Human Dermal Lymphatic Endothelial Cells

Human Dermal Lymphatic Endothelial Cells

Cat.No.: CSC-C8596W

Species: Human

Source: Dermis; Skin

Cell Type: Endothelial Cell

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Cat.No.
CSC-C8596W
Description
Human Dermal Lymphatic Endothelial Cells from Creative Bioarray are isolated from human skin tissue. Human Dermal Lymphatic Endothelial Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based solution for 2 min and incubated in Creative Bioarray’ Culture Complete Growth Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells at passage 3 are detached from flasks and immediately cryopreserved in vails. Each vial contains at least 0.5×10^6 cells per ml. The method we use to isolate endothelial cells was developed based on a combination of established and our proprietary methods. These cells are pre-coated with LYVE1 antibody, following the application of magnetic beads pre-coated with secondary antibody.
Species
Human
Source
Dermis; Skin
Cell Type
Endothelial Cell
Disease
Normal
Quality Control
Human Dermal Lymphatic Endothelial Cells from Creative Bioarray display typical cobblestone with large dark nuclei appearance under light microscopyCells are tested for expression of endothelial cell marker using antibody, CD31 (Catalog No. 550389, BD; CD31/PECAM-1 PE-conjugated Antibody, Catalog No. FAB3567P, R&D), VE-Cadherin (FITC-VE-cadherin Catalog No. 560411, BD) or LYVE1(Catalog No. sc-28190, Santa Cruz) by immunofluorescence staining or FACS. All cells test negative for mycoplasma, bacteria, yeast, and fungi. HIV-1, hepatitis B and hepatitis C are not detected for all donors and/or cell lots. Per request, a Certificate of Analysis will be provided for each cell lot purchased. Cells can be expanded for 3-5 passages under the cell culture conditions specified by Creative Bioarray. Repeated freezing and thawing of cells is not recommended.
Storage and Shipping
Creative Bioarray ships frozen cells on dry ice. On receipt, immediately transfer frozen cells to liquid nitrogen (-180 °C) until ready for experimental use. Live cell shipment is also available on request. Never can primary cells be kept at -20 °C.
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.

Human dermal lymphatic endothelial cells (HDLECs) are a type of monolayer flat epithelium that are tightly arranged on the inner surface of lymphatic vessels, forming the primary structure of the lymphatic vessel wall. Through their precise arrangement and structure, they ensure effective lymph transportation and the normal functioning of the lymphatic system. HDLECs typically lack a complete basement membrane, which endows them with high permeability, favoring the exchange of substances between lymphatic fluid and tissue fluid. Moreover, HDLECs possess numerous invaginations and cytoplasmic vesicles, along with characteristic overlapping intercellular junctions. These structural features enhance the strength of intercellular connections and help maintain the integrity and stability of lymphatic vessels. Additionally, HDLECs exhibit positive reactions to specific immunofluorescence markers such as CD31, Podoplanin, and Lyve1, which are commonly used for the identification and isolation of these cells.

HDLECs play a vital role in maintaining physiological balance and immune functionality within the human body. They not only manage fluid, protein and tissue pressure but also serve as sites for lymphocyte recirculation and immune activity. Lymphocytes travel efficiently throughout the body, performing immune functions such as infection prevention and tumour surveillance via lymphatic vessels. Moreover, HDLECs are involved in various pathologic processes including wound healing, lymphoedema, and spreading of inflammation. Several new studies have shown that HDLECs play a pivotal role in tumor metastasis, modulating the spread routes of cancer cells through control of the creation and function of lymphatic vessels In research, HDLECs are often used in making models of lymphatic diseases, including lymphangioma, lymphangitis and lymphatic tuberculosis, in order to understand how these conditions can be treated. Besides these, HDLECs are widely applied to determine how lymphatic endothelial cells multiply, migrate and differentiate, and the molecular signalling networks controlling those functions.

Human dermal lymphatic endothelial cells stained with DAPI (blue nuclei) and immuno-stained with CD31.Fig. 1. Human dermal lymphatic endothelial cells. DAPI: blue nuclei. Corresponding bright field images of CD31 and podoplanin immuno-stained cells appear to the right of each immuno-stained image. (Kong AM, Lim SY, et al., 2022).

Stearic Acid Selectively Induced Apoptosis in Lymphatic Endothelial Cells Through ER Stress and Reactive Oxygen Species

To investigate the in vitro effects of saturated fatty acids (SFAs) on lymphatic and vascular endothelial cells, human dermal lymphatic endothelial cells (HDLECs), human umbilical vein endothelial cells (HUVECs), and human dermal microvascular endothelial cells (HDMECs) were exposed to increasing concentrations of several different fatty acids, and cell death was evaluated using a trypan blue exclusion assay.

Increasing concentrations of the stearic acid (SA) and palmitic acid (PA) resulted in dose-dependent cell death in HDLECs, to a greater extent than HUVECs and HDMECs, indicating that HDLECs are more susceptible to lipotoxicity (Fig. 1A,B,C). These findings suggest that LECs are more susceptible to SFA-induced lipotoxicity than vascular endothelial cells. SA treatment significantly increased reactive oxygen species (ROS) production in HDLECs, with mitochondrial ROS levels elevated by sixfold and intracellular ROS levels elevated by fivefold (Fig. 1D,E,F). In addition, western blot analysis revealed a dose-dependent increase in sXBP-1 and CHOP expression following SA treatment, suggesting that ER stress also contributes to SA-induced cell death in LECs. These findings demonstrate that ROS and ER stress contribute to SA-induced cell death in LECs.

Stearic acid promotes apoptosis in lymphatic endothelial cells via reactive oxygen species (ROS) and ER stress.
Fig. 1. Stearic acid promotes apoptosis in lymphatic endothelial cells via reactive oxygen species (ROS) and ER stress (Gomes, Karina P., et al., 2025).

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