Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Relative protein expression of mucin 1 (MUC1) in colon mucosa biopsy samples of the control group and MASLD group ( n = 30 per group). b Representative immunofluorescence staining of MUC1 in colon mucosa biopsy samples of control and patients with MASLD. Scale bar, 50 μm. c Correlations between intestinal MUC1 protein expression and BMI, serum TG, TC, ALT, and AST levels in colon mucosa biopsy samples ( n = 60). The correlation analysis was performed using Pearson’s product-moment correlation (two-sided without adjustment). d Relative protein expression of MUC1 in colon tissues of mice fed with ND and HFD for 16 weeks ( n = 6 per group). e Representative immunofluorescence staining of MUC1 in colon tissues of mice fed with ND and HFD for 16 weeks. Scale bar, 50 μm. f Structural schematic diagram of the membrane MUC1 protein. The diagram of the membrane and MUC1 was created in BioRender. Li, Z. (2025) https://BioRender.com/b1gercd and https://BioRender.com/7jqtxz6 . g , h Representative transmission electron microscopy images of the glycocalyx in human colon ( g ) and mouse colon ( h ). Scale bar, 200 nm (left), 100 nm (right). i Schematic diagram of peanut agglutinin (PNA)-specific recognition of O-glycan patterns. The diagram of peanut agglutinin was created in BioRender. Li, Z. (2025) https://BioRender.com/txue94i . Ser (Serine), Thr (Threonine). j The expression levels of O-glycans (PNA) on colonic MUC1 were assessed in both the control group and the patient with MASLD group under conditions of equivalent MUC1 levels. k The expression levels of O-glycans (PNA) on colonic MUC1 were assessed in mice fed with ND and HFD under conditions of equivalent MUC1 levels. Data are presented as mean ± SEM. P -values were calculated by a two-tailed unpaired t -test. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: To induce intestinal Muc1 disruption, Muc1 Flox/Flox and β-catenin Flox/Flox mice were crossed with Villin-Cre mice (kindly provided by Cyagen), resulting in the generation of Muc1 EKO and β-catenin EKO mice.

Techniques: Expressing, Control, Immunofluorescence, Staining, Membrane, Transmission Assay, Electron Microscopy, Glycoproteomics, Two Tailed Test, Western Blot

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Western blot analysis showing the stability of MUC1 after the administration of 50 nM O-glycosidase in complete media for 30 mins follow by cycloheximide (CHX, translation inhibitor) for 24 h in HT-29 cells. b Western blot analysis was performed to detect specified proteins in HT-29 cells that were transfected with deglycosylated MUC1 vectors, specifically MUC1-10TRs or MUC1-5TRs. c Western blots for the indicated proteins from HT-29 cells treated with O-glycosidase for 30 mins follow by 50 μM lysosome inhibitor CQ for 24 h or 10 μM proteasome inhibitor MG132 for 6 h, or DMSO as a control. d Western blots for the indicated proteins from HT-29 cells treated with DMSO, Golgi inhibitor BFA (8 μM), clathrin-dependent endocytosis inhibitor CPZ (10 μM), cavolin-dependent endocytosis inhibitor MβCD (5 mM), or lysosome inhibitor HCQ (50 μM) for 24 h. e Western blots for the indicated proteins in MUC1 of colonic HT-29 cells treated with treated O-glycosidase for 30 mins. f Western blots were used to detect MUC1 protein in co-immunoprecipitation with MUC1 protein or NEDD4 protein in the HT-29 cell line. g Western blots for the indicated proteins from HT-29 cells transfected shNEDD4-#1 and shNEDD4-#2 treated with O-Glycosidase for 30 mins. h A schematic of NEDD4 protein which included C2, WW1/2/3/4 and HECT domain. C2 (Calcium - dependent lipid - binding domain), WW1 (WW domains 1), WW2 (WW domains 2), WW3 (WW domains 3), WW4 (WW domains 4), HECT (Homologous to the E6 - AP Carboxyl Terminus domain), C1046/1197/1286 A (Cysteine residues at positions 1046, 1197, and 1286 were individually mutated to alanine). i Western blots for the indicated proteins from HT-29 cells transfected together with NEDD4 WT or NEDD4 C1046A , NEDD4 C1197A , NEDD4 C1286A . j HEK293T cells transfected with the indicated plasmids were treated with CQ (100 μM) for 24 h, and submitted to in vivo ubiquitination assay. k HT-29 cells co-transfected with Flag-MUC1, His-NEDD4(WT or C1046A), HA-Ub (Ub WT or K48, K63) were treated with CQ (100 μM) for 24 h, and submitted to in vivo ubiquitination assay. l Western blots for the indicated proteins from HT-29 cells transfected with MUC1-WT or MUC1-K1231R mutants were treated with glycosidase for 30 mins. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: To induce intestinal Muc1 disruption, Muc1 Flox/Flox and β-catenin Flox/Flox mice were crossed with Villin-Cre mice (kindly provided by Cyagen), resulting in the generation of Muc1 EKO and β-catenin EKO mice.

