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Cell Signaling Technology Inc cd206
Cd206, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+cd206/pmc12992974-282-11-13
Average 86 stars, based on 1 article reviews

cd206 - by Bioz Stars, 2026-10

86/100 stars

Images

Immunofluorescence:

Article Title: Stem cell-derived biomimetic apoptotic vesicles enhance macrophage efferocytosis via C1qbp to accelerate diabetic wound healing
Article Snippet: Samples were analyzed using a flow cytometer and the data were processed with FlowJo software. .. For immunofluorescence staining, RAW264.7 cells were fixed in 4% PFA, permeabilized with 1% Triton X-100 for 10 min, blocked with 1% BSA for 1 h at room temperature, and incubated overnight at 4 °C with the following primary antibodies: anti-CD206 and anti-CD86 (Cell Signaling Technology, USA). ..

Staining:

Incubation:

Article Title: Regorafenib and Nifuroxazide exert enhanced suppression of hepatocellular carcinoma by inhibiting STAT3 and immune remodeling
Article Snippet: Sections were then blocked with 5% normal goat serum (Beyotime Biotechnology, cat. no. C0265) for 30 min at room temperature to eliminate non-specific antibody binding. .. The prepared tumor sections were incubated with the following primary antibodies: anti-CD3 (1:200; OmnimAbs; cat. no. OM244830 ); anti-CD4 (1:200; Cell Signaling Technology, Inc.; cat. no. 25229); anti-CD8 (1:400; Cell Signaling Technology, Inc.; cat. no. 98941); anti-CD206 (1:800; Cell Signaling Technology, Inc.; cat. no. 24595S); anti-CD86 (1:200, Novus Biologicals LLC; cat. no. NBP2-25208); or anti-Ki67 (1:100, Bioworld Technology, Inc.; cat. no. BS90769) according to the manufacturer's protocol, overnight at 4°C. .. After washing with PBS, sections were incubated with the fluorescent-tagged secondary antibody (1:200; Shanghai Abways Biotechnology Co., Ltd.; cat. no. CY3101) for 30 min at room temperature.

Article Title: Disruption of the circadian rhythm induces acute pancreatitis via amino acid metabolism-mediated macrophage infiltration.
Article Snippet: .. The sections were incubated overnight at 4°C with the following primary antibodies: anti-F4/80 (1:500, #70076 , CST), anti-CD86 (1:100, #19589, CST), anti-CD206 (1:500, #24595, CST), anti-Bmal1 (1:1000, #ab230822, Abcam), anti-amylase alpha (1:300, #12540-1-AP, Proteintech). .. The next day, after twice washing with PBS, the sections were labeled in the dark for 1 h with secondary antibody, then stained with DAPI for 10 min and imaged under a confocal microscope (Nikon, Tokyo, Japan).

other:

Article Title: COX5A induces M2 macrophage polarization in chronic rhinosinusitis with nasal polyps through ROS generation
Article Snippet: After boiling in a citric acid buffer (Servicebio, G1202) for antigen recovery, the tissue sections were blocked with 5% Bovine Serum Albumin (BSA) (Beyotime, P0023B) in TBST (Servicebio, G0001) and then incubated with primary antibodies against CD206(1:400,Cell Signaling Technology (CST), 24595), COX5A (1:500, ABclonal, A6437), and TOM20 (1:400, CST, 42406), followed by secondary antibody incubationThe slides were then washed, counterstained with DAPI.

Article Title: COX5A induces M2 macrophage polarization in chronic rhinosinusitis with nasal polyps through ROS generation.
Article Snippet: Immunofluorescence(mIF) After boiling in a citric acid buffer (Servicebio, G1202) for antigen recovery, the tissue sections were blocked with 5% Bovine Serum Albumin (BSA) (Beyotime, P0023B) in TBST (Servicebio, G0001) and then incubated with primary antibodies against CD206(1:400,Cell Signaling Technology (CST), 24595), COX5A (1:500, ABclonal, A6437), and TOM20 (1:400, CST, 42406), followed by secondary antibody incubationThe slides were then washed, counterstained with DAPI.

