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endothelial cell growth media microvascular 2 ecgm mv2  (PromoCell)


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    PromoCell endothelial cell growth media microvascular 2 ecgm mv2
    Endothelial Cell Growth Media Microvascular 2 Ecgm Mv2, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 123 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ecgm+mv2/Endothelial+Cell+Growth+Medium+MV+2+Kit/pmc13135260-48-17-23
    Average 96 stars, based on 123 article reviews
    endothelial cell growth media microvascular 2 ecgm mv2 - by Bioz Stars, 2026-09
    96/100 stars

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    Cell Culture:

    Article Title: Coordinating Effect of VEGFC and Oleic Acid Participates to Tumor Lymphangiogenesis
    Article Snippet: .. Human dermal lymphatic endothelial cells (HDLECs) were purchased from Promocell (Promocell, Heidelberg, Germany), cultured in ECGM-MV2 (Promocell, Heidelberg, Germany) medium and used between passages 2 and 6. .. Human recombinant VEGFC was from R&D systems (Minneapolis, MN, USA).

    Article Title: Blood flow diverts extracellular vesicles from endothelial degradative compartments to promote angiogenesis
    Article Snippet: VeravecTM are HUVECs human endothelial cells adapted to longer term culture using a single adenovirus protein, E4ORF1 (Angiocrine Biosciences). .. They were cultured in ECGM MV2 (Promocell) complemented with 20% of FBS and 1% PS. ..

    Article Title: Blood flow diverts extracellular vesicles from endothelial degradative compartments to promote angiogenesis
    Article Snippet: HUVEC cells (Human Umbilical Vein Endothelial Cell, Promocell) were grown in Endothelial Growth Medium (ECGM, Promocell) complemented with supplemental mix (SupplementMix, Promocell) and 1per cent PS. .. VeravecTM HUVECs human endothelial cells (Angiocrine Biosciences), referred here as vHUVECs, were cultured in ECGM MV2 (Promocell) complemented with 20per cent of FBS and 1per cent PS. ..

    Article Title: HDACs regulate the differentiation of endothelial cells from human iPSCs.
    Article Snippet: Funding information National Natural Science Foundation of China, Grant/Award Numbers: 81870201, 201806725012; National Institutes of Health, Grant/Award Numbers: NIH R01 R01GM099688, NIH R24OD021606‐03S1; University of California Davis Innovative Development Award; Dickenson's Catalyst Fund Abstract Human induced pluripotent stem cells (hiPSCs) possess the potential to differentiate toward vascular cells including endothelial cells (ECs), pericytes, and smooth muscle cells.. Epigenetic mechanisms including DNA methylation and histone modification play a crucial role in regulating lineage differentiation and specification.. Herein, we utilized a three‐stage protocol to induce differentiation of mesoderm, vascular progenitors, and ECs from hiPSCs and investigated the regulatory effects of histone acetylation on the differentiation processes.

    Article Title: Isolation and characterisation of lymphatic endothelial cells from lung tissues affected by lymphangioleiomyomatosis.
    Article Snippet: From lung cell suspension, we isolated CD45- lung cells using CD45 MicroBeads (Miltenyi Biotec, San Diego, USA) and an autoMACS Pro Separator (Miltenyi Biotec). .. Isolated CD45- lung cells were seeded onto collagen I-coated 6-well plates (Iwaki, Tokyo, Japan) or 10 cm dishes (Iwaki, Tokyo, Japan) according to the number of isolated cells, and cultured with a complete growth medium consisting of ECGM-MV2 (PromoCell, Heidelberg, Germany)/5% FBS (PromoCell)/100 U/ml of penicillin/streptomycin in a humidified incubator with a gas mixture of 21%O2, 5%CO2, and balance N2 at 37 °C until 70–80% confluence was achieved (usually reached in 7–10 days). .. Next, we fractionated LECs from cultured CD45-lung cells using a fluorescence-activated cell sorting (FACS) Aria Fusion Cell Sorter (BD Biosciences, San Jose, USA) according to our previous protocol with some modification15.

    Flow Cytometry:

    Article Title: Negative regulation of p53 by the poliovirus receptor PVR is a target of a human cytomegalovirus immune evasion molecule
    Article Snippet: .. Once expanded, all endothelial cells (HUVEC, hCMEC/D3, HDLEC, HDBEC, and BOECs) were maintained in either ECGM or ECGM MV2 (Promocell) and endothelial phenotype regularly assessed by flow cytometry using anti-CD31-AF488 and anti-VE-cadherin-Biotin antibodies. ..

    other:

    Article Title: Increased Anti-Inflammatory Therapeutic Potential and Progenitor Marker Expression of Corneal Mesenchymal Stem Cells Cultured in an Optimized Propagation Medium
    Article Snippet: Primary lymphatic and blood endothelial cells (LEC and BEC, respectively) were purchased from PromoCell and maintained in supplemented ECGM MV2 (endothelial cell growth medium) culture medium according to manufacturer’s instructions.

