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Proteintech p cadherin

Podocyte-specific TLR4 deletion mitigated STZ-induced DKD, podocyte injury, and proteinuria in mice. (A) Schematic description of the strategy for generating STZ-induced diabetic mouse model in NPHS2 -Cre; TLR4 fl/fl ( TLR4 CKO) mice and in TLR4 fl/fl mice (CTL). (B) Monthly monitoring of plasma glucose levels in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; ## P < 0.01 vs. CKO-NC. (C) Monthly monitoring of body weight in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ### P < 0.01 vs. CTL-STZ. (D) Representative images of PAS and MASSON staining of the glomeruli in mice at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (E) Representative images of HE staining of the kidney in mice at 12 and 16 weeks. Scale bar, 50 μm ( n = 8). (F) Representative IF images of the expression of SD proteins <t>p-cadherin</t> and synaptopodin in glomeruli at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (G) The expression of a mesenchymal marker desmin was detected in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.05 ( n = 8). (H) Representative images of TEM in podocyte ultrastructural alterations in mice. FPs effacement (blue arrow), ER dilation (red arrow) and GBM thickness were observed in podocytes in STZ-induced CTL diabetic mice, and were attenuated in TLR4 CKO diabetic mice at 16 weeks. Scale bar, 1 μm ( n = 8). (I) Determination of proteinuria in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ## P < 0.05 vs. CTL-STZ; # ### P < 0.01 vs. CTL-STZ.

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1) Product Images from "Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation"

Article Title: Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation

Journal: Journal of Advanced Research

doi: 10.1016/j.jare.2025.07.013

Figure Legend Snippet: Podocyte-specific TLR4 deletion mitigated STZ-induced DKD, podocyte injury, and proteinuria in mice. (A) Schematic description of the strategy for generating STZ-induced diabetic mouse model in NPHS2 -Cre; TLR4 fl/fl ( TLR4 CKO) mice and in TLR4 fl/fl mice (CTL). (B) Monthly monitoring of plasma glucose levels in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; ## P < 0.01 vs. CKO-NC. (C) Monthly monitoring of body weight in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ### P < 0.01 vs. CTL-STZ. (D) Representative images of PAS and MASSON staining of the glomeruli in mice at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (E) Representative images of HE staining of the kidney in mice at 12 and 16 weeks. Scale bar, 50 μm ( n = 8). (F) Representative IF images of the expression of SD proteins p-cadherin and synaptopodin in glomeruli at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (G) The expression of a mesenchymal marker desmin was detected in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.05 ( n = 8). (H) Representative images of TEM in podocyte ultrastructural alterations in mice. FPs effacement (blue arrow), ER dilation (red arrow) and GBM thickness were observed in podocytes in STZ-induced CTL diabetic mice, and were attenuated in TLR4 CKO diabetic mice at 16 weeks. Scale bar, 1 μm ( n = 8). (I) Determination of proteinuria in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ## P < 0.05 vs. CTL-STZ; # ### P < 0.01 vs. CTL-STZ.

Techniques Used: Clinical Proteomics, Staining, Expressing, Marker, Western Blot

Activation of TLR4/MyD88/PKCδ/SHP-1 signaling cascade was involved in hyperglycemic podocyte damage in vivo and in vitro . (A) The protein levels of TLR4 were determined in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05 ( n = 8). (B) Representative western blot of the expression of MyD88, p-PKCδ (Y311), PKCδ and SHP-1 in renal cortex from mice at 12 and 16 weeks. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.01; ### P < 0.01 ( n = 8). (C) Representative double IF staining of glomerular SHP-1 and synaptopodin expression in mice at 16 weeks. Scale bar, 20 μm ( n = 8). (D) The expression of TLR4, MyD88, p-PKCδ, PKCδ and SHP-1 in cultured mouse podocytes from treatments of LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ## P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments). (E) IF staining of podocyte proteins p-cadherin and synaptopodin after LG or HG stimulation for 48 h with or without transfection of TLR4, PKCδ, MCP-1 or scrambled shRNAs, or pretreatment of 4-PBA. Magnification 400 × . ( n = 3 independent experiments). (F) Determination of SD protein podocin and injury marker desmin in podocytes treated with LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments).

