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medium fst 14184 09 dissecting scissors (Taiji Group)

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Taiji Group medium fst 14184 09 dissecting scissors
Medium Fst 14184 09 Dissecting Scissors, supplied by Taiji Group, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 86 stars, based on 1 article reviews

medium fst 14184 09 dissecting scissors - by Bioz Stars, 2026-10

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Article Title: Preparation of cleared whole-mount urethra and urinary bladder from transcardially perfused mice for immunolabeling and analysis by CLSM.
Article Snippet: .. Dissecting scissors, medium FST 14184–09 Dissecting scissors, fine 14 cm straight FST 15020–15 Forceps, fine FST 11252–50 Forceps, coarse FST 11992–12 Clamp (artery clamp) FST 13018–14 TAIJI-IE Small Animal Anesthesia Machine RWD TAIJI-IE Infusion bottle (1000 mL, clear, Stopper Infusion 32 mm) or Infusion bottle, for example Braun’s isotonic sodium chloride solution 0.9% Packsys Braun 10000263 PZN:08646871/ EAN4030539036313 Glass-tubing cutter Merck Z150770-1EA Pravaz needle with LL mount, blunt version, size 1 diameter 0.9 mm at least 38 mm length or Laboratory pipetting needle with 90 ◦ blunt ends, gauge 20, L 4 in., 304 stainless steel hub Acufirm Merck 1400 LL CAD7950-12EA Scienceware® trays; L 3 W 3 H 30 cm 3 41 cm 3 7.6 cm Merck Z503797-1EA Stainless steel perforated sheet, square hole 10 mm - thickness 2.00 mm; L 3 W 31 cm 3 42 cm Elbemetal www.elbemetall.de Intrafix® SafeSet with LL mount 180 cm with 3 3 4.1 mm tubing Braun PZN 01900697/EAN 4022495869517 Syring 1 mL Braun PZN 00896456 EAN 4022495252074 Injection needle (pierce the filter) 21G34 4/5; 0,8 3 120 mm Braun PZN 04291448/EAN 4022495052414 Injection needle (injection of Heparin) 26G31; 0,45 3 25 mm Braun PZN 2050858 EAN 4022495001016 Metal multi-hook for glass infusion bottles Braun PZN 04800507/EAN 4022495260161 Infusion accessories Heidelberg extensions 75 cm Braun PZN 02133113/EAN 4022495004758 Braunostat® U Universal infusion stand Braun 8727902 Discofix®-3 three-way tap with connecting pipe, 50 cm, blue Braun PZN 07128507/EAN 4022495005007 Zeiss LSM 710 Confocal Inverted Microscope Zeiss RRID:SCR_018063 Leica STELLARIS 5 Microscope Leica RRID:SCR_024663 Pre-rinse solution Reagent Final concentration Amount Polyvinylpyrrolidone K30 a 2.5% 25 g Sodium chloride 0.9% 9 g Procaine hydrochloride a 0.5% 5 g Heparin natrium 25.000 I.E./5 mL a 10000 I.E./l 2 mL ddH 2 O N/A 1000 mL Total N/A 1000 mL Stored for up to 4 days at 2 ◦ C–8 ◦ C or freeze at − 20 ◦ C. a Harmful or toxic; handle with care. ..

