, DBZ or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bar, 500 μm. B RT-qPCR analysis of the RNA levels of enterocytic ( KRT20 , CA1 , KLF4 and FABP2 ) and mucosecretory ( AGR2 , TFF2 and TFF3 ) genes in organoids from patients #47, #86, #110, #130 for 48 h and #47, #110, #130, #159 for 72 h cultured in DIFF (red), BMP4 (blue), DBZ (orange) or B + D (green) media in the absence (vehicle) or presence of calcitriol (100 nM). * P < 0.05, ** P < 0.01, *** P < 0.001. C RT-qPCR analysis of the RNA levels of stemness genes in organoids from the same patients and in the same conditions as in B. D Western blot analysis and quantification of the effect of calcitriol on the expression of enterocytic (CA1) and mucosecretory (TFF2) marker proteins in organoids from four patients incubated in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM) for 48 h. The stemness PTK7 protein was used as control of differentiation and GAPDH as loading control. * P < 0.05. E Immunofluorescence analysis of the expression of enterocytic and mucosecretory protein markers in organoids (patient #158) cultured for 48 h in PROL or B + D media in the absence (vehicle) or presence of calcitriol (100 nM). Scale bars, 30 µm. Box-plots show the quantification of fluorescence intensity (Log 2 MGV) (patients #92, #158 and #166; the number of organoids analyzed was 68 for KLF4, 104 for KRT19, 110 for AGR2 and 79 for TFF2). ** P < 0.01, *** P < 0.001. F Western blot analysis and quantification of the level of phospho(P)-SMAD1/5/8 in organoid cultures that were incubated for 24 h with calcitriol (100 nM) or vehicle before incubation in DIFF medium or BMP4 medium (50 ng/mL) during the indicated times. MGV: mean gray value.

    Article Snippet: Whole-cell extracts (15–30 μg or 80 μg the case of phospho-SMAD analyses) were separated by SDS-PAGE, transferred to PVDF membranes and incubated with the following primary antibodies: rabbit polyclonal-CA1 (CUSABIO, TX, USA, #CSBPA004364GA01HU), mouse monoclonal-GAPDH (Abcam, Cambridge, UK, #ab8245), rabbit monoclonal-PTK7 (Cell Signalling, MA, USA, #25618), rabbit polyclonal-SMAD1/5/8 (Santa Cruz, TX, USA, #sc6031-R), rabbit monclonal-Phospho-SMAD1/5/8 (Cell Signalling, #9511 S) and rabbit polyclonal-TFF2 (Proteintech, IL, USA, #13681-1-AP).

    Techniques: Light Microscopy, Cell Culture, Quantitative RT-PCR, Western Blot, Expressing, Marker, Incubation, Control, Immunofluorescence, Fluorescence

    ( A, B, C ) Activation of biological processes at different stages of the disease assessed by Ingenuity Pathway Analysis (IPA). Heat maps represent activation z-score change over the course of disease progression and indicate pathways that are activated at 6M ( A ), 12M ( B ) and 18M ( C ). Data were obtained from four biological replicates per group for each time point. Z-score is calculated based on experimental protein expression data (log 2 AD/control ratio) and the theoretical information stored in the IPA Knowledge Base. Positive value of z-score indicates an activation of biological pathway or function. Distribution of the quantified proteins at 2M ( D ), 6M ( E ), 12M ( F ) and 18M ( G ) based on log 2 ratio AD/Control and p-value (t-test) by time point. The pie charts represent the number of quantified non-regulated proteins (grey), significantly different proteins between 3×Tg-AD and control samples, t-test p-value 0.05 (pink) and significantly regulated proteins with more than 50% expression change in comparison to the control (red). ( H–I ) Dynamics of protein expression over the course of AD progression for a selection of the most regulated proteins based on their function. Proteins involved in mRNA processing and transport ( H ) that are upregulated over time and serine protease inhibitors ( I ) that are downregulated. ( J–M ) Putative presymptomatic protein markers of the disease. ( J ) Top 10 significantly up- and downregulated proteins in 3×Tg-AD mice at presymptomatic time point (2M). ( K ) Immunoblot analysis of most regulated hits. Soluble fractions of brain proteins were analyzed from four 2-month-old control and 3×Tg-AD mice animals, respectively. Hebp1 and Glo1 levels were consistently elevated in the transgenic animals as compared to wild type controls. Ca1 levels were reduced in transgenic animals. Presymptomatic markers that remain up- ( L ) or downregulated ( M ) across the AD progression. 10.7554/eLife.47498.007 Figure 2—source data 1. Full list of quantified proteins in the soluble brain fraction of 3×Tg-AD and wild-type mice.

