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mouse cardiac endothelial cell line (Cedarlane)

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Cedarlane mouse cardiac endothelial cell line
Mouse Cardiac Endothelial Cell Line, supplied by Cedarlane, used in various techniques. Bioz Stars score: 93/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 41 article reviews

mouse cardiac endothelial cell line - by Bioz Stars, 2026-05

93/100 stars

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MCECs were seeded overnight, and upon reaching full confluence, were treated with the indicated dose of oleic acid (OA) for the specified times. A – D Representative immunofluorescence images of Bodipy staining and plate-read fluorescence intensity quantification showing that OA increased LD formation in a dose- and time-dependent manner. E – I MCECs were pretreated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) or 10 µM DGAT2 inhibitor PF-06424439 (DGAT2i) overnight, followed by treatment with 500 µM OA for 6 h. Representative Bodipy-stained images ( E ) and plate-read fluorescence intensity quantification ( F ) indicated that DGAT1 inhibition blocked OA-induced LD formation. G Plin2 mRNA levels were measured, showing no significant effect of DGAT1 inhibition on transcription. H , I Representative immunoblots and quantification of PLIN2 protein levels demonstrate that DGAT1 inhibition significantly reduces OA-induced PLIN2 expression. Original uncropped WB bands for Fig. 1H were presented in Supplementary Fig. . J – L MCECs were transfected with 20 nM siRNA targeting Dgat1 (si- Dgat1 ) or control siRNA (si- Ctrl ) for 24 h, followed by 500 µM OA treatment for 6 h. Bodipy staining ( J ) and plate-reader fluorescence intensity quantification ( K ) show that Dgat1 knockdown blocked OA-induced LD formation. L Dgat1 mRNA levels confirming successful knockdown. RFU, relative fluorescence unit. Images in A , C , E and J were acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar =20 µm. Data in B , D , F , G , and L are shown as fold-changes relative to control (CTRL = 1), whereas I and K are normalized to the OA group (OA = 1). All datasets analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test ( B , D , F – H , K ) or by the Mann–Whitney test ( L ). * P < 0.05 vs. 0 ( B , D ), CTRL ( F – H ), or si-C ( K , L ); # P < 0.05 vs. OA ( F , I ) or si-C + OA ( K ). n = 4.

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching full confluence, were treated with the indicated dose of oleic acid (OA) for the specified times. A – D Representative immunofluorescence images of Bodipy staining and plate-read fluorescence intensity quantification showing that OA increased LD formation in a dose- and time-dependent manner. E – I MCECs were pretreated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) or 10 µM DGAT2 inhibitor PF-06424439 (DGAT2i) overnight, followed by treatment with 500 µM OA for 6 h. Representative Bodipy-stained images ( E ) and plate-read fluorescence intensity quantification ( F ) indicated that DGAT1 inhibition blocked OA-induced LD formation. G Plin2 mRNA levels were measured, showing no significant effect of DGAT1 inhibition on transcription. H , I Representative immunoblots and quantification of PLIN2 protein levels demonstrate that DGAT1 inhibition significantly reduces OA-induced PLIN2 expression. Original uncropped WB bands for Fig. 1H were presented in Supplementary Fig. . J – L MCECs were transfected with 20 nM siRNA targeting Dgat1 (si- Dgat1 ) or control siRNA (si- Ctrl ) for 24 h, followed by 500 µM OA treatment for 6 h. Bodipy staining ( J ) and plate-reader fluorescence intensity quantification ( K ) show that Dgat1 knockdown blocked OA-induced LD formation. L Dgat1 mRNA levels confirming successful knockdown. RFU, relative fluorescence unit. Images in A , C , E and J were acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar =20 µm. Data in B , D , F , G , and L are shown as fold-changes relative to control (CTRL = 1), whereas I and K are normalized to the OA group (OA = 1). All datasets analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test ( B , D , F – H , K ) or by the Mann–Whitney test ( L ). * P < 0.05 vs. 0 ( B , D ), CTRL ( F – H ), or si-C ( K , L ); # P < 0.05 vs. OA ( F , I ) or si-C + OA ( K ). n = 4.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Immunofluorescence, Staining, Fluorescence, Inhibition, Western Blot, Expressing, Transfection, Control, Knockdown, MANN-WHITNEY