Figure Legend Snippet: Activation of TLR4/MyD88/PKCδ/SHP-1 signaling cascade was involved in hyperglycemic podocyte damage in vivo and in vitro . (A) The protein levels of TLR4 were determined in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05 ( n = 8). (B) Representative western blot of the expression of MyD88, p-PKCδ (Y311), PKCδ and SHP-1 in renal cortex from mice at 12 and 16 weeks. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.01; ### P < 0.01 ( n = 8). (C) Representative double IF staining of glomerular SHP-1 and synaptopodin expression in mice at 16 weeks. Scale bar, 20 μm ( n = 8). (D) The expression of TLR4, MyD88, p-PKCδ, PKCδ and SHP-1 in cultured mouse podocytes from treatments of LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ## P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments). (E) IF staining of podocyte proteins p-cadherin and synaptopodin after LG or HG stimulation for 48 h with or without transfection of TLR4, PKCδ, MCP-1 or scrambled shRNAs, or pretreatment of 4-PBA. Magnification 400 × . ( n = 3 independent experiments). (F) Determination of SD protein podocin and injury marker desmin in podocytes treated with LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments).

Techniques Used: Activation Assay, In Vivo, In Vitro, Western Blot, Expressing, Staining, Cell Culture, Transfection, Marker

Immunostaining:

Article Title: E-Cadherin Is Expressed in Epithelial Cells of the Choroid Plexus in Human and Mouse Brains.
Article Snippet: .. Immunostaining with the mouse anti-E-cadherin (Dako) (A,D) or P-cadherin (G,J,M) antibody (visu- alized as green) and the rabbit anti-N-cadherin (B,E,K,N) or E-cadherin (ProteinTech) (H) antibody (visualized as red), nuclear staining by TO-PRO-3 (visualized as blue), and merged images (C,F,I,L,O) are shown. ..

Article Title: Denticleless E3 ubiquitin protein ligase (DTL) maintains the proliferation and differentiation of epidermis and hair follicles during skin development.
Article Snippet: Institute of Life Sciences, College of Life and Environmental Science, Wenzhou University, Wenzhou, China School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China Laboratory of Tumor Targeted Therapy and Translational Medicine, Jilin Medical University, Jilin, China Key Laboratory of Interventional Pulmonology of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China Central Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China Department of Endodontics, The First Affiliated Hospital of Harbin Medical University, Harbin, China Department of Histology and Embryology, Harbin Medical University, Harbin, China

Staining:

Incubation:

Article Title: Vincetoxicum arnottianum modulates motility features and metastatic marker expression in pediatric rhabdomyosarcoma by stabilizing the actin cytoskeleton
Article Snippet: .. Briefly, for protein detection, primary antibodies anti-β-Actin ((C4) #sc-47,778; Santa Cruz, Dallas, USA), anti-PCNA ((PC10) #sc-56; Santa Cruz, Dallas, USA), anti-AMT (#10633–1-AP; Proteintech Europe, Manchester, UK), anti-GCSH (#16726–1-AP; Proteintech Europe, Manchester, UK), anti-SGPL1 ((H-300) #sc-67,368; Santa Cruz, Dallas, USA), anti-Ezrin ((3C12) #sc-58,758; Santa Cruz, Dallas, USA), anti-CXCR4 (#11073–2-AP; Proteintech Europe, Manchester, UK) P-Cadherin (#13773–1-AP; Proteintech Europe, Manchester, UK) and Stathmin (#3352; Cell Signaling, Danvers, USA) were incubated overnight at 4 °C followed by labelling with a horseradish peroxidase (HPR)-conjugated secondary antibody (mouse #7076; rabbit #7074P2; Cell Signaling, Danvers, USA) for 1 h at room temperature. .. Finally, the protein signals were visualized with the ClarityTM Western ECL Chemiluminescent Substrate (Bio-Rad Laboratories Inc., USA).

Article Title: Long noncoding RNA ENST00000458139 promotes mitochondrial dysfunction and apoptosis of podocytes in diabetic kidney disease through binding with SNRPA1.
Article Snippet: Diabetic kidney disease (DKD) is recognized as the leading cause of end-stage renal disease (ESRD) and is related to progressive albuminuria, consequent to kidney destruction that involves podocyte mitochondrial dysfunction and apoptosis.. Burgeoning evidence has reported that long Noncoding RNAs (lncRNAs) exert a vital role in DKD; however, their mechanism is largely unknown.. Previously, we performed RNA sequencing (GSE199838) in human DKD samples and identified that lncRNA ENST00000458139 (lnc458) was significantly upregulated in DKD patients compared with healthy controls.