    Isolation:

    Article Title: Isolation and characterisation of lymphatic endothelial cells from lung tissues affected by lymphangioleiomyomatosis.
    Article Snippet: From lung cell suspension, we isolated CD45- lung cells using CD45 MicroBeads (Miltenyi Biotec, San Diego, USA) and an autoMACS Pro Separator (Miltenyi Biotec). .. Isolated CD45- lung cells were seeded onto collagen I-coated 6-well plates (Iwaki, Tokyo, Japan) or 10 cm dishes (Iwaki, Tokyo, Japan) according to the number of isolated cells, and cultured with a complete growth medium consisting of ECGM-MV2 (PromoCell, Heidelberg, Germany)/5% FBS (PromoCell)/100 U/ml of penicillin/streptomycin in a humidified incubator with a gas mixture of 21%O2, 5%CO2, and balance N2 at 37 °C until 70–80% confluence was achieved (usually reached in 7–10 days). .. Next, we fractionated LECs from cultured CD45-lung cells using a fluorescence-activated cell sorting (FACS) Aria Fusion Cell Sorter (BD Biosciences, San Jose, USA) according to our previous protocol with some modification15.



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    Effects of activin‐A treatment of BMPR‐II expression and BMP downstream targets in PMECs and PAECs in low serum and supplemented media conditions. (A–G) Human pulmonary microvascular <t>endothelial</t> cells (PMECs, n = 3) and human pulmonary artery endothelial cells (PAECs) were treated with activin‐A (20 ng/mL; ActA) for 1, 6, and 24 h in low serum (0.1% FBS) conditions, where indicated. RNA was isolated and SMAD7 (A), ID1 (B), and BMPR2 (C) mRNA expression was assessed by normalizing to three housekeeping (HK) genes— BACT , B2M , and HPRT . (D) In PMECs, protein lysates were immunoblotted for phospho‐Smad1/5, phospho‐Smad2, total Smad1, total Smad2, and reprobed for β‐actin as a loading control. (E) Densitometry of the ratio between pSmad1/5 and total Smad1, and densitometry of the ratio between pSmad2/3 and total Smad2, both normalized to β‐actin. (F) In PMECs and PAECs, proteins were lysed after 6‐h ActA treatment and subsequently immunoblotted for BMPR‐II and reprobed for α‐tubulin as a loading control. (G) Densitometry of the ratio between BMPR‐II and α‐tubulin. (H–N) PAECs were treated with ActA (20 ng/mL) for either 1, 6, or 24 h in supplemented endothelial cell growth media, where indicated. RNA was isolated and SMAD7 (H), ID1 (I), and BMPR2 (J) mRNA expression assessed by normalizing to three HK genes. (K) PAECs ( n = 5) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for phospho‐Smad3, using an antibody which cross‐reacts with phospho‐Smad1. Protein lysates were also immunoblotted for total Smad1 and total Smad3 and reprobed for β‐actin. (L) Densitometry of the ratio between pSmad1 and total Smad1, pSmad3 and total Smad3, normalized to β‐actin. (M) PAECs ( n = 6) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (N) Densitometry of the ratio between BMPR‐II and β‐actin. (O) PAECs ( n = 3) were treated with or without Act‐A (20 ng/mL) and/or BMP9 (0.3 ng/mL) for 6 h in 0.1% FBS. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (P) Densitometry of the ratio between BMPR‐II and α‐tubulin. Two‐way ANOVA (A, B, and E). One‐way ANOVA (H, I, J, L, and P). Wilcoxon matched pairs test (I). * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. Error bars represent mean ± SEM.
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    Effects of activin‐A treatment of BMPR‐II expression and BMP downstream targets in PMECs and PAECs in low serum and supplemented media conditions. (A–G) Human pulmonary microvascular endothelial cells (PMECs, n = 3) and human pulmonary artery endothelial cells (PAECs) were treated with activin‐A (20 ng/mL; ActA) for 1, 6, and 24 h in low serum (0.1% FBS) conditions, where indicated. RNA was isolated and SMAD7 (A), ID1 (B), and BMPR2 (C) mRNA expression was assessed by normalizing to three housekeeping (HK) genes— BACT , B2M , and HPRT . (D) In PMECs, protein lysates were immunoblotted for phospho‐Smad1/5, phospho‐Smad2, total Smad1, total Smad2, and reprobed for β‐actin as a loading control. (E) Densitometry of the ratio between pSmad1/5 and total Smad1, and densitometry of the ratio between pSmad2/3 and total Smad2, both normalized to β‐actin. (F) In PMECs and PAECs, proteins were lysed after 6‐h ActA treatment and subsequently immunoblotted for BMPR‐II and reprobed for α‐tubulin as a loading control. (G) Densitometry of the ratio between BMPR‐II and α‐tubulin. (H–N) PAECs were treated with ActA (20 ng/mL) for either 1, 6, or 24 h in supplemented endothelial cell growth media, where indicated. RNA was isolated and SMAD7 (H), ID1 (I), and BMPR2 (J) mRNA expression assessed by normalizing to three HK genes. (K) PAECs ( n = 5) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for phospho‐Smad3, using an antibody which cross‐reacts with phospho‐Smad1. Protein lysates were also immunoblotted for total Smad1 and total Smad3 and reprobed for β‐actin. (L) Densitometry of the ratio between pSmad1 and total Smad1, pSmad3 and total Smad3, normalized to β‐actin. (M) PAECs ( n = 6) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (N) Densitometry of the ratio between BMPR‐II and β‐actin. (O) PAECs ( n = 3) were treated with or without Act‐A (20 ng/mL) and/or BMP9 (0.3 ng/mL) for 6 h in 0.1% FBS. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (P) Densitometry of the ratio between BMPR‐II and α‐tubulin. Two‐way ANOVA (A, B, and E). One‐way ANOVA (H, I, J, L, and P). Wilcoxon matched pairs test (I). * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. Error bars represent mean ± SEM.