Techniques: Western Blot, Transfection, Control, Immunoprecipitation, Binding Assay, In Vivo, Ubiquitin Proteomics

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Experimental schematic of Muc1 Flox/Flox and Muc1 EKO mice after 16 weeks of ND or HFD diet. The diagram of the mouse was created in BioRender. Li, Z. (2025) https://BioRender.com/e2kqno5 . Mice were housed at room temperature (RT, 21 °C) or thermoneutrality (TN, 29 °C). CLAMS, Comprehensive Laboratory Animal Monitoring System. Villin-Cre (Villin promoter-driven Cre recombinase), Muc1 Flox/Flox (Muc1 with loxP sites flanking the gene), Muc1 EKO (Epithelial-Knockout of Muc1), ND (Normal Diet), HFD (High-Fat Diet). b Typical liver H&E staining, oil red O staining, Sirius red staining, and Immunohistochemical staining of F4/80. Scale bars: 25 μm. c Body weight, liver weight. d Glucose tolerance test (GTT). e Insulin tolerance test (ITT). f Quantitative analysis of Serum TG, Hepatic TG, ALT, and AST. g , h Inflammation-related ( g ) and Fibrosis-related ( h ) Gene expression in liver tissues. Data are mean ± s.e.m. n = 8 mice per group. P -values were calculated by a two-tailed unpaired t -test. Source data are provided as a Source data file.

Article Snippet: To induce intestinal Muc1 disruption, Muc1 Flox/Flox and β-catenin Flox/Flox mice were crossed with Villin-Cre mice (kindly provided by Cyagen), resulting in the generation of Muc1 EKO and β-catenin EKO mice.

Techniques: Knock-Out, Staining, Immunohistochemical staining, Gene Expression, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a LPS Concentration were measured in the serum of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). b Bacterial DNA/Whole DNA in blood was measured by RT-qPCR ( n = 8 per group). c Plasmatic 4KDa FITC Dextran Flux concentration 4 h after gavage by 750 µg/g bodyweight ( n = 8 per group). d Representative transmission electron microscopy images and Width of colonic epithelial cell zonula adherence in mice ( n = 8). Scale bars: 1 µm (left), 200 nm (right). e Fluorescent confocal images of colon tissue sections of mice and humans with MASLD and their control group. Scale bars: 40 μm. f Relative protein expression of MUC1 and β-Catenin in colon tissues of the control group and MASLD group ( n = 30 per group). g Relative protein expression of MUC1 and β-Catenin in colon tissues of mice fed with ND and HFD ( n = 6 per group). h Fluorescent confocal images of colon tissue sections of Muc1 Flox/Flox and Muc1 EKO mice. Scale bars: 40 μm. i Relative protein expression of MUC1, β-Catenin, and Phospho-β-Catenin in colon tissues of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). j Western blots for the indicated proteins from HT-29 cells transfected with shCTL or shMUC1 treated with 50 μM lysosome inhibitor CQ for 24 h or 10 μM proteasome inhibitor MG132 for 6 h, or DMSO as a control. CHX (Cycloheximide), DMSO (Dimethyl sulfoxide), CQ (Chloroquine), shCTL (shRNA Control), shMUC1 (shRNA targeting MUC1). Data are means ± SEM. P -values were calculated by a two-tailed unpaired t -test. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: To induce intestinal Muc1 disruption, Muc1 Flox/Flox and β-catenin Flox/Flox mice were crossed with Villin-Cre mice (kindly provided by Cyagen), resulting in the generation of Muc1 EKO and β-catenin EKO mice.