Membrane:

Image Search Results

Mapping the O -Man dependent E-cadherin interactome using IP screening. A , Schematic diagrams and structural model of CDH1 EC domains : ( left ) CDH1 is a transmembrane protein with five EC domains that form cis- and trans interactions; ( middle ) TMTC2 mediates O -Man on CDH1 EC B-strands, while TMTC3 mediates glycosylations on G-strands ( O -Man structures were grafted onto an AlphaFold model of EC4 using the GlycoShape tool – the mannoses are depicted as green sticks and translucent surfaces on recipient serine and threonine residues ); ( right ) schematic of the β-strand arrangement of an EC domain, highlighting O -Man sites ( green dots ) on the B- ( red ) and G- ( blue ) strands of EC2-4. B , Schematic diagram of the IP-MS-based interactome screen applied to CDH1 : Cryomilled cells are distributed to a 96-well plate and combined with different extractants; CDH1-associated complexes are affinity enriched from each extract using an antibody coupled magnetic medium and then analyzed by protein MS; the compositions of the enriched macromolecular assemblies will vary according to the stabilizing/destabilizing responses of the protein constituents and a putative interactome is constituted by the combined results. C , Results of the IP screen using 32 extraction conditions : ( upper ) silver-stained SDS-PAGE gel showing CDH1 capture by IP screening; ( lower ) hierarchical clustering of MS data, with log 2 -transformed protein abundance values from Proteome Discoverer displayed by color. Grey shading in the heatmap indicates proteins not detected (ND). Six extractants, highlighted in red, were selected for further quantitative analysis. Selected reagents present in extraction solutions are labeled with colored dots.

Journal: Molecular & Cellular Proteomics : MCP

Article Title: O -Mannose Glycosylations Influence E-Cadherin Functional Interactions

doi: 10.1016/j.mcpro.2026.101559

Figure Lengend Snippet: Mapping the O -Man dependent E-cadherin interactome using IP screening. A , Schematic diagrams and structural model of CDH1 EC domains : ( left ) CDH1 is a transmembrane protein with five EC domains that form cis- and trans interactions; ( middle ) TMTC2 mediates O -Man on CDH1 EC B-strands, while TMTC3 mediates glycosylations on G-strands ( O -Man structures were grafted onto an AlphaFold model of EC4 using the GlycoShape tool – the mannoses are depicted as green sticks and translucent surfaces on recipient serine and threonine residues ); ( right ) schematic of the β-strand arrangement of an EC domain, highlighting O -Man sites ( green dots ) on the B- ( red ) and G- ( blue ) strands of EC2-4. B , Schematic diagram of the IP-MS-based interactome screen applied to CDH1 : Cryomilled cells are distributed to a 96-well plate and combined with different extractants; CDH1-associated complexes are affinity enriched from each extract using an antibody coupled magnetic medium and then analyzed by protein MS; the compositions of the enriched macromolecular assemblies will vary according to the stabilizing/destabilizing responses of the protein constituents and a putative interactome is constituted by the combined results. C , Results of the IP screen using 32 extraction conditions : ( upper ) silver-stained SDS-PAGE gel showing CDH1 capture by IP screening; ( lower ) hierarchical clustering of MS data, with log 2 -transformed protein abundance values from Proteome Discoverer displayed by color. Grey shading in the heatmap indicates proteins not detected (ND). Six extractants, highlighted in red, were selected for further quantitative analysis. Selected reagents present in extraction solutions are labeled with colored dots.

Article Snippet: Membrane was incubated for 1h at RT in agitation with primary monoclonal antibodies Anti CDH3 (MAB861, R&D systems 1:500 in blocking milk).

