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human pulmonary artery smooth muscle cells hpasmcs  (ATCC)


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    Structured Review

    ATCC human pulmonary artery smooth muscle cells hpasmcs
    The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) <t>HPASMCs</t> were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.
    Human Pulmonary Artery Smooth Muscle Cells Hpasmcs, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 95 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pulmonary+artery+smooth+muscle+cells+hpasmcs/Primary+Pulmonary+Artery+Smooth+Muscle+Cells%3B+Normal%2C+Human/pmc13225285-69-7-25
    Average 99 stars, based on 95 article reviews
    human pulmonary artery smooth muscle cells hpasmcs - by Bioz Stars, 2026-08
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    1) Product Images from "MicroRNA-661 Suppresses Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells and Endothelial Cells by Targeting CCND2"

    Article Title: MicroRNA-661 Suppresses Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells and Endothelial Cells by Targeting CCND2

    Journal: Biologics : Targets & Therapy

    doi: 10.2147/BTT.S592879

    The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) HPASMCs were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.
    Figure Legend Snippet: The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) HPASMCs were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.

    Techniques Used: RNA Sequencing, Quantitative RT-PCR, Expressing



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    The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) <t>HPASMCs</t> were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.
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    Effect of mitoTEMPO treatment on HIF‐1α stabilization in vitro. HIF‐1α protein levels were assessed by western blot, and steady‐state mRNA levels for lactate dehydrogenase A ( Ldha ) and pyruvate dehydrogenase kinase 1 ( Pdk1 ) by quantitative real‐time PCR in (a) CMT167 cells, (b) <t>hPASMCs,</t> and (c) mPASMCs, exposed to normoxia (21% O 2 ), severe hypoxia (1% O 2 ), or mild hypoxia (10% O 2 ) for 24 h and treated with triphenylphosphonium (TPP + ) (blue dots) or mitoTEMPO (MT) (red dots). Immunoblots shown are representative of three independent experiments. CMT167: mouse lung carcinoma epithelial cells; hPASMCs: human pulmonary artery smooth muscle cells; mPASMCs: mouse pulmonary artery smooth muscle cells. Densitometric analysis of HIF‐1α bands normalized to β‐Actin. Data are presented as mean ± SD. Statistical comparisons were made using two‐way ANOVA with Tukey's post hoc test ( n = 3 per group). (ns: no signal). Quantitative real‐time PCR data reflect mean ΔCt ± SD ( n = 3 per experimental group).
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    Effect of mitoTEMPO treatment on HIF‐1α stabilization in vitro. HIF‐1α protein levels were assessed by western blot, and steady‐state mRNA levels for lactate dehydrogenase A ( Ldha ) and pyruvate dehydrogenase kinase 1 ( Pdk1 ) by quantitative real‐time PCR in (a) CMT167 cells, (b) <t>hPASMCs,</t> and (c) mPASMCs, exposed to normoxia (21% O 2 ), severe hypoxia (1% O 2 ), or mild hypoxia (10% O 2 ) for 24 h and treated with triphenylphosphonium (TPP + ) (blue dots) or mitoTEMPO (MT) (red dots). Immunoblots shown are representative of three independent experiments. CMT167: mouse lung carcinoma epithelial cells; hPASMCs: human pulmonary artery smooth muscle cells; mPASMCs: mouse pulmonary artery smooth muscle cells. Densitometric analysis of HIF‐1α bands normalized to β‐Actin. Data are presented as mean ± SD. Statistical comparisons were made using two‐way ANOVA with Tukey's post hoc test ( n = 3 per group). (ns: no signal). Quantitative real‐time PCR data reflect mean ΔCt ± SD ( n = 3 per experimental group).
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    Image Search Results


    The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) HPASMCs were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.