Techniques: Concentration Assay, Quantitative RT-PCR, Transmission Assay, Electron Microscopy, Control, Expressing, Western Blot, Transfection, shRNA, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Schematics of mice cytoplasmic-tail-deleted MUC1 constructs. S (Signal Sequence), VNTR (Variable Number of Tandem Repeats), SEA (Sea urchin sperm protein-Enterokinase-Agrin domain), TM (Transmembrane Domain), CT (Cytoplasmic Tail), ΔCT (Cytoplasmic Tail Deletion). b Experimental schematic of Control, Muc1 ΔCT EOE , and Muc1 EOE mice after 16 weeks of HFD. The diagram of the mouse was created in BioRender. Li, Z. (2025) https://BioRender.com/e2kqno5 . Mice were housed at room temperature (RT, 21 °C) or thermoneutrality (TN, 29 °C). CLAMS, Comprehensive Laboratory Animal Monitoring System. Villin-Cre (Villin promoter-driven Cre recombinase), AAV9 (Adeno-Associated Virus Serotype 9), ΔCT (Cytoplasmic Tail Deletion), EOE (Epithelial Overexpression), HFD (High-Fat Diet). c Representative transmission electron microscopy images of the glycocalyx. Scale bar, 100 nm (left), 200 nm (right). d Typical liver H&E staining, oil red O staining. Scale bars: 25 μm. e Body weight, and Liver weight. f Glucose tolerance test (GTT). g Insulin tolerance test (ITT). h Quantitative analysis of Serum TG, Hepatic TG, ALT, and AST. i LPS Concentration was measured in the serum and Plasmatic 4KDa FITC Dextran Flux concentration 4 h after gavage by 750 µg/g bodyweight. Data are means ± SEM, n = 8 mice/group. P -values were calculated by a two-tailed unpaired t -test. Source data are provided as a Source data file.

Article Snippet: To induce intestinal Muc1 disruption, Muc1 Flox/Flox and β-catenin Flox/Flox mice were crossed with Villin-Cre mice (kindly provided by Cyagen), resulting in the generation of Muc1 EKO and β-catenin EKO mice.

Techniques: Construct, Sequencing, Control, Virus, Over Expression, Transmission Assay, Electron Microscopy, Staining, Concentration Assay, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Relative protein expression of mucin 1 (MUC1) in colon mucosa biopsy samples of the control group and MASLD group ( n = 30 per group). b Representative immunofluorescence staining of MUC1 in colon mucosa biopsy samples of control and patients with MASLD. Scale bar, 50 μm. c Correlations between intestinal MUC1 protein expression and BMI, serum TG, TC, ALT, and AST levels in colon mucosa biopsy samples ( n = 60). The correlation analysis was performed using Pearson’s product-moment correlation (two-sided without adjustment). d Relative protein expression of MUC1 in colon tissues of mice fed with ND and HFD for 16 weeks ( n = 6 per group). e Representative immunofluorescence staining of MUC1 in colon tissues of mice fed with ND and HFD for 16 weeks. Scale bar, 50 μm. f Structural schematic diagram of the membrane MUC1 protein. The diagram of the membrane and MUC1 was created in BioRender. Li, Z. (2025) https://BioRender.com/b1gercd and https://BioRender.com/7jqtxz6 . g , h Representative transmission electron microscopy images of the glycocalyx in human colon ( g ) and mouse colon ( h ). Scale bar, 200 nm (left), 100 nm (right). i Schematic diagram of peanut agglutinin (PNA)-specific recognition of O-glycan patterns. The diagram of peanut agglutinin was created in BioRender. Li, Z. (2025) https://BioRender.com/txue94i . Ser (Serine), Thr (Threonine). j The expression levels of O-glycans (PNA) on colonic MUC1 were assessed in both the control group and the patient with MASLD group under conditions of equivalent MUC1 levels. k The expression levels of O-glycans (PNA) on colonic MUC1 were assessed in mice fed with ND and HFD under conditions of equivalent MUC1 levels. Data are presented as mean ± SEM. P -values were calculated by a two-tailed unpaired t -test. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Expressing, Control, Immunofluorescence, Staining, Membrane, Transmission Assay, Electron Microscopy, Glycoproteomics, Two Tailed Test, Western Blot