Techniques: Protein-Protein interactions, Extraction, Staining, SDS Page, Transformation Assay, Quantitative Proteomics, Labeling

Effects of TMTC knock - out on CDH1 and CDH3 abundance and localization. A , Western blot analysis of endogenous CDH3 abundance in BG1 cells with different TMTC KO statuses. B , Flow cytometry analysis of cell surface CDH1 and CDH3 : ( left ) representative histograms comparing fluorescence intensities in BG1 CDH1::HA cells ( green ), BG1 CDH1::HA/KO:TMTC1-4 cells ( pink ), and BG1 KO:CDH1 negative control cells ( grey ); signals normalized to mode; ( right ) Quantification of fold-change in median fluorescence intensity for surface CDH1 and CDH3 in BG1 CDH1::HA cells relative to BG1 CDH1::HA/KO:TMTC1-4 cells (n = 3). C , representative immunofluorescence images showing cellular localization of CDH1 ( green ) and CDH3 ( red ) in control BG1 CDH1::HA cells ( top panels ) and BG1 CDH1::HA/ KO :TMTC1-4 cells ( bottom panels ). Nuclei were counter-stained with DAPI ( blue ). Scale bar = 10 μm. D , Schematic model of the O-Man-dependent CDH1 interactome : some CDH1 interactors are modulated by O- Man, leading to their decreased or increased co-enrichment, based on changes e.g., in their affinity, localization, and/or abundance.

Journal: Molecular & Cellular Proteomics : MCP

Article Title: O -Mannose Glycosylations Influence E-Cadherin Functional Interactions

doi: 10.1016/j.mcpro.2026.101559

Figure Lengend Snippet: Effects of TMTC knock - out on CDH1 and CDH3 abundance and localization. A , Western blot analysis of endogenous CDH3 abundance in BG1 cells with different TMTC KO statuses. B , Flow cytometry analysis of cell surface CDH1 and CDH3 : ( left ) representative histograms comparing fluorescence intensities in BG1 CDH1::HA cells ( green ), BG1 CDH1::HA/KO:TMTC1-4 cells ( pink ), and BG1 KO:CDH1 negative control cells ( grey ); signals normalized to mode; ( right ) Quantification of fold-change in median fluorescence intensity for surface CDH1 and CDH3 in BG1 CDH1::HA cells relative to BG1 CDH1::HA/KO:TMTC1-4 cells (n = 3). C , representative immunofluorescence images showing cellular localization of CDH1 ( green ) and CDH3 ( red ) in control BG1 CDH1::HA cells ( top panels ) and BG1 CDH1::HA/ KO :TMTC1-4 cells ( bottom panels ). Nuclei were counter-stained with DAPI ( blue ). Scale bar = 10 μm. D , Schematic model of the O-Man-dependent CDH1 interactome : some CDH1 interactors are modulated by O- Man, leading to their decreased or increased co-enrichment, based on changes e.g., in their affinity, localization, and/or abundance.

Article Snippet: Membrane was incubated for 1h at RT in agitation with primary monoclonal antibodies Anti CDH3 (MAB861, R&D systems 1:500 in blocking milk).

Techniques: Knock-Out, Western Blot, Flow Cytometry, Fluorescence, Negative Control, Immunofluorescence, Control, Staining

Journal: Journal of Advanced Research

Article Title: Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation

doi: 10.1016/j.jare.2025.07.013

Figure Lengend Snippet: Podocyte-specific TLR4 deletion mitigated STZ-induced DKD, podocyte injury, and proteinuria in mice. (A) Schematic description of the strategy for generating STZ-induced diabetic mouse model in NPHS2 -Cre; TLR4 fl/fl ( TLR4 CKO) mice and in TLR4 fl/fl mice (CTL). (B) Monthly monitoring of plasma glucose levels in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; ## P < 0.01 vs. CKO-NC. (C) Monthly monitoring of body weight in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ### P < 0.01 vs. CTL-STZ. (D) Representative images of PAS and MASSON staining of the glomeruli in mice at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (E) Representative images of HE staining of the kidney in mice at 12 and 16 weeks. Scale bar, 50 μm ( n = 8). (F) Representative IF images of the expression of SD proteins p-cadherin and synaptopodin in glomeruli at 12 and 16 weeks. Scale bar, 20 μm ( n = 8). (G) The expression of a mesenchymal marker desmin was detected in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.05 ( n = 8). (H) Representative images of TEM in podocyte ultrastructural alterations in mice. FPs effacement (blue arrow), ER dilation (red arrow) and GBM thickness were observed in podocytes in STZ-induced CTL diabetic mice, and were attenuated in TLR4 CKO diabetic mice at 16 weeks. Scale bar, 1 μm ( n = 8). (I) Determination of proteinuria in mice. Data are presented as mean ± SD. ** P < 0.01 vs. CTL-NC; # P < 0.05 vs. CKO-NC; # # P < 0.01 vs. CKO-NC; # ## P < 0.05 vs. CTL-STZ; # ### P < 0.01 vs. CTL-STZ.