Gene Expression:

Article Title: CX3CL1-CX3CR1 signaling orchestrates malignant progression of prostate cancer through luminal progenitor-macrophage crosstalk.
Article Snippet: Imaging was performed using a confocal laser scanning microscope (Nikon A2, Japan). .. The following primary antibodies were used: anti-F4/80 (1:200, Cat# 70076, Cell Signaling Technology, USA), anti-CD206 (1:300, Cat# 24595, Cell Signaling Technology, USA), anti-CX3CR1 (1:250, Cat# ab250888, Abcam, USA), anti-CX3CL1 (1:200, Cat# 67735-1-Ig, Proteintech, Wuhan, China), anti-CD80 cycling conditions were as follows: 95 °C for 30 s, followed by 40 cycles of 95 °C for 5 s and 60 °C for 34 s. Gene expression was normalized to Gapdh and analyzed using the 2–ΔΔCt method. ..

Western Blot:

Article Title: M2 macrophage-mediated tigecycline nanoparticles for combating CRKP pneumonia via antibacterial and immunomodulatory therapy.
Article Snippet: Pneumonia caused by carbapenem-resistant Klebsiella pneumoniae (CRKP) has a high mortality rate and exhibits multiple drug resistance, making current antibacterial treatments of limited efficacy.. To address the challenges of ineffective drug accumulation at the infection site and excessive inflammation leading to tissue damage, this study developed a cell-based nanobionic drug delivery system (denoted as PT@M2, PLGA-TIG nanoparticles loaded into M2 macrophages).. This system encapsulates poly(lactic-co-glycolic acid) (PLGA) loaded with tigecycline within M2-type macrophages, thereby achieving stable circulation, rapid release in acidic microenvironments, and targeted delivery to the lungs.

Image Search Results

LA released from T-gel degradation induces macrophage M2 polarization and promotes fibroblast activation and collagen production. (A) Flow cytometry analysis of the association between T-gel degradation products and macrophage M2 polarization ( n = 3, data represent mean ± s.d.). ∗∗∗∗P < 0.0001. (B) RNA-seq analysis of M2 macrophage marker expression in tissues one week after ID and SC injection of T-gel. (C–D) Immunofluorescence analysis of CD206 (C) and FAPα (D) expression in tissues ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (E) Schematic diagram of the co-culture system showing RAW264.7 macrophages pretreated with T-gel extract medium that were subsequently co-cultured with L929 fibroblasts. (F–G) Collagen expression in L929 cells from the co-culture system assessed by Western blot (F) and ELISA (G). “C” represents RAW264.7 pretreated with blank medium; “T” represents RAW264.7 pretreated with T-gel extract medium. n = 3, data represent mean ± s.d. ∗P < 0.05 and ∗∗P < 0.01. (H) ELISA analysis of TGFβ expression in RAW264.7 cells treated with T-gel extract medium ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (I) Schematic representation of LA, released during T-gel degradation, programming macrophages toward an M2 phenotype and subsequently promoting fibroblast activation and collagen secretion.

Journal: Bioactive Materials

Article Title: Injection site dictates the immune response to a biodegradable polymer and corresponding collagen regeneration

doi: 10.1016/j.bioactmat.2026.04.004

Figure Lengend Snippet: LA released from T-gel degradation induces macrophage M2 polarization and promotes fibroblast activation and collagen production. (A) Flow cytometry analysis of the association between T-gel degradation products and macrophage M2 polarization ( n = 3, data represent mean ± s.d.). ∗∗∗∗P < 0.0001. (B) RNA-seq analysis of M2 macrophage marker expression in tissues one week after ID and SC injection of T-gel. (C–D) Immunofluorescence analysis of CD206 (C) and FAPα (D) expression in tissues ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (E) Schematic diagram of the co-culture system showing RAW264.7 macrophages pretreated with T-gel extract medium that were subsequently co-cultured with L929 fibroblasts. (F–G) Collagen expression in L929 cells from the co-culture system assessed by Western blot (F) and ELISA (G). “C” represents RAW264.7 pretreated with blank medium; “T” represents RAW264.7 pretreated with T-gel extract medium. n = 3, data represent mean ± s.d. ∗P < 0.05 and ∗∗P < 0.01. (H) ELISA analysis of TGFβ expression in RAW264.7 cells treated with T-gel extract medium ( n = 3, data represent mean ± s.d.). ∗∗P < 0.01. (I) Schematic representation of LA, released during T-gel degradation, programming macrophages toward an M2 phenotype and subsequently promoting fibroblast activation and collagen secretion.