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Activin A induces excessive ET-1 (endothelin-1) production in pulmonary artery endothelial cells (PAECs), reversible by follistatin or bosentan. A and B , Quantitative real-time polymerase chain reaction analysis of ET-1 mRNA expression ( A , n=6 biologically independent samples per group) and ELISA measurement of ET-1 concentration in culture medium ( B , n=3–4) from PAECs treated for 6 hours with recombinant activin A (100 ng/mL) or vehicle. C and D , ET-1 mRNA expression ( C , n=6) and secreted ET-1 concentration ( D , n=4-5) in PAECs 48 hours after INHBA (inhibin β-A) overexpression (OE) or GFP (green fluorescent protein) control retroviral transfection. E and F , INHBA mRNA expression ( E , n=6) and activin A concentration in culture medium ( F , n=4) in PAECs treated for 6 hours with recombinant ET-1 (100 nmol/L) or vehicle. G , ET-1 mRNA expression in PAECs treated for 6 hours with vehicle or recombinant activin A in the presence of vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or both (FST+BOS; n=4). H , ET-1 mRNA expression in PAECs 48 hours after INHBA OE or GFP transfection, followed by 24 hours of treatment with VEH, FST (100 ng/mL), BOS (10 μM), or FST+BOS (n=4). I , ET-1 mRNA expression in PAECs treated for 6 hours with vehicle or recombinant activin A in the presence of VEH or ACTRIIA-Fc (activin receptor type IIa fusion protein; 2500 ng/mL; n=3-4). J , ET-1 mRNA expression in PAECs 48 hours after INHBA OE or GFP transfection, followed by 24 hours of treatment with VEH or ACTRIIA-Fc (2500 ng/mL; n=4). Data are mean±SEM. P <0.05 is deemed statistically significant. Statistical tests: 2-sided Student t test for A through F ; 1-way ANOVA with Tukey post hoc test for G and H .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: Activin A induces excessive ET-1 (endothelin-1) production in pulmonary artery endothelial cells (PAECs), reversible by follistatin or bosentan. A and B , Quantitative real-time polymerase chain reaction analysis of ET-1 mRNA expression ( A , n=6 biologically independent samples per group) and ELISA measurement of ET-1 concentration in culture medium ( B , n=3–4) from PAECs treated for 6 hours with recombinant activin A (100 ng/mL) or vehicle. C and D , ET-1 mRNA expression ( C , n=6) and secreted ET-1 concentration ( D , n=4-5) in PAECs 48 hours after INHBA (inhibin β-A) overexpression (OE) or GFP (green fluorescent protein) control retroviral transfection. E and F , INHBA mRNA expression ( E , n=6) and activin A concentration in culture medium ( F , n=4) in PAECs treated for 6 hours with recombinant ET-1 (100 nmol/L) or vehicle. G , ET-1 mRNA expression in PAECs treated for 6 hours with vehicle or recombinant activin A in the presence of vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or both (FST+BOS; n=4). H , ET-1 mRNA expression in PAECs 48 hours after INHBA OE or GFP transfection, followed by 24 hours of treatment with VEH, FST (100 ng/mL), BOS (10 μM), or FST+BOS (n=4). I , ET-1 mRNA expression in PAECs treated for 6 hours with vehicle or recombinant activin A in the presence of VEH or ACTRIIA-Fc (activin receptor type IIa fusion protein; 2500 ng/mL; n=3-4). J , ET-1 mRNA expression in PAECs 48 hours after INHBA OE or GFP transfection, followed by 24 hours of treatment with VEH or ACTRIIA-Fc (2500 ng/mL; n=4). Data are mean±SEM. P <0.05 is deemed statistically significant. Statistical tests: 2-sided Student t test for A through F ; 1-way ANOVA with Tukey post hoc test for G and H .

Article Snippet: For indicated experiments, PAECs were treated for 24 hours with FST (100 ng/mL; no. 4889-FN-025; R&D Systems), bosentan (10 μM; no. SML1265; Sigma-Aldrich), ALK (activin receptor–like kinase) 4/5/7 inhibitor SB505124 (5 μM; no. S2186; Selleck), ALK1/2/6 inhibitor K02288 (1 μM; no. S7359; Selleck), the activin receptor type IIA fusion protein ACTRIIA-Fc (activin receptor type IIA fusion protein; 2500 ng/mL), or vehicle.

Techniques: Real-time Polymerase Chain Reaction, Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Recombinant, Over Expression, Control, Retroviral, Transfection

Activin A–driven ET-1 (endothelin-1) contributes to pulmonary artery endothelial cell (PAEC) dysfunction. A and B , Representative images ( A ) and quantification ( B ) of chord length and number of branching points in a Matrigel tube formation assay (n=3–4) using PAECs transfected with GFP (green fluorescent protein) or INHBA (inhibin β-A) overexpression (OE), treated with vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or both (FST+BOS). C and D , Representative images ( C ) and quantification ( D ) of apoptotic cells assessed by TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining (n=3–4) under serum starvation. Apoptotic cells are indicated by white arrows. E , Cell proliferation measured by WST-1 (water-soluble tetrazolium-1) assay in GFP- or INHBA OE–transfected PAECs treated with VEH, FST, BOS, or FST+BOS (n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Statistical test: 1-way ANOVA with Tukey post hoc test for B , D , and E . AU indicates a bsorbance units; and DAPI, 4′,6-diamidino-2-phenylindole.