Article Snippet: The following primary antibodies were used: f4/80 (29414–1-AP), desmin (16520–1-AP), MCP-1 (26161–1-AP), podocin (20384–1-AP), synaptopodin (21064–1-AP), TLR4 (66350–1-Ig), β-actin (66009–1-Ig), PKCδ(14188–1-AP), ATF6 (24169–1-AP), p-cadherin (13773–1-AP) were from Proteintech (IL, USA); phospho-PKCδ (Y311) (ab76181), PKCdelta (ab182126), SHP-1 (ab227503), HA (ab9110) were from Abcam (MA, USA); BIP (M010300), MyD88 (P012343) were from Epizyme, Shanghai, China); and ATF4 (11815), sXBP-1 (40435) were from Cell Signaling Technology (MA, USA).

Techniques: Clinical Proteomics, Staining, Expressing, Marker, Western Blot

Journal: Journal of Advanced Research

Article Title: Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation

doi: 10.1016/j.jare.2025.07.013

Figure Lengend Snippet: Activation of TLR4/MyD88/PKCδ/SHP-1 signaling cascade was involved in hyperglycemic podocyte damage in vivo and in vitro . (A) The protein levels of TLR4 were determined in renal tissues from mice at 12 and 16 weeks by western blot analysis. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05 ( n = 8). (B) Representative western blot of the expression of MyD88, p-PKCδ (Y311), PKCδ and SHP-1 in renal cortex from mice at 12 and 16 weeks. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; # P < 0.05; ## P < 0.01; ### P < 0.01 ( n = 8). (C) Representative double IF staining of glomerular SHP-1 and synaptopodin expression in mice at 16 weeks. Scale bar, 20 μm ( n = 8). (D) The expression of TLR4, MyD88, p-PKCδ, PKCδ and SHP-1 in cultured mouse podocytes from treatments of LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ## P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments). (E) IF staining of podocyte proteins p-cadherin and synaptopodin after LG or HG stimulation for 48 h with or without transfection of TLR4, PKCδ, MCP-1 or scrambled shRNAs, or pretreatment of 4-PBA. Magnification 400 × . ( n = 3 independent experiments). (F) Determination of SD protein podocin and injury marker desmin in podocytes treated with LG or HG for 48 h with or without transfection of TLR4, MyD88 or scrambled shRNAs. P values were determined by one-way ANOVA and data are presented as mean ± SD. **** P < 0.01; ### P < 0.01; #### P < 0.01 ( n = 3 independent experiments).

Techniques: Activation Assay, In Vivo, In Vitro, Western Blot, Expressing, Staining, Cell Culture, Transfection, Marker

Knockdown of LAMC2 attenuates airway remodeling and EMT in a COPD model. ( A ) Schematic overview of the animal experimental design and grouping. ( B ) Representative Masson staining on mice lung sections from different groups (n = 5 per group). ( C ) Quantitative staining of Masson content in different groups (n = 5 per group). ( D ) Representative airway Fibronectin immunohistochemical staining and ( E ) quantitative staining of Fibronectin intensity on lung sections of different groups (n = 5 per group). ( F ) Representative airway N-cadherin immunohistochemical staining and ( G ) quantitative staining of N-cadherin intensity on lung sections of different groups (n=5 per group). ( H ) Representative airway E-cadherin immunohistochemical staining and ( I ) quantitative staining of E-cadherin intensity on lung sections of different groups (n=5 per group). ( J – M ) Western blot analysis and quantification of EMT-related proteins (Fibronectin, N-cadherin, and E-cadherin) in lung tissues from the different treatment groups. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bars: 100μm.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 attenuates airway remodeling and EMT in a COPD model. ( A ) Schematic overview of the animal experimental design and grouping. ( B ) Representative Masson staining on mice lung sections from different groups (n = 5 per group). ( C ) Quantitative staining of Masson content in different groups (n = 5 per group). ( D ) Representative airway Fibronectin immunohistochemical staining and ( E ) quantitative staining of Fibronectin intensity on lung sections of different groups (n = 5 per group). ( F ) Representative airway N-cadherin immunohistochemical staining and ( G ) quantitative staining of N-cadherin intensity on lung sections of different groups (n=5 per group). ( H ) Representative airway E-cadherin immunohistochemical staining and ( I ) quantitative staining of E-cadherin intensity on lung sections of different groups (n=5 per group). ( J – M ) Western blot analysis and quantification of EMT-related proteins (Fibronectin, N-cadherin, and E-cadherin) in lung tissues from the different treatment groups. * P < 0.05, ** P < 0.01, *** P < 0.001. Scale bars: 100μm.