    Journal: eLife

    Article Title: Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity

    doi: 10.7554/eLife.47498

    Figure Lengend Snippet: ( A, B, C ) Activation of biological processes at different stages of the disease assessed by Ingenuity Pathway Analysis (IPA). Heat maps represent activation z-score change over the course of disease progression and indicate pathways that are activated at 6M ( A ), 12M ( B ) and 18M ( C ). Data were obtained from four biological replicates per group for each time point. Z-score is calculated based on experimental protein expression data (log 2 AD/control ratio) and the theoretical information stored in the IPA Knowledge Base. Positive value of z-score indicates an activation of biological pathway or function. Distribution of the quantified proteins at 2M ( D ), 6M ( E ), 12M ( F ) and 18M ( G ) based on log 2 ratio AD/Control and p-value (t-test) by time point. The pie charts represent the number of quantified non-regulated proteins (grey), significantly different proteins between 3×Tg-AD and control samples, t-test p-value 0.05 (pink) and significantly regulated proteins with more than 50% expression change in comparison to the control (red). ( H–I ) Dynamics of protein expression over the course of AD progression for a selection of the most regulated proteins based on their function. Proteins involved in mRNA processing and transport ( H ) that are upregulated over time and serine protease inhibitors ( I ) that are downregulated. ( J–M ) Putative presymptomatic protein markers of the disease. ( J ) Top 10 significantly up- and downregulated proteins in 3×Tg-AD mice at presymptomatic time point (2M). ( K ) Immunoblot analysis of most regulated hits. Soluble fractions of brain proteins were analyzed from four 2-month-old control and 3×Tg-AD mice animals, respectively. Hebp1 and Glo1 levels were consistently elevated in the transgenic animals as compared to wild type controls. Ca1 levels were reduced in transgenic animals. Presymptomatic markers that remain up- ( L ) or downregulated ( M ) across the AD progression. 10.7554/eLife.47498.007 Figure 2—source data 1. Full list of quantified proteins in the soluble brain fraction of 3×Tg-AD and wild-type mice.

    Article Snippet: The following primary antibodies were used for immunoblotting: rabbit Hebp1 (1:1000, Invitrogen, PA5-30609), mouse Glo1 (1:1000, GeneTex, Irvine, CA, GTX628890), rabbit CA1 (1:250, Novus Biologicals, Abingdon, UK, NBP1-88191), mouse α-tubulin (1:5000, Synaptic Systems, Göttingen, Germany, 302 211), rabbit β-actin (1:5000, Synaptic Systems, 251 003), rabbit GFP (1:5000, Synaptic Systems, 132 002), mouse Rab5 (1:1000, Synaptic Systems, 108 111), rabbit Rab6 (1:1000, Synaptic Systems, 273 003), rabbit Lamp1 (1:500, Abcam, ab24170), mouse Mic60 (1:1000, Abcam, ab110329), rabbit Cox4 (1:1000, Synaptic Systems, 298 002), rabbit Cyt C (1:1000, Cell Signaling, Beverly, MA, USA, 11940S), rabbit caspase 9 (1:1000, Abcam, Cambridge, UK, ab185719), mouse Sodium Potassium ATPase, subunit α1 (1:1000, Abcam, Cambridge, UK, ab7671), mouse syntaxin 1 (1:1000, Synaptic Systems, 110 001), mouse VAMP2 (1:10000, Synaptic Systems, 104 211), rabbit phospho-tau (Ser400;Thr403;Ser404) (1:1000, Cell Signaling, Beverly, MA, USA, 11837S).