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: Activin A–driven ET-1 (endothelin-1) contributes to pulmonary artery endothelial cell (PAEC) dysfunction. A and B , Representative images ( A ) and quantification ( B ) of chord length and number of branching points in a Matrigel tube formation assay (n=3–4) using PAECs transfected with GFP (green fluorescent protein) or INHBA (inhibin β-A) overexpression (OE), treated with vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or both (FST+BOS). C and D , Representative images ( C ) and quantification ( D ) of apoptotic cells assessed by TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining (n=3–4) under serum starvation. Apoptotic cells are indicated by white arrows. E , Cell proliferation measured by WST-1 (water-soluble tetrazolium-1) assay in GFP- or INHBA OE–transfected PAECs treated with VEH, FST, BOS, or FST+BOS (n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Statistical test: 1-way ANOVA with Tukey post hoc test for B , D , and E . AU indicates a bsorbance units; and DAPI, 4′,6-diamidino-2-phenylindole.

Techniques: Tube Formation Assay, Transfection, Over Expression, TUNEL Assay, Staining

Endothelial cell (EC)–derived activin A–induced ET-1 (endothelin-1) alters vasoconstrictive properties of the pulmonary vasculature. A , eNOS (endothelial NO synthase) mRNA expression in pulmonary artery endothelial cells (PAECs) 48 hours after GFP (green fluorescent protein) or INHBA (inhibin β-A) overexpression (OE), treated with vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or FST+BOS for 24 hours (n=3). B , Representative immunoblots and quantification of p-eNOS (phosphorylated eNOS) and total eNOS under the same conditions (n=3–4). C , ET-1 concentration in pulmonary artery smooth muscle cell (PASMC) culture medium after coculture with PAECs treated with recombinant activin A for 24 or 48 hours (n=3). D , ET-1 and INHBA mRNA expression in PASMCs cocultured for 48 hours with GFP- or INHBA OE–PAECs, with VEH, FST, BOS, or FST+BOS added for the last 24 hours (n=3–4). E , PASMC mRNA expression of PCNA (proliferating cell nuclear antigen), fibronectin, SM22α (smooth muscle protein 22-α), and α-SMA (α-smooth muscle actin) under the same conditions (n=3–4). F , Representative immunoblots and quantification of MYH11 (myosin heavy chain 11), SM22α, and MMP2 (matrix metalloproteinase-2) in PASMCs cocultured with GFP- or INHBA OE–PAECs, treated as in E (n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 2-sided Student t test for C ; 1-way ANOVA with Tukey post hoc test for A , B , D through F .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: Endothelial cell (EC)–derived activin A–induced ET-1 (endothelin-1) alters vasoconstrictive properties of the pulmonary vasculature. A , eNOS (endothelial NO synthase) mRNA expression in pulmonary artery endothelial cells (PAECs) 48 hours after GFP (green fluorescent protein) or INHBA (inhibin β-A) overexpression (OE), treated with vehicle (VEH), FST (follistatin; 100 ng/mL), bosentan (BOS; 10 μM), or FST+BOS for 24 hours (n=3). B , Representative immunoblots and quantification of p-eNOS (phosphorylated eNOS) and total eNOS under the same conditions (n=3–4). C , ET-1 concentration in pulmonary artery smooth muscle cell (PASMC) culture medium after coculture with PAECs treated with recombinant activin A for 24 or 48 hours (n=3). D , ET-1 and INHBA mRNA expression in PASMCs cocultured for 48 hours with GFP- or INHBA OE–PAECs, with VEH, FST, BOS, or FST+BOS added for the last 24 hours (n=3–4). E , PASMC mRNA expression of PCNA (proliferating cell nuclear antigen), fibronectin, SM22α (smooth muscle protein 22-α), and α-SMA (α-smooth muscle actin) under the same conditions (n=3–4). F , Representative immunoblots and quantification of MYH11 (myosin heavy chain 11), SM22α, and MMP2 (matrix metalloproteinase-2) in PASMCs cocultured with GFP- or INHBA OE–PAECs, treated as in E (n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 2-sided Student t test for C ; 1-way ANOVA with Tukey post hoc test for A , B , D through F .