MCECs were seeded overnight, and upon reaching sub-confluence, were pre-treated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) for 30 min, followed by treatment with 250 µM OA for 6 h. A , B Representative immunofluorescence images of SREBP1 or 2, and their nuclear intensities summary. An isotype-matched IgG control (mouse or rabbit) was included as a negative control to confirm staining specificity. C – G Transcriptional level of key lipogenesis genes, including Srebf1 , Scd1, Acaca , Fasn and Fads1 . H , I Transcriptional level of lipolysis genes: Atgl and Lipa . J – N Transcriptional level of FAO genes, including Pdk4 , Cpt1α , Slc25a20, Pparβ/δ , and Cpt2 . Images in A and B acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar =20 µm. Data are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs CTRL, # vs OA, P < 0.05, n = 4.

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching sub-confluence, were pre-treated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) for 30 min, followed by treatment with 250 µM OA for 6 h. A , B Representative immunofluorescence images of SREBP1 or 2, and their nuclear intensities summary. An isotype-matched IgG control (mouse or rabbit) was included as a negative control to confirm staining specificity. C – G Transcriptional level of key lipogenesis genes, including Srebf1 , Scd1, Acaca , Fasn and Fads1 . H , I Transcriptional level of lipolysis genes: Atgl and Lipa . J – N Transcriptional level of FAO genes, including Pdk4 , Cpt1α , Slc25a20, Pparβ/δ , and Cpt2 . Images in A and B acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar =20 µm. Data are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs CTRL, # vs OA, P < 0.05, n = 4.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Immunofluorescence, Control, Negative Control, Staining

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching sub-confluence, were pre-treated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) for 30 min, followed by treatment with 250 µM OA for 6 h. A – J Transcriptional level changes of ER-stress related genes, including Ern1, Atf6, Eif2ak3, Bip, Eif2s1, Ppp1r15a, Atf3, Trib3, Chac1, and Ddit3 . K – L Representative immunofluorescence images of CHOP staining ( K ) and summary of positive cells percentage ( L ). An isotype-matched rabbit IgG control was included as a negative control to confirm staining specificity. Images in K acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar = 20 µm. Data in A – J are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs CTRL, # vs OA, P < 0.05, n = 4.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Immunofluorescence, Staining, Control, Negative Control

MCECs were seeded overnight, and upon reaching sub-confluence, followed by treatment with different doses of OA for 6 h. A – H Effect of different doses of OA on mitochondrial functions, including basal respiration ( B ), maximal respiration ( C ), spare respiration capacity ( D ), ATP production ( E ), proton leak ( F ), non-mitochondrial respiration ( G ), and basal ECAR ( H ). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs 0, P < 0.05, n = 4. OCR, oxygen consumption rate, ECAR extracellular acidification rate.

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching sub-confluence, followed by treatment with different doses of OA for 6 h. A – H Effect of different doses of OA on mitochondrial functions, including basal respiration ( B ), maximal respiration ( C ), spare respiration capacity ( D ), ATP production ( E ), proton leak ( F ), non-mitochondrial respiration ( G ), and basal ECAR ( H ). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs 0, P < 0.05, n = 4. OCR, oxygen consumption rate, ECAR extracellular acidification rate.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques:

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching sub-confluence, were pre-treated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) for 30 min, followed by treatment with indicated doses of OA for 6 h. A–H Effect of OA and DGAT1i on mitochondrial functions, including basal respiration ( B ), maximal respiration ( C ), spare respiration capacity ( D ), ATP production ( E ), proton leak ( F ), non-mitochondrial respiration ( G ), and basal ECAR ( H ). I , J Representative confocal images of MitoTracker-labeled mitochondria ( I ). Quantification of mean mitochondrial fluorescence intensity ( J ). 1 µM rotenone 6 h was included as a positive control for mitochondrial disruption. Data in J are shown as fold-changes relative to control (CTRL = 1). Images in I were acquired using a 100× oil-immersion objective and a standard 10× eyepiece, with 2× digital zoom (effective ×2000 magnification). Scale bar= 5 µm. All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * P < 0.05 vs. CTRL without OA (0 µM), # P < 0.05 vs. CTRL treated with the same concentration of OA. n = 4. OCR, oxygen consumption rate; ECAR, extracellular acidification rate.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Labeling, Fluorescence, Positive Control, Disruption, Control, Concentration Assay

