Hlmvecs

Manufactured by Thermo Fisher Scientific

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HLMVECs are primary human lung microvascular endothelial cells. They are isolated from the microvasculature of normal human lung tissue. HLMVECs are suitable for use in in vitro studies of lung endothelial cell biology and function.

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Lab products found in correlation

Q5 site directed mutagenesis kit, by New England Biolabs (1 mentions) Lipofectamine rnaimax transfection reagent, by Thermo Fisher Scientific (1 mentions) Lipopolysaccharide lps, by Merck Group (1 mentions) Hlmvec, by Cell Applications (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions) Lipofectamine 2000 reagent, by Thermo Fisher Scientific (1 mentions) Ebm 2, by Lonza (1 mentions)

2 protocols using hlmvecs

Modulating RhoA Activity in Endothelial Cells

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Plasmid DNA coding RhoA have been described previously [23 (link)]. The C16, 20, 159S triple mutant RhoA was generated by Q5^® Site- Directed Mutagenesis Kit (NEB, Ipswich, MA) and confirmed by DNA sequencing. The antibody against RhoA was purchased from Cell Signaling. The G⁺-bacterial toxin, listeriolysin (LLO), was purified as described previously [7 (link)].
GSNOR/TRX genes were transiently silenced using siRNA. The siRNA targeting GSNOR (siRNA ID: s1071) and TRX (siRNA ID: s2) as well as validated non-targeting controls were purchased from Applied Biosystems (Carlsbad, California). Lipofectamine^® RNAi- MAX transfection reagent was used to deliver the siRNA in HLMVECs (Invitrogen, Grand Island, NY).

Chen F., Wang Y., Rafikov R., Haigh S., Zhi W.B., Kumar S., Doulias P.T., Rafikova O., Pillich H., Chakraborty T., Lucas R., Verin A.D., Catravas J.D., She J.X., Black S.M, & Fulton D.J. (2016). RhoA S-nitrosylation as a regulatory mechanism influencing endothelial barrier function in response to G+-bacterial toxins. Biochemical pharmacology, 127, 34-45.

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Investigating Autophagy Regulation in HLMVEC

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Human lung microvascular endothelial cells (HLMVECs) (Cell Applications Inc., CA, USA) were cultured in EBM-2 (containing endothelial growth factor, CC3162, Lonza, MD, USA) supplemented with 5% FBS (Gibco, CA, USA) at 37°C, 5% CO₂, and 95% humidity and passaged every 3–5 days. P4–P7 cells were utilized in the next stage of the experiment. Lipopolysaccharide (LPS) (Sigma-Aldrich, MO, USA; 10 μg/mL) treatment for 1 day was applied on HLMVECs for the in vitro model. Then, 50 μM HYP or 3 mM 3-MA was used to investigate the regulatory role of HYP on autophagy. For Atg13 silencing (si-Atg13 : 5′-AAGUCCCUUCUUGCUAUAACUAGTTCUAGUUAUAGCAAGAAGGGACUUTT-3′), siRNA against Atg13 was used to transfect into HLMVECs using Lipofectamine 2000 reagent (Invitrogen, Carlsbad, CA, USA). After transfection for 48 hr, HLMVECs cells were harvested for use in subsequent experiments.

Mai J., He Q., Liu Y, & Hou Y. (2023). Hyperoside Attenuates Sepsis-Induced Acute Lung Injury (ALI) through Autophagy Regulation and Inflammation Suppression. Mediators of Inflammation, 2023, 1257615.

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