Article Snippet: The membranes were blocked with 5% bovine serum albumin for 1 hour at room temperature and then incubated overnight at 4°C with the following primary antibodies: GAPDH (1:5000; Cell Signaling Technology, Danvers, MA, USA), LAMC2 (1:1000; Proteintech, China), E-Cadherin (1:1000; Cell Signaling Technology), N-Cadherin (1:1000; Cell Signaling Technology), Fibronectin (1:1000; HUABIO, China), AKT (1:1000; Cell Signaling Technology), and phospho-AKT (p-AKT, 1:1000; Cell Signaling Technology).

Techniques: Knockdown, Staining, Immunohistochemical staining, Western Blot

LAMC2 expression is upregulated in bronchial epithelial cells following TGF-β1 stimulation. ( A and B ) Volcano plots illustrating DEGs from ( A ) GSE104908 and ( B ) GSE40374 datasets, with corresponding LAMC2 expression levels. Significantly upregulated genes (red) and downregulated genes (blue) are indicated (fold change >1.5, adjusted P < 0.05). ( C ) The mRNA levels of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. ( D ) Western blot and ( E – H ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: LAMC2 expression is upregulated in bronchial epithelial cells following TGF-β1 stimulation. ( A and B ) Volcano plots illustrating DEGs from ( A ) GSE104908 and ( B ) GSE40374 datasets, with corresponding LAMC2 expression levels. Significantly upregulated genes (red) and downregulated genes (blue) are indicated (fold change >1.5, adjusted P < 0.05). ( C ) The mRNA levels of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. ( D ) Western blot and ( E – H ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after treatment with different concentrations of TGF-β1 for 24 hours. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques: Expressing, Western Blot

Knockdown of LAMC2 reverses TGF-β1-induced EMT marker expression and inhibits 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with different siLAMC2 constructs. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after siLAMC2 transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after siLAMC2 transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. ** P < 0.01, *** P < 0.001.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Knockdown of LAMC2 reverses TGF-β1-induced EMT marker expression and inhibits 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with different siLAMC2 constructs. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after siLAMC2 transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after siLAMC2 transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. ** P < 0.01, *** P < 0.001.

Techniques: Knockdown, Marker, Expressing, Migration, Transfection, Construct, Western Blot, Wound Healing Assay

Overexpression of LAMC2 promotes TGF-β1-induced EMT and enhances 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with LAMC2 plasmid and TGF-β1treatment. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after LAMC2 plasmid vector transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after LAMC2 plasmid vector transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Article Title: LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway

doi: 10.2147/COPD.S580964

Figure Lengend Snippet: Overexpression of LAMC2 promotes TGF-β1-induced EMT and enhances 16HBE cell migration. ( A ) LAMC2 mRNA expression levels following transfection with LAMC2 plasmid and TGF-β1treatment. ( B ) mRNA expression of Fibronectin, N-cadherin, and E-cadherin after LAMC2 plasmid vector transfection and subsequent TGF-β1 treatment. ( C ) Western blot and ( D – F ) the relative protein level of Fibronectin, N-cadherin, E-cadherin, and LAMC2 after LAMC2 plasmid vector transfection and TGF-β1 treatment. ( G ) Representative images of wound healing and transwell migration assays under different treatment conditions. Scale bar: 20 μm. ( H ) Quantification of migration rate (%) from wound healing assay and ( I ) Cell migration numbers counted from transwell assays. The data are the mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001.

Techniques: Over Expression, Migration, Expressing, Transfection, Plasmid Preparation, Western Blot, Wound Healing Assay

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