Article Snippet: Following permeabilization, cells were stained with Phycoerythrin (PE)-conjugated anti-mouse CD206 antibody (Elabscience, E-AB-F1135D) for 30 min at 4 °C in the dark.

Techniques: Activation Assay, Flow Cytometry, RNA Sequencing, Marker, Expressing, Injection, Immunofluorescence, Co-Culture Assay, Cell Culture, Western Blot, Enzyme-linked Immunosorbent Assay

Evaluation of mucosal status after tracheal mucosal injury in rabbits . (a) Gross morphology and Masson staining of mucosal defects (n = 3). (b – f) Tracheal samples were collected on Day 10, and RNA sequencing was performed to assess biological differences between Native and Model groups (n = 3). (b) Principal components analysis of samples. (c) Volcano plot of DEGs. (d) KEGG enrichment analysis of DEGs. (e) Chord plot of enriched KEGG terms. (f) Heatmaps of DEGs associated with inflammation and oxidative stress. (g) IF staining of FISH (marker of bacteria, pink), iNOS (marker of M1 macrophages, orange), CD206 (marker of M2 macrophages, green), and immunohistochemical staining of CD31 (marker of endothelial cells) in various samples, blood vessels are denoted by triangles.

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Evaluation of mucosal status after tracheal mucosal injury in rabbits . (a) Gross morphology and Masson staining of mucosal defects (n = 3). (b – f) Tracheal samples were collected on Day 10, and RNA sequencing was performed to assess biological differences between Native and Model groups (n = 3). (b) Principal components analysis of samples. (c) Volcano plot of DEGs. (d) KEGG enrichment analysis of DEGs. (e) Chord plot of enriched KEGG terms. (f) Heatmaps of DEGs associated with inflammation and oxidative stress. (g) IF staining of FISH (marker of bacteria, pink), iNOS (marker of M1 macrophages, orange), CD206 (marker of M2 macrophages, green), and immunohistochemical staining of CD31 (marker of endothelial cells) in various samples, blood vessels are denoted by triangles.

Article Snippet: Cells were then incubated overnight at 4 °C with rabbit polyclonal antibodies against CD86 or CD206 (1:200, Proteintech), followed by 1 h incubation with Alexa Fluor 488-conjugated or CoraLite Plus 594-conjugated goat anti-rabbit IgG secondary antibodies (1:200, Proteintech).

Techniques: Staining, RNA Sequencing, Marker, Bacteria, Immunohistochemical staining

Effects of Gel-AgNA/MgGA MN on oxidative stress, macrophage polarization, and angiogenesis after treatment with Gel, Gel-MgGA, or Gel-AgNA/MgGA MN. (a) Representative fluorescence images of DCFH-DA staining (marker of ROS, green) and quantitative analysis of ROS levels in RAW264.7 cells (n = 3). (b – c) Immunofluorescence images and quantitative analysis of CD86+ and CD206+ macrophages in RAW264.7 cells after different treatments (n = 3). (d) Flow cytometry analysis of RAW264.7 macrophages (n = 3). (e) Schematic illustration of HUVECs co-cultured with various MN. (f) Representative images and quantification of Transwell assays in HUVECs (n = 3). (g) Representative images and quantification of EdU assays in HUVECs (n = 3). (h) RT-PCR analysis of angiogenesis-related gene expression in HUVECs after co-culture with MN for 3 days (n = 3).

