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anti cd206  (R&D Systems)


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    R&D Systems anti cd206
    Anti Cd206, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 378 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mmr+cd206/pmc13108569-265-123-126?v=R%26D+Systems
    Average 96 stars, based on 378 article reviews
    anti cd206 - by Bioz Stars, 2026-07
    96/100 stars

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    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 <t>CD206</t> (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.
    Anti Mouse Cd206 Antibody, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    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 <t>CD206-positive</t> macrophages. (D) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.
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    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 <t>CD206-positive</t> macrophages. (D) Cell migration analysis by transwell migration assay. ∗ P < 0.05, ∗∗ P < 0.01 and ∗∗∗ P < 0.001.
    Anti Cd206, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems cd206
    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and <t>CD206</t> (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.
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    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and <t>CD206</t> (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.
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    Bio-Techne corporation mouse mmr/cd206 antibody
    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and <t>CD206</t> (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.
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    Elabscience Biotechnology apc anti mouse cd206 mmr antibody
    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and <t>CD206</t> (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.
    Apc Anti Mouse Cd206 Mmr Antibody, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems anti mmr cd206
    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and <t>CD206</t> (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.
    Anti Mmr Cd206, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    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

    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.

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

    Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and CD206 (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.

    Journal: Aging Cell

    Article Title: Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction

    doi: 10.1111/acel.70490

    Figure Lengend Snippet: Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and CD206 (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.

    Article Snippet: For immunofluorescence (IF), the following antibodies were used: CD206 (R&D Systems, AF2534, 1:75); CD80 (Abclonal A23688, 1:50); CD68 (Invitrogen, MA5‐1324, 1:75); F4/80 (Abcam, ab16911, 1:50); TERT (Biossusa, bs‐1411R, 1:50).

    Techniques: Starch, Reverse Transcription Polymerase Chain Reaction, Expressing, Staining

    AT abnormalities in LysM‐ Tert KO mice. (a) Senescence‐associated β‐galactosidase staining of VAT from 20‐month‐old female mice. (b) Senescence‐associated β‐galactosidase staining of adherent cells from VAT in (a). Arrows: Senescent cells. (c) Flow cytometry on VAT from A, revealing a lower frequency of mG+ macrophages expressing CD206 in KO mice. (d) Flow cytometry on SAT, revealing a higher frequency of mG+ macrophages expressing CD86 in KO mice. (e) IF with antibodies against CD68 and CD206 reveals a lower frequency of CD206+ macrophages (red arrows) in SAT of KO mice. IF with antibodies against perilipin‐1 and F4/80 reveals comparable adipocyte size in SAT of WT and KO mice. (f) Trichrome staining reveals fibrosis (arrows) in SAT of KO mice. In (d, e) 4‐month‐old male mice fed an atherogenic diet were used. Scale bar: 50 μm.

    Journal: Aging Cell

    Article Title: Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction

    doi: 10.1111/acel.70490

    Figure Lengend Snippet: AT abnormalities in LysM‐ Tert KO mice. (a) Senescence‐associated β‐galactosidase staining of VAT from 20‐month‐old female mice. (b) Senescence‐associated β‐galactosidase staining of adherent cells from VAT in (a). Arrows: Senescent cells. (c) Flow cytometry on VAT from A, revealing a lower frequency of mG+ macrophages expressing CD206 in KO mice. (d) Flow cytometry on SAT, revealing a higher frequency of mG+ macrophages expressing CD86 in KO mice. (e) IF with antibodies against CD68 and CD206 reveals a lower frequency of CD206+ macrophages (red arrows) in SAT of KO mice. IF with antibodies against perilipin‐1 and F4/80 reveals comparable adipocyte size in SAT of WT and KO mice. (f) Trichrome staining reveals fibrosis (arrows) in SAT of KO mice. In (d, e) 4‐month‐old male mice fed an atherogenic diet were used. Scale bar: 50 μm.

    Article Snippet: For immunofluorescence (IF), the following antibodies were used: CD206 (R&D Systems, AF2534, 1:75); CD80 (Abclonal A23688, 1:50); CD68 (Invitrogen, MA5‐1324, 1:75); F4/80 (Abcam, ab16911, 1:50); TERT (Biossusa, bs‐1411R, 1:50).

    Techniques: Staining, Flow Cytometry, Expressing

    Lung abnormalities in LysM‐ Tert KO mice. (a) IF with antibodies against F4/80 and CD206 reveals a lower frequency of CD206+ macrophages (red arrows) in lungs of 6 month‐old chow‐fed KO mice, compared to WT mice. (b) Data quantification for 10 view fields from A. * p < 0.05 (two‐sided Student's t ‐test). (c) Trichrome staining reveals fibrosis (arrows) in 20‐month‐old lungs of KO mice. (d) q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of Tgfb1 and Cola1a in lungs of KO male and female mice. Shown are mean+/− SEM (error bars). * p < 0.0001 (two‐sided Student's t ‐test). ** p < 0.01. In (a), (b), and (d), 6‐month‐old male mice fed a chow diet were used. Scale bar: 50 μm.

    Journal: Aging Cell

    Article Title: Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction

    doi: 10.1111/acel.70490

    Figure Lengend Snippet: Lung abnormalities in LysM‐ Tert KO mice. (a) IF with antibodies against F4/80 and CD206 reveals a lower frequency of CD206+ macrophages (red arrows) in lungs of 6 month‐old chow‐fed KO mice, compared to WT mice. (b) Data quantification for 10 view fields from A. * p < 0.05 (two‐sided Student's t ‐test). (c) Trichrome staining reveals fibrosis (arrows) in 20‐month‐old lungs of KO mice. (d) q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of Tgfb1 and Cola1a in lungs of KO male and female mice. Shown are mean+/− SEM (error bars). * p < 0.0001 (two‐sided Student's t ‐test). ** p < 0.01. In (a), (b), and (d), 6‐month‐old male mice fed a chow diet were used. Scale bar: 50 μm.

    Article Snippet: For immunofluorescence (IF), the following antibodies were used: CD206 (R&D Systems, AF2534, 1:75); CD80 (Abclonal A23688, 1:50); CD68 (Invitrogen, MA5‐1324, 1:75); F4/80 (Abcam, ab16911, 1:50); TERT (Biossusa, bs‐1411R, 1:50).

    Techniques: Staining, Reverse Transcription Polymerase Chain Reaction, Expressing