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching sub-confluence, were pre-treated with or without 5 µM DGAT1 inhibitor A-922500 (DGAT1i) for 30 min, followed by treatment with 250 µM OA for 6 h. A – L Transcriptional level changes of hypoxia-related genes, including Hif1a, Hif1β, Epas1(Hif2), Egln1, Egln2, Egln3, Siah2, Hilpda, Vegfa, Angptl4, Hk2, and Fgf21 . M , N Representative immunofluorescence images of HIF1a, and its nuclear intensities summary. An isotype-matched rabbit IgG control was included as a negative control to confirm staining specificity. Data in A – L are shown as fold-changes relative to control, while data in N are shown as fold-changes relative to OA. Images in M acquired using a 63× oil-immersion objective and a standard 10× eyepiece (effective ×630 magnification). Scale bar = 10 µm. All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * vs CTRL, # vs OA, P < 0.05, n = 4.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Immunofluorescence, Control, Negative Control, Staining

MCECs were seeded overnight, and upon reaching 70% confluence, were pre-treated with indicated inhibitors or activators for 30 min, followed by treatment with indicated doses OA for specified times. A Ferroptosis inhibitor liproxstatin (LIP) blocked GPX4 inhibitor RSL3-induced cell death after overnight treatment. B OA dose-dependently induced cell death in MCECs after overnight treatment. Effect of LIP ( C ) and ROS inhibitor (N-Acetyl-L-cysteine (NAC)) ( D ) on OA-induced cell death. E RSL3 sensitized OA-induced cell death. F LIP mitigated cell death induced by the combination of OA and RSL-3. G GPX4 activator PKUMDL-LC-101-D04 (PKU) rescued cells from OA-induced cell death. H , I Representative immunofluorescence images and intensity quantification showing overnight OA treatment decreased GPX4 expression. An isotype-matched rabbit IgG control was included as a negative control to confirm staining specificity. Images in H acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar = 20 µm. Data in I are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * P < 0.05 vs. corresponding CTRL lacking RSL3 ( A ), lacking OA ( B , I ), or lacking OA and additional treatments ( C – G ); # P < 0.05 vs. CTRL treated with the same concentration of RSL3 ( A ), the same concentration of OA ( C , D , E , G ), or OA + RSL3 ( F ). n = 4. OD, optical density.

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching 70% confluence, were pre-treated with indicated inhibitors or activators for 30 min, followed by treatment with indicated doses OA for specified times. A Ferroptosis inhibitor liproxstatin (LIP) blocked GPX4 inhibitor RSL3-induced cell death after overnight treatment. B OA dose-dependently induced cell death in MCECs after overnight treatment. Effect of LIP ( C ) and ROS inhibitor (N-Acetyl-L-cysteine (NAC)) ( D ) on OA-induced cell death. E RSL3 sensitized OA-induced cell death. F LIP mitigated cell death induced by the combination of OA and RSL-3. G GPX4 activator PKUMDL-LC-101-D04 (PKU) rescued cells from OA-induced cell death. H , I Representative immunofluorescence images and intensity quantification showing overnight OA treatment decreased GPX4 expression. An isotype-matched rabbit IgG control was included as a negative control to confirm staining specificity. Images in H acquired using a 40× objective and a standard 10× eyepiece (effective ×400 magnification). Scale bar = 20 µm. Data in I are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. * P < 0.05 vs. corresponding CTRL lacking RSL3 ( A ), lacking OA ( B , I ), or lacking OA and additional treatments ( C – G ); # P < 0.05 vs. CTRL treated with the same concentration of RSL3 ( A ), the same concentration of OA ( C , D , E , G ), or OA + RSL3 ( F ). n = 4. OD, optical density.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Immunofluorescence, Expressing, Control, Negative Control, Staining, Concentration Assay