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Effects of Gel-AgNA/MgGA MN on oxidative stress, macrophage polarization, and angiogenesis after treatment with Gel, Gel-MgGA, or Gel-AgNA/MgGA MN. (a) Representative fluorescence images of DCFH-DA staining (marker of ROS, green) and quantitative analysis of ROS levels in RAW264.7 cells (n = 3). (b – c) Immunofluorescence images and quantitative analysis of CD86+ and CD206+ macrophages in RAW264.7 cells after different treatments (n = 3). (d) Flow cytometry analysis of RAW264.7 macrophages (n = 3). (e) Schematic illustration of HUVECs co-cultured with various MN. (f) Representative images and quantification of Transwell assays in HUVECs (n = 3). (g) Representative images and quantification of EdU assays in HUVECs (n = 3). (h) RT-PCR analysis of angiogenesis-related gene expression in HUVECs after co-culture with MN for 3 days (n = 3).

Techniques: Fluorescence, Staining, Marker, Immunofluorescence, Flow Cytometry, Cell Culture, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Co-Culture Assay

Gel-AgNA/MgGA MN remodel the microenvironment after TMI by regulating infection, inflammation, oxidative stress, and vascular disruption. (a) FISH (marker of bacteria, red) staining of harvested samples after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b, c) Quantitative analysis of bacterial coverage and fluorescence intensity of FISH (n = 9). (d) Heatmaps of DEGs related to inflammation and oxidative stress. (e) RT-PCR analysis showing the relative expression levels of IL-1, TNF-α, HIF-1α, and IL-6 (n = 3). (f) IF staining of iNOS (marker of M1 macrophages, red) and CD206 (marker of M2 macrophages, green). (g) Quantitative analysis of iNOS and CD206 fluorescence intensity. (h) RT-PCR analysis showing the relative expression levels of Arg1 and CD206. (i) IF staining of CD31 (marker of blood vessels, red). (j, k) RT-PCR analysis showing the relative expression levels of VEGF and HIF-1α (n = 3).

Journal: Bioactive Materials

Article Title: Spatiotemporally engineered microneedle for microenvironment remodeling propels mucosal regeneration after tracheal mucosal injury

doi: 10.1016/j.bioactmat.2026.01.026

Figure Lengend Snippet: Gel-AgNA/MgGA MN remodel the microenvironment after TMI by regulating infection, inflammation, oxidative stress, and vascular disruption. (a) FISH (marker of bacteria, red) staining of harvested samples after treated with Gel, Gel-AgNA, Gel-MgGA, and Gel-AgNA/MgGA MN. (b, c) Quantitative analysis of bacterial coverage and fluorescence intensity of FISH (n = 9). (d) Heatmaps of DEGs related to inflammation and oxidative stress. (e) RT-PCR analysis showing the relative expression levels of IL-1, TNF-α, HIF-1α, and IL-6 (n = 3). (f) IF staining of iNOS (marker of M1 macrophages, red) and CD206 (marker of M2 macrophages, green). (g) Quantitative analysis of iNOS and CD206 fluorescence intensity. (h) RT-PCR analysis showing the relative expression levels of Arg1 and CD206. (i) IF staining of CD31 (marker of blood vessels, red). (j, k) RT-PCR analysis showing the relative expression levels of VEGF and HIF-1α (n = 3).

Techniques: Infection, Disruption, Marker, Bacteria, Staining, Fluorescence, Reverse Transcription Polymerase Chain Reaction, Expressing