    Techniques: Activation Assay, Biomarker Discovery, Expressing, Control, Comparison, Selection, Western Blot, Transgenic Assay

    Identified presymptomatic brain markers of AD in this study.

    Journal: eLife

    Article Title: Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity

    doi: 10.7554/eLife.47498

    Figure Lengend Snippet: Identified presymptomatic brain markers of AD in this study.

    Article Snippet: The following primary antibodies were used for immunoblotting: rabbit Hebp1 (1:1000, Invitrogen, PA5-30609), mouse Glo1 (1:1000, GeneTex, Irvine, CA, GTX628890), rabbit CA1 (1:250, Novus Biologicals, Abingdon, UK, NBP1-88191), mouse α-tubulin (1:5000, Synaptic Systems, Göttingen, Germany, 302 211), rabbit β-actin (1:5000, Synaptic Systems, 251 003), rabbit GFP (1:5000, Synaptic Systems, 132 002), mouse Rab5 (1:1000, Synaptic Systems, 108 111), rabbit Rab6 (1:1000, Synaptic Systems, 273 003), rabbit Lamp1 (1:500, Abcam, ab24170), mouse Mic60 (1:1000, Abcam, ab110329), rabbit Cox4 (1:1000, Synaptic Systems, 298 002), rabbit Cyt C (1:1000, Cell Signaling, Beverly, MA, USA, 11940S), rabbit caspase 9 (1:1000, Abcam, Cambridge, UK, ab185719), mouse Sodium Potassium ATPase, subunit α1 (1:1000, Abcam, Cambridge, UK, ab7671), mouse syntaxin 1 (1:1000, Synaptic Systems, 110 001), mouse VAMP2 (1:10000, Synaptic Systems, 104 211), rabbit phospho-tau (Ser400;Thr403;Ser404) (1:1000, Cell Signaling, Beverly, MA, USA, 11837S).

    Techniques: Binding Assay, Clinical Proteomics, Membrane

    ( A ) Expression of Hebp1 in 12-month-old control and 3×Tg-AD mice by brain region. ( B ) Hebp1 immunostaining of the fronto-temporal cortex depicting primary motor and somatosensory areas and hippocampus (coronal sections). CA1 region is marked with the white dashed line. ( C ) Co-staining of Hebp1 with markers of CA1 and dentate gyrus neurons (Ctip2), astrocytes (GFAP) and microglia (IBA-1) in the hippocampus of 3×Tg-AD mice. Hepb1 is expressed predominantly in Ctip2-positive cells of hippocampus (neurons). All images were acquired from 12-month-old control or 3×Tg-AD mice. Scale bar is 100 µm. All data shown are representative of results obtained from three independent experiments.

    Journal: eLife

    Article Title: Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity

    doi: 10.7554/eLife.47498

    Figure Lengend Snippet: ( A ) Expression of Hebp1 in 12-month-old control and 3×Tg-AD mice by brain region. ( B ) Hebp1 immunostaining of the fronto-temporal cortex depicting primary motor and somatosensory areas and hippocampus (coronal sections). CA1 region is marked with the white dashed line. ( C ) Co-staining of Hebp1 with markers of CA1 and dentate gyrus neurons (Ctip2), astrocytes (GFAP) and microglia (IBA-1) in the hippocampus of 3×Tg-AD mice. Hepb1 is expressed predominantly in Ctip2-positive cells of hippocampus (neurons). All images were acquired from 12-month-old control or 3×Tg-AD mice. Scale bar is 100 µm. All data shown are representative of results obtained from three independent experiments.