MCECs were seeded overnight, and upon reaching 70% confluence, were pre-treated with indicated inhibitors for 30 min, followed by treatment with indicated doses OA for specified times. A Inhibition of DGAT1 exacerbated OA-induced ferroptosis. B Pan-caspase inhibitor (50 µM Z-VAD-FMK), caspase-3 inhibitor (20 µM Z-DEVD-FMK), caspase-1 inhibitor (30 µg/ml AC-YVAD-CMK), lysosome inhibitors chloroquine (5 µM CQ) and bafilomycin (10 nM BAF), and autophagy inhibitor spautin-1 (10 µM SP-1) had minimal or no effect on OA and DGAT1i-induced cell death. C Flow cytometric analysis revealed DGAT1 inhibition enhanced OA-induced lipid peroxidation measured by Liper-Fluo, a key marker for ferroptosis. D – J Transcriptional changes in ferroptosis-related genes, including Gpx4, Slc7a11, Slc3a2, Acsl4, Lpcat3, Fth1 and Hmox1 . K Dgat1 gene knockdown exacerbated OA-induced ferroptosis. Data in D – J are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. In A , K , * P < 0.05 vs. corresponding CTRL or si-C lacking OA and additional treatments; # P < 0.05 vs. CTRL or si-C treated with the same concentration of OA; & P < 0.05 vs. DGAT1i or si- Dgat1 with same concentration of OA. In B , * P < 0.05 vs. corresponding CTRL lacking OA and DGAT1i; # P < 0.05 vs. CTRL treated OA + DGAT1i. In C – J , * P <0.05 vs CTRL, # P <0.05 vs OA. n = 4. OD, optical density.

Journal: Cell Death Discovery

Article Title: Defective lipid droplet biogenesis exacerbates oleic acid-induced cellular homeostasis disruption and ferroptosis in mouse cardiac endothelial cells

doi: 10.1038/s41420-025-02669-5

Figure Lengend Snippet: MCECs were seeded overnight, and upon reaching 70% confluence, were pre-treated with indicated inhibitors for 30 min, followed by treatment with indicated doses OA for specified times. A Inhibition of DGAT1 exacerbated OA-induced ferroptosis. B Pan-caspase inhibitor (50 µM Z-VAD-FMK), caspase-3 inhibitor (20 µM Z-DEVD-FMK), caspase-1 inhibitor (30 µg/ml AC-YVAD-CMK), lysosome inhibitors chloroquine (5 µM CQ) and bafilomycin (10 nM BAF), and autophagy inhibitor spautin-1 (10 µM SP-1) had minimal or no effect on OA and DGAT1i-induced cell death. C Flow cytometric analysis revealed DGAT1 inhibition enhanced OA-induced lipid peroxidation measured by Liper-Fluo, a key marker for ferroptosis. D – J Transcriptional changes in ferroptosis-related genes, including Gpx4, Slc7a11, Slc3a2, Acsl4, Lpcat3, Fth1 and Hmox1 . K Dgat1 gene knockdown exacerbated OA-induced ferroptosis. Data in D – J are shown as fold-changes relative to control (CTRL = 1). All datasets were analyzed by the Kruskal–Wallis test with Dunn’s multiple-comparisons post hoc test. In A , K , * P < 0.05 vs. corresponding CTRL or si-C lacking OA and additional treatments; # P < 0.05 vs. CTRL or si-C treated with the same concentration of OA; & P < 0.05 vs. DGAT1i or si- Dgat1 with same concentration of OA. In B , * P < 0.05 vs. corresponding CTRL lacking OA and DGAT1i; # P < 0.05 vs. CTRL treated OA + DGAT1i. In C – J , * P <0.05 vs CTRL, # P <0.05 vs OA. n = 4. OD, optical density.

Article Snippet: The immortalized mouse cardiac endothelial cells (MCECs) line was purchased from Cedarlane (CLU510).

Techniques: Inhibition, Marker, Knockdown, Control, Concentration Assay

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: mCECs , Cedarlane , CLU510.

Techniques: Recombinant, Lysis, Staining, Modification, Sequencing, Synthesized, Blocking Assay, Enzyme-linked Immunosorbent Assay, Ab Array, Bicinchoninic Acid Protein Assay, SYBR Green Assay, Mass Spectrometry, Knock-Out, Software, Imaging