EHF promotes lung cancer cell malignancy and M2 macrophage polarization. A549 and H520 cells were transfected with control (Ctrl) or EHF-knockdown (KD-EHF) plasmids. (A-B) Western blot and quantification of EHF protein levels in A549 and H520 cells. (C-D) EdU staining and quantification of EdU + cells in A549 and H520 cells, assessing proliferation. (E-H) Glucose uptake and lactate production assays were conducted using commercial kits to evaluate glycolytic output. (I-J) Flow cytometric analysis of apoptosis. (K-L) Transwell assay was employed to examine cell migration. (M − P) THP-1 cells were differentiated into THP-1-M0 macrophages with 100 ng/mL PMA for 24 h. Culture supernatants from Ctrl- or KD-EHF–transfected A549 and H520 cells were collected and co-incubated with THP-1-M0 macrophages. (M − N) Flow cytometric analysis was performed to assess the proportion of CD206 + M2-polarized macrophages. (O–P) ELISA was conducted to quantify the secretion of M2-associated cytokines (TGF-β1, IL-10, and VEGFA) in the supernatants of THP-1-M0 macrophages. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Journal: Regenerative Therapy

Article Title: Lung cancer cell-derived exosomal EHF drives M2 macrophage polarization via transcriptional activation of RNF41 to promote tumor progression

doi: 10.1016/j.reth.2026.101104

Figure Lengend Snippet: EHF promotes lung cancer cell malignancy and M2 macrophage polarization. A549 and H520 cells were transfected with control (Ctrl) or EHF-knockdown (KD-EHF) plasmids. (A-B) Western blot and quantification of EHF protein levels in A549 and H520 cells. (C-D) EdU staining and quantification of EdU + cells in A549 and H520 cells, assessing proliferation. (E-H) Glucose uptake and lactate production assays were conducted using commercial kits to evaluate glycolytic output. (I-J) Flow cytometric analysis of apoptosis. (K-L) Transwell assay was employed to examine cell migration. (M − P) THP-1 cells were differentiated into THP-1-M0 macrophages with 100 ng/mL PMA for 24 h. Culture supernatants from Ctrl- or KD-EHF–transfected A549 and H520 cells were collected and co-incubated with THP-1-M0 macrophages. (M − N) Flow cytometric analysis was performed to assess the proportion of CD206 + M2-polarized macrophages. (O–P) ELISA was conducted to quantify the secretion of M2-associated cytokines (TGF-β1, IL-10, and VEGFA) in the supernatants of THP-1-M0 macrophages. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Article Snippet: Membranes were blocked with 5% skim milk in TBST, incubated with primary antibodies against EHF (1:1000, Catalog #: 27195-1-AP, Proteintech, Wuhan, China), TSG101 (1:1000, Catalog #: 14497-1-AP, Proteintech), Calnexin (1:1000, Catalog #: 10427-2-AP, Proteintech), CD9 (1:2000, Catalog #: 60232-1-Ig, Proteintech), RNF41 (1:500, Catalog #: 17233-1-AP, Proteintech), CD206 (1:1000, Catalog #: 18704-1-AP, Proteintech), TGF-β1 (1:1000, Catalog #: 26155-1-AP, Proteintech), VEGFA (1:1000, Catalog #: ab46154, Abcam, Cambridge, UK), and β-actin (1:1000, Catalog #: 66009-1-Ig, Proteintech) overnight at 4 °C, followed by HRP-conjugated secondary antibodies (1:5000, Catalog #: ab6721/ab205719, Abcam) for 1 h at room temperature.

Techniques: Transfection, Control, Knockdown, Western Blot, Staining, Transwell Assay, Migration, Incubation, Enzyme-linked Immunosorbent Assay

Exosomal EHF reprograms THP-1-M0 macrophages to promote lung cancer cell malignancy and angiogenesis via paracrine signaling. (A) Schematic of the paracrine co-culture system: Exosomes from control (Ctrl) or EHF-knockdown (KD-EHF) A549/H520 cells were co-incubated with THP-1-M0 macrophages. The medium from these macrophages was used to treat A549/H520 cells or HUVECs. (B-E) THP-1-M0 macrophages were treated with three conditions: blank control (no exosome), exosomes from control-transfected A549/H520 cells (Exo Ctrl ), or exosomes from EHF-knockdown A549/H520 cells (Exo KD−EHF ). (B–C) Flow cytometry analysis of CD206 + M2 macrophage proportions in THP-1-M0 cells. (D-E) ELISA measurement of M2-associated cytokines (TGF-β1, IL-10, and VEGFA). (F-M) The medium from exosome treated macrophages was then used to incubate A549/H520 cells or HUVECs. (F-G) EdU staining and quantification of EdU + proliferating A549 and H520 cells. (H–I) Flow cytometric analysis of apoptosis in A549 and H520 cells. (J-K) Transwell migration assays and quantification of migrated A549 and H520 cells. (L-M) Tube formation assays and quantification of tube numbers in HUVECs. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Journal: Regenerative Therapy

