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pulmonary artery smooth muscle cells pasmcs  (ATCC)


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    ATCC pulmonary artery smooth muscle cells pasmcs
    Pulmonary Artery Smooth Muscle Cells Pasmcs, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 97 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+pulmonary+artery+smooth+muscle+cells+pasmcs/Primary+Pulmonary+Artery+Smooth+Muscle+Cells%3B+Normal%2C+Human/pm41997928-246-11-18
    Average 99 stars, based on 97 article reviews
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    Article Title: Mid-old cells are a potential target for anti-aging interventions in the elderly
    Article Snippet: .. Primary pulmonary artery smooth muscle cells (PASMCs) were purchased from American Tissue Culture Collections (ATCC, Rockville, MD) and were cultured in vascular cell basal medium (PCS-100-030, ATCC) supplemented with vascular smooth muscle cell growth kit (PCS-100-042, ATCC) at 37 °C in a humidified incubator with 5% CO 2 . .. Human pulmonary alveolar epithelial cells (HPAEpiC) and human primary colonic epithelial cells (HCoEpiC) were purchase from ScienCell Research Laboratories, Inc. (Carlsbad, CA) and Cell Biologics, Inc. (Chicago, IL), respectively, and were cultured in Alveolar Epithelial Cell Medium (ScienCell Research Laboratories, Inc.) and Human Epithelial Cell Basal Medium (Cell Biologics, Inc.), respectively.

    Article Title: Mid-old cells are a potential target for anti-aging interventions in the elderly.
    Article Snippet: .. Primary pulmonary artery smooth muscle cells (PASMCs) were purchased from American Tissue Culture Collections (ATCC, Rockville, MD) and were cultured in vascular cell basal medium (PCS-100-030, ATCC) supplemented with vascular smooth muscle cell growth kit (PCS-100-042, ATCC) at 37 °C in a humidified incubator with 5% CO2. .. Human pulmonary alveolar epithelial cells (HPAEpiC) and human primary colonic epithelial cells (HCoEpiC) were purchase from ScienCell Research Laboratories, Inc. (Carlsbad, CA) and Cell Biologics, Inc. (Chicago, IL), respectively, and were cultured in Alveolar Epithelial Cell Medium (ScienCell Research Laboratories, Inc.) and Human Epithelial Cell Basal Medium (Cell Biologics, Inc.), respectively.



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    Excess BCAAs promoted a pro-ferroptotic phenotype in <t>human</t> <t>PASMC</t> . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.
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    Excess BCAAs promoted a pro-ferroptotic phenotype in <t>human</t> <t>PASMC</t> . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.
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    Excess BCAAs promoted a pro-ferroptotic phenotype in <t>human</t> <t>PASMC</t> . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.
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    Excess BCAAs promoted a pro-ferroptotic phenotype in <t>human</t> <t>PASMC</t> . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.
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    Excess BCAAs promoted a pro-ferroptotic phenotype in <t>human</t> <t>PASMC</t> . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.
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    Excess BCAAs promoted a pro-ferroptotic phenotype in human PASMC . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.

    Journal: bioRxiv

    Article Title: Impaired Lung BCAA Metabolism Promotes Ferroptosis and Resultant Pulmonary Arterial Hypertension-Associated Hepatopathy

    doi: 10.1101/2025.09.03.672819

    Figure Lengend Snippet: Excess BCAAs promoted a pro-ferroptotic phenotype in human PASMC . (A) Representative confocal micrographs of PASMC stained with MitoTracker Orange and quantification of mitochondrial organization in control and BCAA-treated PASMC (Control PASMC [Con]: 1.1±0.6, BCAA-Treated PASMC [BCAA]: 0.7±0.3); p -values determined by Mann-Whitney U-test. (B) Confocal micrographs of TRME-stained PASMC in control and BCAA-treated media, with corresponding quantification of mitochondrial membrane hyperpolarization, indicated by fluorescence intensity (Con: 8.3±17.2, BCAA: 42.7±9.7). p -values determined by Mann-Whitney U-test. (C) Excess BCAAs increase mitochondrial ROS, demonstrated by confocal micrographs of control and BCAA-treated PASMCs stained with MitoSox Red (Con: 6.4±2.1, BCAA: 14.5±6.9 MFI). p -values determined by Mann-Whitney U-test. (D) Representative confocal micrographs of control, BCAA-treated, and BCAA and ferrostatin-1-treated PASMCs incubated with 50 μM oleate and 50 μM palmitate and stained for lipid peroxidation using BODIPY (Con: 1.8±0.3, BCAA: 1.4±0.1, BCAA-treated with 5 μM ferrostatin-1 [BCAA-FER1]: 1.7±0.3). p -values determined by Kruskal-Wallis test and Dunn’s multiple comparisons test. (E) Incubation with BCAAs induces ferroptotic cell death, demonstrated by viability staining of control, BCAA-treated, and BCAA-treated with ferrostatin-1 PASMCs via Trypan Blue (Con: 9.4±7.5, BCAA: 31.7±11.7, BCAA-FER1: 13.0±11.1). White arrows indicate trypan blue-positive cells. p -values determined by ordinary one-way ANOVA with Tukey’s multiple comparison test.

    Article Snippet: Human PASMC (ATCC PCS-100-023) were grown with Sigma Basic Eagle Medium (Sigma, B1522-500) with supplements (Lonza, CC-3182) and passaged with subculture reagents (Lonza CC-5034).

    Techniques: Staining, Control, MANN-WHITNEY, Membrane, Fluorescence, Incubation, Comparison