Immortalized Human Cardiac Microvascular Endothelial Cells-SV40

Cat.No.: CSC-I9075L

Species: homo sapiens

Source: Cardiac Microvascular

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I9075L
Description
Immortalized Human Cardiac Microvascular Endothelial Cells-SV40 were developed from human tissues transduced with a lentiviral expression vector containing the SV40T gene. The cell line was continuously cultured for more than 30 passages without showing signs of growth retardation or replicative senescence.
Species
homo sapiens
Source
Cardiac Microvascular
Recommended Medium
SuperCult® Immortalized Human Cardiac Microvascular Endothelial Cell Medium (Cat No.: CM-I9075L)
Freezing Medium
Complete medium supplemented with 10% (v/v) DMSO
Culture Properties
Adherent
Morphology
Polygonal
Immortalization Method
SV40 large T antigen
Markers
vWF, CD31, podoplanin, Dil-Ac-LDL uptake
Application
For Research Use Only
Growth Properties
Cells are cultured as a monolayer at 37°C in a humidified atmosphere with 5% CO2.
Storage
Directly and immediately transfer cells from dry ice to liquid nitrogen upon receiving and keep the cells in liquid nitrogen until cell culture needed for experiments.

Note: Never can cells be kept at -20 °C.
Shipping
Dry Ice.
Recommended Products
CSC-C1464 Human Cardiac Microvascular Endothelial Cells
CIK-HT003 HT® Lenti-SV40T Immortalization Kit
Quality Control
Real Time PCR was used to quantify SV40T gene expression in immortalized cell line.
free from contaminations (bacteria incl. mycoplasma, fungi, HIV, HAV, HBV, HCV, Parvo-B19) and cross-contaminations
BioSafety Level
II
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

Immortalized Human Cardiac Microvascular Endothelial Cells - SV40 are primary human cardiac microvascular endothelial cells (HCMVECs) that have been immortalized through the introduction of SV40 large T antigen, allowing for long-term and stable propagation. They maintain important characteristics of the cardiac microvascular endothelium while also providing increased practicality over primary endothelial cells due to extended lifespan and reduced donor variability, making them particularly well-suited for mechanistic studies and high-throughput screening.

The hallmark of these cells is their maintenance of a microvascular endothelial identity that is specific to the heart. They exhibit typical cobblestone morphology, establish tight cell-cell junctions, and express common endothelial markers such as CD31, VE-cadherin, von Willebrand factor (vWF), and endothelial nitric oxide synthase (eNOS). In terms of function, they respond strongly to shear stress, hypoxia, inflammatory cytokines, and angiogenic factors, which are all stimuli that are of particular relevance to the cardiac microenvironment. Thess cells have been used to study coronary microcirculation, endothelial dysfunction, and cardiac vascular inflammation. In general, they serve as a convenient and reliable in vitro model for the study of mechanisms underlying ischemia-reperfusion injury, diabetic cardiomyopathy, and heart failure-associated microvascular dysfunction.

Sufentanil Enhances the Viability and Inhibits the Apoptosis of OGD/R-Induced HCMECs

Ischemic heart disease is a major cause of death due to chronic myocardial damage from coronary artery ischemia. Here, Wang's team used oxygen and glucose deprivation/reoxygenation (OGD/R) to simulate myocardial I/R injury in HCMECs.

The chemical structure of sufentanil is shown in Fig. 1A. Sufentanil had no significant effect on HCMEC viability (Fig. 1B). OGD/R induction significantly decreased HCMEC viability, but sufentanil treatment partially enhanced it (Fig. 1C). Sufentanil also improved the viability of OGD/R-induced HCMECs in a dose-dependent manner. OGD/R induction increased LDH activity, which was gradually reduced by sufentanil treatment (Fig. 1D), indicating sufentanil's inhibitory effects on LDH activity. OGD/R induction significantly increased HCMEC apoptosis compared to controls, but sufentanil treatment suppressed this increase in a dose-dependent manner. 20 µM sufentanil had the best suppressive effect on apoptosis (Fig. 2A and B). OGD/R induction downregulated Bcl-2 and upregulated Bax, c-caspase-3, and cytochrome c protein expression. However, sufentanil treatment reversed these effects, as shown by upregulated Bcl-2 and downregulated Bax, c-caspase-3, and cytochrome c expression in the OGD/R + 5 µM, OGD/R + 10 µM, and OGD/R + 20 µM groups (Fig. 2C).

Sufentanil enhances the viability of OGD/R-induced HCMECs.

Fig. 1. Sufentanil enhances the viability of OGD/R-induced HCMECs (Wang L G, Ge C L, et al., 2022).

Sufentanil inhibits the apoptosis of OGD/R-induced human cardiac microvascular endothelial cells.

Fig. 2. Sufentanil inhibits the apoptosis of OGD/R-induced human cardiac microvascular endothelial cells (Wang L G, Ge C L, et al., 2022).

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