Article Title: Lung cancer cell-derived exosomal EHF drives M2 macrophage polarization via transcriptional activation of RNF41 to promote tumor progression

doi: 10.1016/j.reth.2026.101104

Figure Lengend Snippet: Exosomal EHF reprograms THP-1-M0 macrophages to promote lung cancer cell malignancy and angiogenesis via paracrine signaling. (A) Schematic of the paracrine co-culture system: Exosomes from control (Ctrl) or EHF-knockdown (KD-EHF) A549/H520 cells were co-incubated with THP-1-M0 macrophages. The medium from these macrophages was used to treat A549/H520 cells or HUVECs. (B-E) THP-1-M0 macrophages were treated with three conditions: blank control (no exosome), exosomes from control-transfected A549/H520 cells (Exo Ctrl ), or exosomes from EHF-knockdown A549/H520 cells (Exo KD−EHF ). (B–C) Flow cytometry analysis of CD206 + M2 macrophage proportions in THP-1-M0 cells. (D-E) ELISA measurement of M2-associated cytokines (TGF-β1, IL-10, and VEGFA). (F-M) The medium from exosome treated macrophages was then used to incubate A549/H520 cells or HUVECs. (F-G) EdU staining and quantification of EdU + proliferating A549 and H520 cells. (H–I) Flow cytometric analysis of apoptosis in A549 and H520 cells. (J-K) Transwell migration assays and quantification of migrated A549 and H520 cells. (L-M) Tube formation assays and quantification of tube numbers in HUVECs. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Techniques: Co-Culture Assay, Control, Knockdown, Incubation, Transfection, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Staining, Migration

RNF41 mediates exosomal EHF-driven pro-tumorigenic effects in lung cancer. (A) Schematic of the rescue co-culture system: THP-1-M0 macrophages (control or RNF41-overexpressing) were incubated with exosomes from control (Exo Ctrl ) or EHF-knockdown (Exo KD−EHF ) A549/H520 cells. The medium from these co-cultures was used to treat A549/H520 cells or HUVECs. (B–C) Flow cytometry was used to analyze the proportion of CD206 + M2-polarized macrophages in THP-1-M0 cells. (D-E) ELISA was employed to quantify the levels of M2-associated cytokines (TGF-β1, IL-10, and VEGFA) in the CM from macrophages. (F-G) EdU assays were carried out to measure the proliferation of A549 and H520 cells. (H–I) Annexin V/PI flow cytometry was used to assess the apoptosis of A549 and H520 cells treated with CM. (J-K) Transwell assays were performed to evaluate the migration of A549 and H520 cells. (L-M) Tube formation assays were conducted on HUVECs treated with CM. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Journal: Regenerative Therapy

Article Title: Lung cancer cell-derived exosomal EHF drives M2 macrophage polarization via transcriptional activation of RNF41 to promote tumor progression

doi: 10.1016/j.reth.2026.101104

Figure Lengend Snippet: RNF41 mediates exosomal EHF-driven pro-tumorigenic effects in lung cancer. (A) Schematic of the rescue co-culture system: THP-1-M0 macrophages (control or RNF41-overexpressing) were incubated with exosomes from control (Exo Ctrl ) or EHF-knockdown (Exo KD−EHF ) A549/H520 cells. The medium from these co-cultures was used to treat A549/H520 cells or HUVECs. (B–C) Flow cytometry was used to analyze the proportion of CD206 + M2-polarized macrophages in THP-1-M0 cells. (D-E) ELISA was employed to quantify the levels of M2-associated cytokines (TGF-β1, IL-10, and VEGFA) in the CM from macrophages. (F-G) EdU assays were carried out to measure the proliferation of A549 and H520 cells. (H–I) Annexin V/PI flow cytometry was used to assess the apoptosis of A549 and H520 cells treated with CM. (J-K) Transwell assays were performed to evaluate the migration of A549 and H520 cells. (L-M) Tube formation assays were conducted on HUVECs treated with CM. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Techniques: Co-Culture Assay, Control, Incubation, Knockdown, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Migration