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Western blot analysis showing the stability of MUC1 after the administration of 50 nM O-glycosidase in complete media for 30 mins follow by cycloheximide (CHX, translation inhibitor) for 24 h in HT-29 cells. b Western blot analysis was performed to detect specified proteins in HT-29 cells that were transfected with deglycosylated MUC1 vectors, specifically MUC1-10TRs or MUC1-5TRs. c Western blots for the indicated proteins from HT-29 cells treated with O-glycosidase for 30 mins follow by 50 μM lysosome inhibitor CQ for 24 h or 10 μM proteasome inhibitor MG132 for 6 h, or DMSO as a control. d Western blots for the indicated proteins from HT-29 cells treated with DMSO, Golgi inhibitor BFA (8 μM), clathrin-dependent endocytosis inhibitor CPZ (10 μM), cavolin-dependent endocytosis inhibitor MβCD (5 mM), or lysosome inhibitor HCQ (50 μM) for 24 h. e Western blots for the indicated proteins in MUC1 of colonic HT-29 cells treated with treated O-glycosidase for 30 mins. f Western blots were used to detect MUC1 protein in co-immunoprecipitation with MUC1 protein or NEDD4 protein in the HT-29 cell line. g Western blots for the indicated proteins from HT-29 cells transfected shNEDD4-#1 and shNEDD4-#2 treated with O-Glycosidase for 30 mins. h A schematic of NEDD4 protein which included C2, WW1/2/3/4 and HECT domain. C2 (Calcium - dependent lipid - binding domain), WW1 (WW domains 1), WW2 (WW domains 2), WW3 (WW domains 3), WW4 (WW domains 4), HECT (Homologous to the E6 - AP Carboxyl Terminus domain), C1046/1197/1286 A (Cysteine residues at positions 1046, 1197, and 1286 were individually mutated to alanine). i Western blots for the indicated proteins from HT-29 cells transfected together with NEDD4 WT or NEDD4 C1046A , NEDD4 C1197A , NEDD4 C1286A . j HEK293T cells transfected with the indicated plasmids were treated with CQ (100 μM) for 24 h, and submitted to in vivo ubiquitination assay. k HT-29 cells co-transfected with Flag-MUC1, His-NEDD4(WT or C1046A), HA-Ub (Ub WT or K48, K63) were treated with CQ (100 μM) for 24 h, and submitted to in vivo ubiquitination assay. l Western blots for the indicated proteins from HT-29 cells transfected with MUC1-WT or MUC1-K1231R mutants were treated with glycosidase for 30 mins. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Western Blot, Transfection, Control, Immunoprecipitation, Binding Assay, In Vivo, Ubiquitin Proteomics