(A–C) sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , mLECs, and control mCECs were characterized for size (A) and by sEV protein marker array (B) and transmission electron microscopy (C). Scale bar: 100 nm. (D) BMDM were treated with PKH 26-labeled (red) CSC PDPN+ sEVs to show cell internalization. Scale bar: 25 μm. (E and F) Mass spectrometry analysis of protein content in sEVs derived from TNF-α- and AngII-pretreated mLECs and CSC PDPN+ cells revealed that ~1,000 proteins are commonly expressed by the two groups of sEVs and that ~2,000 proteins were exclusively expressed in the pretreated CSC PDPN+ sEVs (E). Within these 2,000 proteins, ~1,200 were upregulated after TNF-α and AngII treatment, as shown by the volcano plot (F, left) and the heatmap (F, right). (G) Western blot analysis of isolated sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , mLECs, mCECs, and SAA3 knockout (KO)-CSC PDPN+ . (H) SAA3 is highly expressed in CSC PDPN+ cell lysate after TNF-α and AngII pretreatment. Treatment of mCECs with TNF-α and AngII slightly increased SAA3 expression, which was undetectable in the cells’ lysate of CSC PDPN+ isolated from global SAA3 KO mice following the same treatment. Data are presented as mean ± SEM. ** p < 0.002 and **** p < 0.0001. N = 3–5. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: (A–C) sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , mLECs, and control mCECs were characterized for size (A) and by sEV protein marker array (B) and transmission electron microscopy (C). Scale bar: 100 nm. (D) BMDM were treated with PKH 26-labeled (red) CSC PDPN+ sEVs to show cell internalization. Scale bar: 25 μm. (E and F) Mass spectrometry analysis of protein content in sEVs derived from TNF-α- and AngII-pretreated mLECs and CSC PDPN+ cells revealed that ~1,000 proteins are commonly expressed by the two groups of sEVs and that ~2,000 proteins were exclusively expressed in the pretreated CSC PDPN+ sEVs (E). Within these 2,000 proteins, ~1,200 were upregulated after TNF-α and AngII treatment, as shown by the volcano plot (F, left) and the heatmap (F, right). (G) Western blot analysis of isolated sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , mLECs, mCECs, and SAA3 knockout (KO)-CSC PDPN+ . (H) SAA3 is highly expressed in CSC PDPN+ cell lysate after TNF-α and AngII pretreatment. Treatment of mCECs with TNF-α and AngII slightly increased SAA3 expression, which was undetectable in the cells’ lysate of CSC PDPN+ isolated from global SAA3 KO mice following the same treatment. Data are presented as mean ± SEM. ** p < 0.002 and **** p < 0.0001. N = 3–5. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.

Article Snippet: Mouse cardiac endothelial cells (mCECs) were purchased and validated from Cedarlane research Products and was cultured expanded.

Techniques: Derivative Assay, Control, Marker, Transmission Assay, Electron Microscopy, Labeling, Mass Spectrometry, Western Blot, Isolation, Knock-Out, Expressing

$(A) Echocardiography analysis showed a reduction of percent ejection fraction (%EF) and fractional shorting (FS) and an increase in end-systolic volume (ESV) and end-diastolic volume (EDV) in healthy mouse hearts injected with sEVs derived from pretreated CSC PDPN+ or mouse lymphatic endothelial cells (mLECs) compared to mouse hearts injected with control sEVs (pretreated mouse cardiac endothelial cells [mCECs]) or saline. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.002, *** p < 0.0005, and **** p < 0.0001. N = 5–10. Ordinary two-way ANOVA and Tukey’s post hoc test were performed among the groups. (B and C) Histological characterization by Masson’s trichrome staining of mouse hearts injected with pretreated CSC PDPN+ sEVs or mLECs sEVs showed infiltrative epicardial fibrosis (top) when compared to animals injected with control sEVs or saline (bottom). Scale bar: 0.25 mm. (D) Fibrotic tissue was characterized by fibronectin deposition (labeled in green; scale bar: 100 μm) and recruited CD45 + cells infiltrating the fibrotic tissue (D, bottom, labeled in red and quantified in E; scale bar: 10 μm). Data are presented as mean ± SEM. * p < 0.05. N = 5–10. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.$

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: (A) Echocardiography analysis showed a reduction of percent ejection fraction (%EF) and fractional shorting (FS) and an increase in end-systolic volume (ESV) and end-diastolic volume (EDV) in healthy mouse hearts injected with sEVs derived from pretreated CSC PDPN+ or mouse lymphatic endothelial cells (mLECs) compared to mouse hearts injected with control sEVs (pretreated mouse cardiac endothelial cells [mCECs]) or saline. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.002, *** p < 0.0005, and **** p < 0.0001. N = 5–10. Ordinary two-way ANOVA and Tukey’s post hoc test were performed among the groups. (B and C) Histological characterization by Masson’s trichrome staining of mouse hearts injected with pretreated CSC PDPN+ sEVs or mLECs sEVs showed infiltrative epicardial fibrosis (top) when compared to animals injected with control sEVs or saline (bottom). Scale bar: 0.25 mm. (D) Fibrotic tissue was characterized by fibronectin deposition (labeled in green; scale bar: 100 μm) and recruited CD45 + cells infiltrating the fibrotic tissue (D, bottom, labeled in red and quantified in E; scale bar: 10 μm). Data are presented as mean ± SEM. * p < 0.05. N = 5–10. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.