EHF knockdown inhibits tumor growth and downregulates M2-associated molecules in v ivo. Nude mice were subcutaneously implanted with Ctrl or KD-EHF A549 cells. (A) Tumor volume was measured every 5 days over 30 days. (B) Tumor weight. (C) Representative images of excised tumors. (D) Western blot analysis of RNF41, CD206, TGF-β1, and VEGFA expression levels in tumor tissues. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Journal: Regenerative Therapy

Article Title: Lung cancer cell-derived exosomal EHF drives M2 macrophage polarization via transcriptional activation of RNF41 to promote tumor progression

doi: 10.1016/j.reth.2026.101104

Figure Lengend Snippet: EHF knockdown inhibits tumor growth and downregulates M2-associated molecules in v ivo. Nude mice were subcutaneously implanted with Ctrl or KD-EHF A549 cells. (A) Tumor volume was measured every 5 days over 30 days. (B) Tumor weight. (C) Representative images of excised tumors. (D) Western blot analysis of RNF41, CD206, TGF-β1, and VEGFA expression levels in tumor tissues. Data are presented as mean ± SD. P < 0.05 denotes statistical significance.

Techniques: Knockdown, Western Blot, Expressing

The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 2 weeks. (a) Schematic diagram of in vivo experiments of hydrogel treatment of TMJ-OA. HE staining (b), SO/FG staining (c), immunohistochemical staining of COLII (d) and MMP13 (e), immunofluorescence staining of CD86 (f) and CD206 (g) at the synovial, and immunofluorescence staining of IL-1β (h) in the TMJ of rats after 2 weeks of treatment, scale bar = 100 μm. (i) Histological OARSI score of articular cartilage after 2 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (c–h). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

Journal: Bioactive Materials

Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

doi: 10.1016/j.bioactmat.2026.01.031

Figure Lengend Snippet: The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 2 weeks. (a) Schematic diagram of in vivo experiments of hydrogel treatment of TMJ-OA. HE staining (b), SO/FG staining (c), immunohistochemical staining of COLII (d) and MMP13 (e), immunofluorescence staining of CD86 (f) and CD206 (g) at the synovial, and immunofluorescence staining of IL-1β (h) in the TMJ of rats after 2 weeks of treatment, scale bar = 100 μm. (i) Histological OARSI score of articular cartilage after 2 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (c–h). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

Article Snippet: Additionally, the sections were stained with antibodies specific to anti-CD86, CD206, and IL-1β (Boster Biological Technology Co., Ltd., Wuhan, China) for immunofluorescence analysis.

Techniques: In Vivo, Staining, Immunohistochemical staining, Immunofluorescence, Comparison

The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 8 weeks. HE staining (a), SO/FG staining (b), immunohistochemical staining of COLII (c) and MMP13 (d), immunofluorescence staining of CD86 (e) and CD206 (f) at the synovial, and immunofluorescence staining of IL-1β (g) in the TMJ of rats after 8 weeks of treatment, scale bar = 100 μm. (h) Histological OARSI score of articular cartilage after 8 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (b–g). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