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Experimental schematic of Muc1 Flox/Flox and Muc1 EKO mice after 16 weeks of ND or HFD diet. The diagram of the mouse was created in BioRender. Li, Z. (2025) https://BioRender.com/e2kqno5 . Mice were housed at room temperature (RT, 21 °C) or thermoneutrality (TN, 29 °C). CLAMS, Comprehensive Laboratory Animal Monitoring System. Villin-Cre (Villin promoter-driven Cre recombinase), Muc1 Flox/Flox (Muc1 with loxP sites flanking the gene), Muc1 EKO (Epithelial-Knockout of Muc1), ND (Normal Diet), HFD (High-Fat Diet). b Typical liver H&E staining, oil red O staining, Sirius red staining, and Immunohistochemical staining of F4/80. Scale bars: 25 μm. c Body weight, liver weight. d Glucose tolerance test (GTT). e Insulin tolerance test (ITT). f Quantitative analysis of Serum TG, Hepatic TG, ALT, and AST. g , h Inflammation-related ( g ) and Fibrosis-related ( h ) Gene expression in liver tissues. Data are mean ± s.e.m. n = 8 mice per group. P -values were calculated by a two-tailed unpaired t -test. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Knock-Out, Staining, Immunohistochemical staining, Gene Expression, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a LPS Concentration were measured in the serum of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). b Bacterial DNA/Whole DNA in blood was measured by RT-qPCR ( n = 8 per group). c Plasmatic 4KDa FITC Dextran Flux concentration 4 h after gavage by 750 µg/g bodyweight ( n = 8 per group). d Representative transmission electron microscopy images and Width of colonic epithelial cell zonula adherence in mice ( n = 8). Scale bars: 1 µm (left), 200 nm (right). e Fluorescent confocal images of colon tissue sections of mice and humans with MASLD and their control group. Scale bars: 40 μm. f Relative protein expression of MUC1 and β-Catenin in colon tissues of the control group and MASLD group ( n = 30 per group). g Relative protein expression of MUC1 and β-Catenin in colon tissues of mice fed with ND and HFD ( n = 6 per group). h Fluorescent confocal images of colon tissue sections of Muc1 Flox/Flox and Muc1 EKO mice. Scale bars: 40 μm. i Relative protein expression of MUC1, β-Catenin, and Phospho-β-Catenin in colon tissues of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). j Western blots for the indicated proteins from HT-29 cells transfected with shCTL or shMUC1 treated with 50 μM lysosome inhibitor CQ for 24 h or 10 μM proteasome inhibitor MG132 for 6 h, or DMSO as a control. CHX (Cycloheximide), DMSO (Dimethyl sulfoxide), CQ (Chloroquine), shCTL (shRNA Control), shMUC1 (shRNA targeting MUC1). Data are means ± SEM. P -values were calculated by a two-tailed unpaired t -test. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Concentration Assay, Quantitative RT-PCR, Transmission Assay, Electron Microscopy, Control, Expressing, Western Blot, Transfection, shRNA, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Schematics of mice cytoplasmic-tail-deleted MUC1 constructs. S (Signal Sequence), VNTR (Variable Number of Tandem Repeats), SEA (Sea urchin sperm protein-Enterokinase-Agrin domain), TM (Transmembrane Domain), CT (Cytoplasmic Tail), ΔCT (Cytoplasmic Tail Deletion). b Experimental schematic of Control, Muc1 ΔCT EOE , and Muc1 EOE mice after 16 weeks of HFD. The diagram of the mouse was created in BioRender. Li, Z. (2025) https://BioRender.com/e2kqno5 . Mice were housed at room temperature (RT, 21 °C) or thermoneutrality (TN, 29 °C). CLAMS, Comprehensive Laboratory Animal Monitoring System. Villin-Cre (Villin promoter-driven Cre recombinase), AAV9 (Adeno-Associated Virus Serotype 9), ΔCT (Cytoplasmic Tail Deletion), EOE (Epithelial Overexpression), HFD (High-Fat Diet). c Representative transmission electron microscopy images of the glycocalyx. Scale bar, 100 nm (left), 200 nm (right). d Typical liver H&E staining, oil red O staining. Scale bars: 25 μm. e Body weight, and Liver weight. f Glucose tolerance test (GTT). g Insulin tolerance test (ITT). h Quantitative analysis of Serum TG, Hepatic TG, ALT, and AST. i LPS Concentration was measured in the serum and Plasmatic 4KDa FITC Dextran Flux concentration 4 h after gavage by 750 µg/g bodyweight. Data are means ± SEM, n = 8 mice/group. P -values were calculated by a two-tailed unpaired t -test. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Construct, Sequencing, Control, Virus, Over Expression, Transmission Assay, Electron Microscopy, Staining, Concentration Assay, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a Experimental schematic of Muc1 Flox/Flox and Muc1 EKO mice after 16 weeks of ND or HFD diet. The diagram of the mouse was created in BioRender. Li, Z. (2025) https://BioRender.com/e2kqno5 . Mice were housed at room temperature (RT, 21 °C) or thermoneutrality (TN, 29 °C). CLAMS, Comprehensive Laboratory Animal Monitoring System. Villin-Cre (Villin promoter-driven Cre recombinase), Muc1 Flox/Flox (Muc1 with loxP sites flanking the gene), Muc1 EKO (Epithelial-Knockout of Muc1), ND (Normal Diet), HFD (High-Fat Diet). b Typical liver H&E staining, oil red O staining, Sirius red staining, and Immunohistochemical staining of F4/80. Scale bars: 25 μm. c Body weight, liver weight. d Glucose tolerance test (GTT). e Insulin tolerance test (ITT). f Quantitative analysis of Serum TG, Hepatic TG, ALT, and AST. g , h Inflammation-related ( g ) and Fibrosis-related ( h ) Gene expression in liver tissues. Data are mean ± s.e.m. n = 8 mice per group. P -values were calculated by a two-tailed unpaired t -test. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Knock-Out, Staining, Immunohistochemical staining, Gene Expression, Two Tailed Test