Article Snippet: Mouse cardiac endothelial cells (mCECs) were purchased and validated from Cedarlane research Products and was cultured expanded.

Techniques: Injection, Derivative Assay, Control, Saline, Staining, Labeling

(A) qPCR analysis of SAA3 and cytokine mRNA in BMDMs (MΦ) stimulated with sEV-depleted CSC PDPN+ conditioned medium and with CSC PDPN+ sEVs. Data are presented as mean ± SEM. * p < 0.05 and *** p < 0.0005. N = 3. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (B) Western blots showing total cell lysate of BMDMs treated either with recombinant SAA3 (rSAA3), sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , control sEVs derived from similarly treated mCECs, or SAA3-null CSC PDPN+ . BMDMs treated with rSAA3 or CSC PDPN+ sEVs specifically expressed SAA3 in cell lysates compared to BMDMs treated with control sEVs. (C) Western blot showing that BMDMs from TLR2 KO mice did not synthesize SAA3 upon any stimulation. (D) Quantification of SAA3 expression and release via qPCR, western blot, and ELISA analysis of wild-type and TLR2 KO BMDMs after different treatments. Data are presented as mean ± SEM. * p < 0.05, *** p < 0.0005, and **** p < 0.0001. N = 3–5. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (E) Western blot analysis and quantification (right) of p38-MAPK phosphorylation (T180/Y182) in BMDMs after treatment with rSAA3. (F) Western blot analysis and quantification (right) of p38-MAPK phosphorylation (T180/Y182) in BMDMs after treatment with sEVs isolated from TNF-α- and AngII-pretreated CSC PDPN+ , sEVs from similarly treated CSC PDPN+ from SAA3 KO mice or mCECs. sEVs derived from treated CSC PDPN+ from SAA3 KO mice or mCECs only, did not induce p38-MAPK phosphorylation in BMDMs compared to sEVs derived from pretreated CSC PDPN+ . Data are presented as mean ± SEM. * p < 0.05 and ** p < 0.002. N = 3–6. Student’s t test analysis or ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (G) qPCR analysis of SAA3 mRNA in BMDMs shows an important reduction of SAA3 expression after specific inhibition of p38-MAPK with the SB 203580 compound. (H) Western blot analysis of SAA3 protein expression shows an important reduction of SAA3 synthesis after specific inhibition of p38-MAPK with the SB 203580 compound. Data are presented as mean ± SEM. * p < 0.05 and *** p < 0.0005. N = 3–6. Student’s t test analysis or ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: (A) qPCR analysis of SAA3 and cytokine mRNA in BMDMs (MΦ) stimulated with sEV-depleted CSC PDPN+ conditioned medium and with CSC PDPN+ sEVs. Data are presented as mean ± SEM. * p < 0.05 and *** p < 0.0005. N = 3. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (B) Western blots showing total cell lysate of BMDMs treated either with recombinant SAA3 (rSAA3), sEVs derived from TNF-α- and AngII-pretreated CSC PDPN+ , control sEVs derived from similarly treated mCECs, or SAA3-null CSC PDPN+ . BMDMs treated with rSAA3 or CSC PDPN+ sEVs specifically expressed SAA3 in cell lysates compared to BMDMs treated with control sEVs. (C) Western blot showing that BMDMs from TLR2 KO mice did not synthesize SAA3 upon any stimulation. (D) Quantification of SAA3 expression and release via qPCR, western blot, and ELISA analysis of wild-type and TLR2 KO BMDMs after different treatments. Data are presented as mean ± SEM. * p < 0.05, *** p < 0.0005, and **** p < 0.0001. N = 3–5. Ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (E) Western blot analysis and quantification (right) of p38-MAPK phosphorylation (T180/Y182) in BMDMs after treatment with rSAA3. (F) Western blot analysis and quantification (right) of p38-MAPK phosphorylation (T180/Y182) in BMDMs after treatment with sEVs isolated from TNF-α- and AngII-pretreated CSC PDPN+ , sEVs from similarly treated CSC PDPN+ from SAA3 KO mice or mCECs. sEVs derived from treated CSC PDPN+ from SAA3 KO mice or mCECs only, did not induce p38-MAPK phosphorylation in BMDMs compared to sEVs derived from pretreated CSC PDPN+ . Data are presented as mean ± SEM. * p < 0.05 and ** p < 0.002. N = 3–6. Student’s t test analysis or ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups. (G) qPCR analysis of SAA3 mRNA in BMDMs shows an important reduction of SAA3 expression after specific inhibition of p38-MAPK with the SB 203580 compound. (H) Western blot analysis of SAA3 protein expression shows an important reduction of SAA3 synthesis after specific inhibition of p38-MAPK with the SB 203580 compound. Data are presented as mean ± SEM. * p < 0.05 and *** p < 0.0005. N = 3–6. Student’s t test analysis or ordinary one-way ANOVA and Tukey’s post hoc test were performed among the groups.