    Article Snippet: The following primary antibodies were used for immunoblotting: rabbit Hebp1 (1:1000, Invitrogen, PA5-30609), mouse Glo1 (1:1000, GeneTex, Irvine, CA, GTX628890), rabbit CA1 (1:250, Novus Biologicals, Abingdon, UK, NBP1-88191), mouse α-tubulin (1:5000, Synaptic Systems, Göttingen, Germany, 302 211), rabbit β-actin (1:5000, Synaptic Systems, 251 003), rabbit GFP (1:5000, Synaptic Systems, 132 002), mouse Rab5 (1:1000, Synaptic Systems, 108 111), rabbit Rab6 (1:1000, Synaptic Systems, 273 003), rabbit Lamp1 (1:500, Abcam, ab24170), mouse Mic60 (1:1000, Abcam, ab110329), rabbit Cox4 (1:1000, Synaptic Systems, 298 002), rabbit Cyt C (1:1000, Cell Signaling, Beverly, MA, USA, 11940S), rabbit caspase 9 (1:1000, Abcam, Cambridge, UK, ab185719), mouse Sodium Potassium ATPase, subunit α1 (1:1000, Abcam, Cambridge, UK, ab7671), mouse syntaxin 1 (1:1000, Synaptic Systems, 110 001), mouse VAMP2 (1:10000, Synaptic Systems, 104 211), rabbit phospho-tau (Ser400;Thr403;Ser404) (1:1000, Cell Signaling, Beverly, MA, USA, 11837S).

    Techniques: Expressing, Control, Immunostaining, Staining

    Immunostaining of Hebp1 in the hippocampal region of 3×Tg-AD (27-month-old) and control (24-month-old) mice. Boxed regions in CA1 and dentate gyrus show representative regions where Hebp1 expression was elevated in 3×Tg-AD but not control mice. Scale bar is 500 µm.

    Journal: eLife

    Article Title: Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity

    doi: 10.7554/eLife.47498

    Figure Lengend Snippet: Immunostaining of Hebp1 in the hippocampal region of 3×Tg-AD (27-month-old) and control (24-month-old) mice. Boxed regions in CA1 and dentate gyrus show representative regions where Hebp1 expression was elevated in 3×Tg-AD but not control mice. Scale bar is 500 µm.

    Article Snippet: The following primary antibodies were used for immunoblotting: rabbit Hebp1 (1:1000, Invitrogen, PA5-30609), mouse Glo1 (1:1000, GeneTex, Irvine, CA, GTX628890), rabbit CA1 (1:250, Novus Biologicals, Abingdon, UK, NBP1-88191), mouse α-tubulin (1:5000, Synaptic Systems, Göttingen, Germany, 302 211), rabbit β-actin (1:5000, Synaptic Systems, 251 003), rabbit GFP (1:5000, Synaptic Systems, 132 002), mouse Rab5 (1:1000, Synaptic Systems, 108 111), rabbit Rab6 (1:1000, Synaptic Systems, 273 003), rabbit Lamp1 (1:500, Abcam, ab24170), mouse Mic60 (1:1000, Abcam, ab110329), rabbit Cox4 (1:1000, Synaptic Systems, 298 002), rabbit Cyt C (1:1000, Cell Signaling, Beverly, MA, USA, 11940S), rabbit caspase 9 (1:1000, Abcam, Cambridge, UK, ab185719), mouse Sodium Potassium ATPase, subunit α1 (1:1000, Abcam, Cambridge, UK, ab7671), mouse syntaxin 1 (1:1000, Synaptic Systems, 110 001), mouse VAMP2 (1:10000, Synaptic Systems, 104 211), rabbit phospho-tau (Ser400;Thr403;Ser404) (1:1000, Cell Signaling, Beverly, MA, USA, 11837S).

    Techniques: Immunostaining, Control, Expressing