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Hpasmcs

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HPASMCs are primary human pulmonary artery smooth muscle cells, which are suitable for in vitro studies of the pulmonary vasculature. They are isolated from the pulmonary arteries of healthy human donors.

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Lab products found in correlation

Brdu cell proliferation assay, by Merck Group (2 mentions) Human smooth muscle cell growth medium 2, by PromoCell (2 mentions) Lipofectamine rnaimax transfection reagent, by Thermo Fisher Scientific (2 mentions) Dpp4 sirna, by Thermo Fisher Scientific (1 mentions) Hpasmc, by Thermo Fisher Scientific (1 mentions) Smooth muscle cell growth medium 2, by PromoCell (1 mentions) Tipifarnib, by Selleck Chemicals (1 mentions) C 12521, by PromoCell (1 mentions)

4 protocols using hpasmcs

1

Modulating hPASMCs with DPP4 siRNA

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hPASMCs were purchased from PromoCell (Heidelberg, Germany) and cultured in Smooth Muscle Cell Growth Medium 2 (PromoCell) supplemented with 10% fetal bovine serum. hPASMCs were incubated at 37 °C in a 5% CO2 incubator and used at passages 4–6 for all experiments. For small interfering RNA (siRNA) transfection, DPP4 siRNA (Cat# 4392421, siRNA ID: s4255) and non-specific control siRNA (Cat# 4390843, Silencer™ Select Negative Control No. 1 siRNA) were purchased from Thermo Fisher Scientific (Waltham, MA, USA). Using the Lipofectamine™ RNAiMAX Transfection Reagent (Thermo Fisher Scientific), hPASMCs were transfected with siRNA for 48 h according to the manufacturer’s protocol. After the siRNA treatment, the cells were stimulated with recombinant human transforming growth factor-b1 (TGFβ) (PEPROTECH. Cranbury, NJ, USA) at a concentration of 10 ng/mL as previously reported [45 (link)] or with PBS at the same concentration for 24 h.
Okaya T., Kawasaki T., Sato S., Koyanagi Y., Tatsumi K., Hatano R., Ohnuma K., Morimoto C., Kasuya Y., Hasegawa Y., Ohara O, & Suzuki T. (2024). Functional Roles of CD26/DPP4 in Bleomycin-Induced Pulmonary Hypertension Associated with Interstitial Lung Disease. International Journal of Molecular Sciences, 25(2), 748.
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2

Hypoxia Impact on HPASMC Proliferation

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Human pulmonary artery smooth muscle cells (HPASMCs) from PromoCell and Lonza were grown in Human Smooth Muscle Cell Growth Medium 2 (PromoCell). The cells were cultured under normal oxygen tension (20% O2, 5% CO2) or exposed to hypoxia (2% O2, 5% CO2, 92% N2) for 48-72hr. A Bromodeoxyuridine (BrdU) cell proliferation assay (Millipore) was used to assess cell proliferation following manufacturer’s conditions.
Zhao L., Oliver E., Maratou K., Atanur S.S., Dubois O.D., Cotroneo E., Chen C.N., Wang L., Arce C., Chabosseau P.L., Ponsa-Cobas J., Frid M.G., Moyon B., Webster Z., Aldashev A., Ferrer J., Rutter G.A., Stenmark K.R., Aitman T.J, & Wilkins M.R. (2015). The zinc transporter, ZIP12, regulates the pulmonary vascular response to chronic hypoxia. Nature, 524(7565), 356-360.
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3

Hypoxia Impact on HPASMC Proliferation

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Human pulmonary artery smooth muscle cells (HPASMCs) from PromoCell and Lonza were grown in Human Smooth Muscle Cell Growth Medium 2 (PromoCell). The cells were cultured under normal oxygen tension (20% O2, 5% CO2) or exposed to hypoxia (2% O2, 5% CO2, 92% N2) for 48-72hr. A Bromodeoxyuridine (BrdU) cell proliferation assay (Millipore) was used to assess cell proliferation following manufacturer’s conditions.
Zhao L., Oliver E., Maratou K., Atanur S.S., Dubois O.D., Cotroneo E., Chen C.N., Wang L., Arce C., Chabosseau P.L., Ponsa-Cobas J., Frid M.G., Moyon B., Webster Z., Aldashev A., Ferrer J., Rutter G.A., Stenmark K.R., Aitman T.J, & Wilkins M.R. (2015). The zinc transporter, ZIP12, regulates the pulmonary vascular response to chronic hypoxia. Nature, 524(7565), 356-360.
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4

Hypoxic Response in Pulmonary Cells

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Human pulmonary artery endothelial cells (HPAEC; Promocell, C-12241, lot 7121003.5 and 4091902) and smooth muscle cells (HPASMCs; Promocell, C-12521, lot 9033101.6) were cultured, as described in Ref. 4 (link). The cells were used between passages 3–6. The cells were kept under normoxia or were exposed to hypoxia (2% O2) for 2–72 h. In experiments involving a short-term (2 h) exposure to hypoxia, tipifarnib (Selleckchem) was added to the cells 1 h before the hypoxic exposure at 0.1 µmol/L. In experiments involving a more prolonged exposure to hypoxia (24–72 h), tipifarnib was added to the cells at the start of hypoxic exposure.4 (link)
Duluc L., Ahmetaj-Shala B., Mitchell J., Abdul-Salam V.B., Mahomed A.S., Aldabbous L., Oliver E., Iannone L., Dubois O.D., Storck E.M., Tate E.W., Zhao L., Wilkins M.R, & Wojciak-Stothard B. (2017). Tipifarnib prevents development of hypoxia-induced pulmonary hypertension. Cardiovascular Research, 113(3), 276-287.
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