Article Snippet: Mouse cardiac endothelial cells (mCECs) were purchased and validated from Cedarlane research Products and was cultured expanded.

Techniques: Western Blot, Recombinant, Derivative Assay, Control, Expressing, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Isolation, Inhibition

(A and B) Mouse heart sections 30 days after myocardial infarction (MI) (left) and healthy hearts injected with TNF-α- and AngII-pretreated CSC PDPN+ sEVs (center) were stained with thioflavin S (scale bar: 50 μm) and Congo red staining (B) (scale bar: 25 μm). Both showed the presence of amyloid deposits when compared with healthy hearts injected with similarly treated mCECs (a right). Congo red staining also showed specific birefringence (B) of amyloid deposits, observed with a polarized light microscope in mouse hearts 30 days after MI or after treatment with CSC PDPN+ sEVs. (C) Immunohistochemistry analysis further showed that SAA, labeled in green, aggregated in ischemic tissue of mouse hearts 30 days after MI along with ECM, labeled with fibronectin in red (left), and sEVs isolated from pretreated CSC PDPN+ were able to initiate SAA amyloidosis (center) when injected into healthy mouse hearts (right). Conversely, sEVs derived from pretreated SAA3-null CSC PDPN+ failed to induce SAA amyloidosis. Scale bar: 50 μm. N = 7–10. (D and E) Cardiac sections obtained from failing human hearts showed SAA aggregation, labeled in green, in the fibrotic tissue (E) with the same pattern as SAA aggregation in mouse hearts 30 days after MI (D). Scale bar: 50 μm. N = 7–10.

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: (A and B) Mouse heart sections 30 days after myocardial infarction (MI) (left) and healthy hearts injected with TNF-α- and AngII-pretreated CSC PDPN+ sEVs (center) were stained with thioflavin S (scale bar: 50 μm) and Congo red staining (B) (scale bar: 25 μm). Both showed the presence of amyloid deposits when compared with healthy hearts injected with similarly treated mCECs (a right). Congo red staining also showed specific birefringence (B) of amyloid deposits, observed with a polarized light microscope in mouse hearts 30 days after MI or after treatment with CSC PDPN+ sEVs. (C) Immunohistochemistry analysis further showed that SAA, labeled in green, aggregated in ischemic tissue of mouse hearts 30 days after MI along with ECM, labeled with fibronectin in red (left), and sEVs isolated from pretreated CSC PDPN+ were able to initiate SAA amyloidosis (center) when injected into healthy mouse hearts (right). Conversely, sEVs derived from pretreated SAA3-null CSC PDPN+ failed to induce SAA amyloidosis. Scale bar: 50 μm. N = 7–10. (D and E) Cardiac sections obtained from failing human hearts showed SAA aggregation, labeled in green, in the fibrotic tissue (E) with the same pattern as SAA aggregation in mouse hearts 30 days after MI (D). Scale bar: 50 μm. N = 7–10.

Article Snippet: Mouse cardiac endothelial cells (mCECs) were purchased and validated from Cedarlane research Products and was cultured expanded.

Techniques: Injection, Staining, Light Microscopy, Immunohistochemistry, Labeling, Isolation, Derivative Assay

Journal: Cell reports

Article Title: Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction

doi: 10.1016/j.celrep.2025.115408

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Mouse cardiac endothelial cells (mCECs) were purchased and validated from Cedarlane research Products and was cultured expanded.

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