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smooth muscle basal media  (PromoCell)


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    PromoCell smooth muscle basal media
    Smooth Muscle Basal Media, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 74 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/smooth muscle basal media/product/PromoCell
    Average 95 stars, based on 74 article reviews
    smooth muscle basal media - by Bioz Stars, 2026-02
    95/100 stars

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    Smooth Muscle Basal Media, supplied by PromoCell, 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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    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating <t>cell</t> nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha <t>smooth</t> <t>muscle</t> actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="250" height="auto" />
    Smooth Muscle Cell Basal Medium, supplied by Cell Applications Inc, 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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    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating <t>cell</t> nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha <t>smooth</t> <t>muscle</t> actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="250" height="auto" />
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    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating <t>cell</t> nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha <t>smooth</t> <t>muscle</t> actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="250" height="auto" />
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    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating <t>cell</t> nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha <t>smooth</t> <t>muscle</t> actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="250" height="auto" />
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    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating <t>cell</t> nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha <t>smooth</t> <t>muscle</t> actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="250" height="auto" />
    Smooth Muscle Basal Media (Smbm), supplied by Lonza, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/smooth muscle basal media (smbm)/product/Lonza
    Average 90 stars, based on 1 article reviews
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    Image Search Results


    Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating cell nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha smooth muscle actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also <xref ref-type=Figures S8 and . " width="100%" height="100%">

    Journal: Cell Reports Medicine

    Article Title: Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies

    doi: 10.1016/j.xcrm.2025.101964

    Figure Lengend Snippet: Therapeutic effects of barasertib in male rats exposed to Sugen/hypoxia (A) Study design using the Sugen/hypoxia (Su/Hx) rat model. (B) Pulmonary artery acceleration time (PAAT), right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), S wave, stroke volume (SV), and cardiac output (CO) determined by echocardiography at the end of the protocol in control, Su/Hx+Veh, and Su/Hx+barasertib male rats ( n = 4–9/group). (C) Effect of AURKB inhibition on right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure (mPAP), as assessed by right heart catheterization at the end of the protocol ( n = 4–9/group). (D) Representative images of distal PAs stained with Elastica van Gieson (EVG) and quantification of vascular remodeling in control, Su/Hx+Veh, and Su/Hx+barasertib rats ( n = 4–9/group). (E) Representative images of distal PAs labeled with proliferating cell nuclear antigen (PCNA, proliferative marker, red), p16, or p21 ( n = 4–9/group). PASMCs were labeled with alpha smooth muscle actin (αSMA, green). The quantifications of the percentage of PASMCs positive for PCNA, p16, or p21 are shown. Scale bars, 20 μm. Scatter dot plots show individual values and mean ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis’s test followed by Dunnett’s post hoc test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001. See also Figures S8 and .

    Article Snippet: Smooth muscle cell basal medium , Cell Applications , Cat# 310-500.

    Techniques: Control, Inhibition, Staining, Labeling, Marker

    Barasertib reduces vascular remodeling in human precision-cut lung slices (A) Experimental setup for precision-cut lung slices (PCLSs) from control, patients with PAH, and patients with idiopathic pulmonary fibrosis. (B) Representative images of distal PAs stained with Elastica van Gieson (EVG) or labeled with proliferating cell nuclear antigen (PCNA) or p21 in PCLSs prepared from control patients ( n = 5) after exposure or not to a growth factor cocktail (GF, FGF2 + PDGF-BB + ET1) in presence or not to barasertib for 10 days. PASMCs were labeled with alpha smooth muscle actin (αSMA, green). The quantification of vascular remodeling and PASMCs positive for PCNA or p21 is shown. (C) Representative images of distal PAs stained with EVG or labeled with PCNA or p21 in PCLSs from patients with PAH ( n = 6). (D) Representative images of distal PAs stained with EVG or labeled with PCNA or p21 in PCLSs from patients with IPF complicated with pulmonary hypertension (PH) ( n = 2). For each experiment, the quantifications of vascular remodeling and PCNA- or p21-positive PASMCs (average of 40–45 arteries per patient) are shown. Scale bars, 25 μm. Values are represented as means ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using repeated measures one-way ANOVA test followed by Dunnett’s post hoc test or paired Student’s t test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Journal: Cell Reports Medicine

    Article Title: Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies

    doi: 10.1016/j.xcrm.2025.101964

    Figure Lengend Snippet: Barasertib reduces vascular remodeling in human precision-cut lung slices (A) Experimental setup for precision-cut lung slices (PCLSs) from control, patients with PAH, and patients with idiopathic pulmonary fibrosis. (B) Representative images of distal PAs stained with Elastica van Gieson (EVG) or labeled with proliferating cell nuclear antigen (PCNA) or p21 in PCLSs prepared from control patients ( n = 5) after exposure or not to a growth factor cocktail (GF, FGF2 + PDGF-BB + ET1) in presence or not to barasertib for 10 days. PASMCs were labeled with alpha smooth muscle actin (αSMA, green). The quantification of vascular remodeling and PASMCs positive for PCNA or p21 is shown. (C) Representative images of distal PAs stained with EVG or labeled with PCNA or p21 in PCLSs from patients with PAH ( n = 6). (D) Representative images of distal PAs stained with EVG or labeled with PCNA or p21 in PCLSs from patients with IPF complicated with pulmonary hypertension (PH) ( n = 2). For each experiment, the quantifications of vascular remodeling and PCNA- or p21-positive PASMCs (average of 40–45 arteries per patient) are shown. Scale bars, 25 μm. Values are represented as means ± SEM. Assessment of the normality of the data was performed using Shapiro-Wilk test. Statistical analyses were performed using repeated measures one-way ANOVA test followed by Dunnett’s post hoc test or paired Student’s t test; ∗ p < 0.05; ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Article Snippet: Smooth muscle cell basal medium , Cell Applications , Cat# 310-500.

    Techniques: Control, Staining, Labeling

    Journal: Cell Reports Medicine

    Article Title: Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies

    doi: 10.1016/j.xcrm.2025.101964

    Figure Lengend Snippet:

    Article Snippet: Smooth muscle cell basal medium , Cell Applications , Cat# 310-500.

    Techniques: Virus, Plasmid Preparation, Recombinant, Negative Control, Protease Inhibitor, Staining, EdU Assay, TUNEL Assay, Western Blot, SYBR Green Assay, Chromatin Immunoprecipitation, Magnetic Beads, RNA Sequencing Assay, Expressing, Software