Techniques: Derivative Assay, Expressing, Over Expression, Western Blot, Concentration Assay, Recombinant

Activin A–derived ET-1 (endothelin-1) drives multiple proremodeling pathways in pulmonary artery endothelial cells (PAECs). A , mRNA expression of BMP4 (bone morphogenetic protein 4), SLUG (snail family transcriptional repressor 2), SNAIL (snail family transcriptional repressor 1), VE-cadherin (vascular endothelial cadherin), fibronectin, and SOD2 (superoxide dismutase 2) in GFP (green fluorescent protein)- or INHBA (inhibin β-A) overexpression (OE)–PAECs treated with vehicle (VEH), FST (follistatin), bosentan (BOS), or FST+BOS for 24 hours (n=3–4). B , Representative immunoblots and quantification of vimentin, SOD2, and NRF2 (nuclear factor, erythroid 2-related factor 2) under the same conditions (n=3). C , Reactive oxygen species (ROS) production in GFP- or INHBA OE–PAECs treated as in A , measured at 4, 6, 16, and 24 hours (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for A and B ; 2-way ANOVA with Tukey post hoc test for C .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: Activin A–derived ET-1 (endothelin-1) drives multiple proremodeling pathways in pulmonary artery endothelial cells (PAECs). A , mRNA expression of BMP4 (bone morphogenetic protein 4), SLUG (snail family transcriptional repressor 2), SNAIL (snail family transcriptional repressor 1), VE-cadherin (vascular endothelial cadherin), fibronectin, and SOD2 (superoxide dismutase 2) in GFP (green fluorescent protein)- or INHBA (inhibin β-A) overexpression (OE)–PAECs treated with vehicle (VEH), FST (follistatin), bosentan (BOS), or FST+BOS for 24 hours (n=3–4). B , Representative immunoblots and quantification of vimentin, SOD2, and NRF2 (nuclear factor, erythroid 2-related factor 2) under the same conditions (n=3). C , Reactive oxygen species (ROS) production in GFP- or INHBA OE–PAECs treated as in A , measured at 4, 6, 16, and 24 hours (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for A and B ; 2-way ANOVA with Tukey post hoc test for C .

Techniques: Derivative Assay, Expressing, Over Expression, Western Blot

Canonical SMAD2/3 signaling mediates activin A–induced ET-1 (endothelin-1) expression. A , Representative immunoblots and quantification of p-SMAD2/3 (phosphorylated SMAD2/3; small mother against decapentaplegic family member 2/3) and total SMAD2/3 in GFP (green fluorescent protein)- or INHBA (inhibin β-A) overexpression (OE)–pulmonary artery endothelial cells (PAECs) treated with vehicle (VEH), FST (follistatin), bosentan (BOS), or FST+BOS for 24 hours (n=3). B , Immunoblots showing p-SMAD2/3 and total SMAD2/3 in GFP- or INHBA OE–PAECs treated with SB505124 (5 μM) or vehicle for 24 hours. C , ET-1 mRNA expression in GFP- or INHBA OE–PAECs treated with SB505124 or vehicle for 24 hours ( left , n=3) and in PAECs treated for 6 hours with activin A±SB505124 ( right , n=3–4). D , Immunoblots showing SMAD2/3 and β-actin in PAECs pretreated with SMAD2 siRNA (small interfering RNA; siSMAD2), SMAD3 siRNA (siSMAD3), dual SMAD2-SMAD3 siRNA (dual siSMAD), or control siRNA (siNC [siRNA negative control]). E , ET-1 mRNA expression in GFP- or INHBA OE–PAECs pretreated with siSMAD2, siSMAD3, dual siSMAD, or siNC (n=3–4). F , INHBA and ET-1 mRNA expression in PAECs exposed to normoxia or hypoxia (0.1% O 2 , 24 hours; n=6). G and H , ET-1 mRNA expression in PAECs under hypoxia treated with FST ( G ) or SB505124 ( H ; n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for A , C , E , G , and H ; 2-sided Student t test for F .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: Canonical SMAD2/3 signaling mediates activin A–induced ET-1 (endothelin-1) expression. A , Representative immunoblots and quantification of p-SMAD2/3 (phosphorylated SMAD2/3; small mother against decapentaplegic family member 2/3) and total SMAD2/3 in GFP (green fluorescent protein)- or INHBA (inhibin β-A) overexpression (OE)–pulmonary artery endothelial cells (PAECs) treated with vehicle (VEH), FST (follistatin), bosentan (BOS), or FST+BOS for 24 hours (n=3). B , Immunoblots showing p-SMAD2/3 and total SMAD2/3 in GFP- or INHBA OE–PAECs treated with SB505124 (5 μM) or vehicle for 24 hours. C , ET-1 mRNA expression in GFP- or INHBA OE–PAECs treated with SB505124 or vehicle for 24 hours ( left , n=3) and in PAECs treated for 6 hours with activin A±SB505124 ( right , n=3–4). D , Immunoblots showing SMAD2/3 and β-actin in PAECs pretreated with SMAD2 siRNA (small interfering RNA; siSMAD2), SMAD3 siRNA (siSMAD3), dual SMAD2-SMAD3 siRNA (dual siSMAD), or control siRNA (siNC [siRNA negative control]). E , ET-1 mRNA expression in GFP- or INHBA OE–PAECs pretreated with siSMAD2, siSMAD3, dual siSMAD, or siNC (n=3–4). F , INHBA and ET-1 mRNA expression in PAECs exposed to normoxia or hypoxia (0.1% O 2 , 24 hours; n=6). G and H , ET-1 mRNA expression in PAECs under hypoxia treated with FST ( G ) or SB505124 ( H ; n=3). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for A , C , E , G , and H ; 2-sided Student t test for F .