Journal: Nature Communications

Article Title: Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice

doi: 10.1038/s41467-025-67034-7

Figure Lengend Snippet: a LPS Concentration were measured in the serum of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). b Bacterial DNA/Whole DNA in blood was measured by RT-qPCR ( n = 8 per group). c Plasmatic 4KDa FITC Dextran Flux concentration 4 h after gavage by 750 µg/g bodyweight ( n = 8 per group). d Representative transmission electron microscopy images and Width of colonic epithelial cell zonula adherence in mice ( n = 8). Scale bars: 1 µm (left), 200 nm (right). e Fluorescent confocal images of colon tissue sections of mice and humans with MASLD and their control group. Scale bars: 40 μm. f Relative protein expression of MUC1 and β-Catenin in colon tissues of the control group and MASLD group ( n = 30 per group). g Relative protein expression of MUC1 and β-Catenin in colon tissues of mice fed with ND and HFD ( n = 6 per group). h Fluorescent confocal images of colon tissue sections of Muc1 Flox/Flox and Muc1 EKO mice. Scale bars: 40 μm. i Relative protein expression of MUC1, β-Catenin, and Phospho-β-Catenin in colon tissues of Muc1 Flox/Flox and Muc1 EKO mice ( n = 8 per group). j Western blots for the indicated proteins from HT-29 cells transfected with shCTL or shMUC1 treated with 50 μM lysosome inhibitor CQ for 24 h or 10 μM proteasome inhibitor MG132 for 6 h, or DMSO as a control. CHX (Cycloheximide), DMSO (Dimethyl sulfoxide), CQ (Chloroquine), shCTL (shRNA Control), shMUC1 (shRNA targeting MUC1). Data are means ± SEM. P -values were calculated by a two-tailed unpaired t -test. Western blotting data are representative of three independent experiments. Source data are provided as a Source data file.

Article Snippet: Muc1 Flox/Flox and β-Catenin Flox/Flox mice were purchased from Cyagen (S-CKO-03832, S-CKO-01559).

Techniques: Concentration Assay, Quantitative RT-PCR, Transmission Assay, Electron Microscopy, Control, Expressing, Western Blot, Transfection, shRNA, Two Tailed Test