Journal: Bioactive Materials

Article Title: Nanozyme hydrogels remodel pathological microenvironment for temporomandibular joint osteoarthritis therapy via inhibiting MAPK signal pathway

doi: 10.1016/j.bioactmat.2026.01.031

Figure Lengend Snippet: The in vivo therapeutic effect of Mn-NC composite hydrogels on TMJ-OA after 8 weeks. HE staining (a), SO/FG staining (b), immunohistochemical staining of COLII (c) and MMP13 (d), immunofluorescence staining of CD86 (e) and CD206 (f) at the synovial, and immunofluorescence staining of IL-1β (g) in the TMJ of rats after 8 weeks of treatment, scale bar = 100 μm. (h) Histological OARSI score of articular cartilage after 8 weeks of treatment and quantitative data of immunohistochemical positive area and proportion of immunofluorescence positive cells in (b–g). Data represent means ± SD, n = 3. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 indicates a significant difference in comparison to the Sham group. # p < 0.05, ## p < 0.01, and ### p < 0.001 suggests a significant difference in comparison to the MIA group.

Techniques: In Vivo, Staining, Immunohistochemical staining, Immunofluorescence, Comparison

MMP12 silencing inhibited M2 macrophage polarization. THP-1 cells were differentiated into M0 macrophages (THP-1 M0) by treatment with 100 ng/mL PMA for 24 h. (A) Flow cytometry was used to quantify the number of CD68-positive cells. Subsequently, KYSE150 cells were co-cultured with the THP-1-derived macrophages using a Transwell system. (B) The mRNA levels of IL-10, Arg-1, and TGF-β were detected by qRT-PCR. (C) Flow cytometry was used to quantify the number of CD206-positive macrophages. (D) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Journal: Regenerative Therapy

Article Title: WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells

doi: 10.1016/j.reth.2026.101101

Figure Lengend Snippet: MMP12 silencing inhibited M2 macrophage polarization. THP-1 cells were differentiated into M0 macrophages (THP-1 M0) by treatment with 100 ng/mL PMA for 24 h. (A) Flow cytometry was used to quantify the number of CD68-positive cells. Subsequently, KYSE150 cells were co-cultured with the THP-1-derived macrophages using a Transwell system. (B) The mRNA levels of IL-10, Arg-1, and TGF-β were detected by qRT-PCR. (C) Flow cytometry was used to quantify the number of CD206-positive macrophages. (D) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Article Snippet: Additionally, to determine the proportion of CD206-positive macrophages, single-cell suspensions of these cells were incubated with a FITC-conjugated anti-CD206 antibody (E-AB-F1161E, Elabscience).

Techniques: Flow Cytometry, Cell Culture, Derivative Assay, Quantitative RT-PCR, Migration, Transwell Migration Assay

WTAP silencing inhibited M2 macrophage polarization by regulating MMP12. THP-1 cells were differentiated into M0 macrophages (THP-1 M0) by treatment with 100 ng/mL PMA for 24 h. KYSE150 cells were transfected with si-WTAP, MMP12 overexpression plasmid, or the matched control (si-NC and oe-NC). Subsequently, these KYSE150 cells were co-cultured with the THP-1-derived macrophages using a Transwell system. (A) The mRNA levels of IL-10, Arg-1, and TGF-β were detected by qRT-PCR. (B) Flow cytometry was used to quantify the number of CD206-positive macrophages. (C) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Journal: Regenerative Therapy

Article Title: WTAP stabilizes MMP12 expression to promote the malignant phenotypes of esophageal cancer cells

doi: 10.1016/j.reth.2026.101101

Figure Lengend Snippet: WTAP silencing inhibited M2 macrophage polarization by regulating MMP12. THP-1 cells were differentiated into M0 macrophages (THP-1 M0) by treatment with 100 ng/mL PMA for 24 h. KYSE150 cells were transfected with si-WTAP, MMP12 overexpression plasmid, or the matched control (si-NC and oe-NC). Subsequently, these KYSE150 cells were co-cultured with the THP-1-derived macrophages using a Transwell system. (A) The mRNA levels of IL-10, Arg-1, and TGF-β were detected by qRT-PCR. (B) Flow cytometry was used to quantify the number of CD206-positive macrophages. (C) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Techniques: Transfection, Over Expression, Plasmid Preparation, Control, Cell Culture, Derivative Assay, Quantitative RT-PCR, Flow Cytometry, Migration, Transwell Migration Assay

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