Techniques: Expressing, Western Blot, Over Expression, Small Interfering RNA, Control, Negative Control

In vivo activin A inhibition improves pulmonary hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary artery muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung ECs isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .

Journal: Arteriosclerosis, Thrombosis, and Vascular Biology

Article Title: Activin A–Endothelin-1 Axis Governs Pulmonary Vascular Remodeling: Mechanistic Basis for Emerging Therapies in PAH

doi: 10.1161/ATVBAHA.125.323681

Figure Lengend Snippet: In vivo activin A inhibition improves pulmonary hypertension (PH) phenotype comparably or more than ET-1 (endothelin-1) blockade. A , Experimental design: wild-type (WT) and VE-cadherin (vascular endothelial cadherin)–INHBA (inhibin β-A)-Tg (TG/transgenic) mice were exposed to hypoxia (10% O 2 ) for 3 weeks, with vehicle (VEH), FST (follistatin; 8.5 μg/kg), bosentan (BOS; 30 mg/kg), or FST+BOS administered during the final 2 weeks. B , Right ventricular systolic pressure (RVSP; n=4–9). C , Fulton index (RV/[LV+S] [right ventricle to left ventricle plus septum] ratio; n=4–8). D , Representative hematoxylin and eosin–stained lung sections. Blue arrows indicate vessels. E , Representative immunofluorescent staining of α-SMA (α-smooth muscle actin protein; green, SMC [smooth muscle cell] marker), vWF (von Willebrand Factor; red, endothelial cell [EC] marker), and DAPI (4′,6-diamidino-2-phenylindole; blue, nuclei). White arrows indicate vessels. F , Quantification of pulmonary artery muscularization (non-, partial-, full; n=12–15 fields from 3–4 mice). PA indicates pulmonary artery. G , Lung ET-1 mRNA expression (n=3–4). H , mRNA expression of INHBA, ET-1, eNOS (endothelial NO synthase), SOD2 (superoxide dismutase 2), fibronectin, SLUG (snail family transcriptional repressor 2), CD31 (cluster of differentiation 31), and BMP4 (bone morphogenetic protein 4) in lung ECs isolated from WT and TG mice (n=3–4). Data are mean±SEM. P <0.05 is deemed statistically significant. Tests: 1-way ANOVA with Tukey post hoc test for B , C , and G ; 2-way ANOVA with Tukey post hoc test for F ; 2-sided Student t test for H .

Techniques: In Vivo, Inhibition, Transgenic Assay, Staining, Marker, Expressing, Isolation

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