    Journal: Pulmonary Circulation

    Article Title: Activin‐A Regulates Bone Morphogenetic Protein Signaling in Pulmonary Endothelial Cells Without Affecting Bone Morphogenetic Protein Type‐II Receptor Expression

    doi: 10.1002/pul2.70095

    Figure Lengend Snippet: Effects of activin‐A treatment of BMPR‐II expression and BMP downstream targets in PMECs and PAECs in low serum and supplemented media conditions. (A–G) Human pulmonary microvascular endothelial cells (PMECs, n = 3) and human pulmonary artery endothelial cells (PAECs) were treated with activin‐A (20 ng/mL; ActA) for 1, 6, and 24 h in low serum (0.1% FBS) conditions, where indicated. RNA was isolated and SMAD7 (A), ID1 (B), and BMPR2 (C) mRNA expression was assessed by normalizing to three housekeeping (HK) genes— BACT , B2M , and HPRT . (D) In PMECs, protein lysates were immunoblotted for phospho‐Smad1/5, phospho‐Smad2, total Smad1, total Smad2, and reprobed for β‐actin as a loading control. (E) Densitometry of the ratio between pSmad1/5 and total Smad1, and densitometry of the ratio between pSmad2/3 and total Smad2, both normalized to β‐actin. (F) In PMECs and PAECs, proteins were lysed after 6‐h ActA treatment and subsequently immunoblotted for BMPR‐II and reprobed for α‐tubulin as a loading control. (G) Densitometry of the ratio between BMPR‐II and α‐tubulin. (H–N) PAECs were treated with ActA (20 ng/mL) for either 1, 6, or 24 h in supplemented endothelial cell growth media, where indicated. RNA was isolated and SMAD7 (H), ID1 (I), and BMPR2 (J) mRNA expression assessed by normalizing to three HK genes. (K) PAECs ( n = 5) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for phospho‐Smad3, using an antibody which cross‐reacts with phospho‐Smad1. Protein lysates were also immunoblotted for total Smad1 and total Smad3 and reprobed for β‐actin. (L) Densitometry of the ratio between pSmad1 and total Smad1, pSmad3 and total Smad3, normalized to β‐actin. (M) PAECs ( n = 6) were treated with ActA for 6 h in supplemented media. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (N) Densitometry of the ratio between BMPR‐II and β‐actin. (O) PAECs ( n = 3) were treated with or without Act‐A (20 ng/mL) and/or BMP9 (0.3 ng/mL) for 6 h in 0.1% FBS. Protein lysates were immunoblotted for BMPR‐II and reprobed for α‐tubulin. (P) Densitometry of the ratio between BMPR‐II and α‐tubulin. Two‐way ANOVA (A, B, and E). One‐way ANOVA (H, I, J, L, and P). Wilcoxon matched pairs test (I). * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, **** p ≤ 0.0001. Error bars represent mean ± SEM.

    Article Snippet: PAECs or pulmonary microvascular endothelial cells (PMECs; Promocell or Lonza) were maintained in Endothelial Cell Growth Medium (ECGM)‐2 plus 2% fetal bovine serum (FBS) or ECGM‐MV2 plus 5% FBS, respectively, including supplement mix and antibiotic‐antimycotic (penicillin, streptomycin, and amphotericin B; Invitrogen).

    Techniques: Expressing, Isolation, Control