    Journal: Biologics : Targets & Therapy

    Article Title: MicroRNA-661 Suppresses Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells and Endothelial Cells by Targeting CCND2

    doi: 10.2147/BTT.S592879

    Figure Lengend Snippet: The negative correlation between miR-661 and CCND2 in pulmonary hypertension patients. ( A ) HPASMCs were overexpressed with miR-661, followed by RNA-seq analysis. The heatmap result showed the differentially expressed genes as indicated. ( B ) qRT-PCR was used to detect the expression level of miR-661 and CCND2 in serum of patients with pulmonary hypertension and healthy volunteers, then the correlation analysis were performed. ( C ) Statistics of KEGG pathway were performed after overexpressed with miR-661 in HPASMCs, the green highlighted text indicates that the cell cycle pathway was significantly inhibited.

    Article Snippet: The human embryonic Kidney 293T cells (HEK293T), human pulmonary artery smooth muscle Cells (HPASMCs) and human pulmonary artery endothelial cells (HPAECs) were obtained from the American Type Culture Collection.

    Techniques: RNA Sequencing, Quantitative RT-PCR, Expressing

    Effect of mitoTEMPO treatment on HIF‐1α stabilization in vitro. HIF‐1α protein levels were assessed by western blot, and steady‐state mRNA levels for lactate dehydrogenase A ( Ldha ) and pyruvate dehydrogenase kinase 1 ( Pdk1 ) by quantitative real‐time PCR in (a) CMT167 cells, (b) hPASMCs, and (c) mPASMCs, exposed to normoxia (21% O 2 ), severe hypoxia (1% O 2 ), or mild hypoxia (10% O 2 ) for 24 h and treated with triphenylphosphonium (TPP + ) (blue dots) or mitoTEMPO (MT) (red dots). Immunoblots shown are representative of three independent experiments. CMT167: mouse lung carcinoma epithelial cells; hPASMCs: human pulmonary artery smooth muscle cells; mPASMCs: mouse pulmonary artery smooth muscle cells. Densitometric analysis of HIF‐1α bands normalized to β‐Actin. Data are presented as mean ± SD. Statistical comparisons were made using two‐way ANOVA with Tukey's post hoc test ( n = 3 per group). (ns: no signal). Quantitative real‐time PCR data reflect mean ΔCt ± SD ( n = 3 per experimental group).

    Journal: Physiological Reports

    Article Title: The effect of mitoTEMPO on the development of hypoxia‐induced pulmonary hypertension in male mice

    doi: 10.14814/phy2.70804

    Figure Lengend Snippet: Effect of mitoTEMPO treatment on HIF‐1α stabilization in vitro. HIF‐1α protein levels were assessed by western blot, and steady‐state mRNA levels for lactate dehydrogenase A ( Ldha ) and pyruvate dehydrogenase kinase 1 ( Pdk1 ) by quantitative real‐time PCR in (a) CMT167 cells, (b) hPASMCs, and (c) mPASMCs, exposed to normoxia (21% O 2 ), severe hypoxia (1% O 2 ), or mild hypoxia (10% O 2 ) for 24 h and treated with triphenylphosphonium (TPP + ) (blue dots) or mitoTEMPO (MT) (red dots). Immunoblots shown are representative of three independent experiments. CMT167: mouse lung carcinoma epithelial cells; hPASMCs: human pulmonary artery smooth muscle cells; mPASMCs: mouse pulmonary artery smooth muscle cells. Densitometric analysis of HIF‐1α bands normalized to β‐Actin. Data are presented as mean ± SD. Statistical comparisons were made using two‐way ANOVA with Tukey's post hoc test ( n = 3 per group). (ns: no signal). Quantitative real‐time PCR data reflect mean ΔCt ± SD ( n = 3 per experimental group).

    Article Snippet: Mouse lung carcinoma epithelial (CMT167) cells (10032302, Merck, Germany) and human PASMCs (hPASMCs) (C‐12521, PromoCell, Germany) were purchased.

    Techniques: In Vitro, Western Blot, Real-time Polymerase Chain Reaction