Human Aortic Endothelial Cells: Asthma: HAOEC-AS
Human Aortic Endothelial Cells: Asthma (HAOEC-AS) from asthma donors represent a specialized macrovascular endothelial cell population isolated from the luminal layer of the human aorta of individuals clinically diagnosed with asthma.
Description
Human Aortic Endothelial Cells: Asthma (HAOEC-AS) from asthma donors represent a specialized macrovascular endothelial cell population isolated from the luminal layer of the human aorta of individuals clinically diagnosed with asthma. As a primary cell type rather than an immortalized cell line, HAOEC-AS provide a translationally relevant human model to explore how chronic respiratory conditions potentially intersect with macrovascular biology. These cells may retain a disease-associated imprint shaped by the donor’s in vivo inflammatory environment. This potential cellular imprint depends on the specific asthma phenotype, overall disease severity, donor medication history (such as corticosteroid use), active comorbidities, and the time elapsed since the donor’s last acute exacerbation. Characterization protocols verify that these cells maintain classic baseline endothelial markers—such as CD31 (PECAM-1) and von Willebrand factor—though their exact gene expression profiles and surface configurations can exhibit notable donor-to-donor heterogeneity.
In the human body, these vascular endothelial cells form the innermost large-vessel monolayer lining the lumen of the thoracic and abdominal aorta segments. It is important to note that asthma is primarily an airway-localized disease, and many patients exhibit localized inflammation confined to the respiratory tract with limited systemic spillover. Pronounced systemic Th2 cytokine elevations and active circulating eosinophils typically occur only in specific subsets, such as severe eosinophilic asthma. Consequently, the sustained exposure of large-vessel walls to these inflammatory mediators varies greatly by patient phenotype and treatment status. While a typical cell panel for respiratory research relies on tissue-specific environments—such as airway epithelial cells, pulmonary microvascular cells, or direct sampling of lung tissues—evaluating macrovascular cells from the same donor allows investigators to study potential systemic vascular cross-talk. Understanding these cells helps researchers evaluate changes in the aortic wall, though direct links between asthma and macrovascular remodeling or an increased risk of a thoracic or abdominal aortic aneurysm are not established general findings and remain a subject of active epidemiological and mechanistic investigation.
The primary function of healthy aortic endothelial cells is to maintain vascular homeostasis by acting as a semipermeable barrier, managing arterial tone, and preventing unprovoked leukocyte recruitment. In asthmatic patients—particularly those with severe or poorly controlled allergic asthma—this baseline functional state may be altered if the vascular wall is exposed to systemic inflammatory signals. When active, these systemic loops can prompt endothelial activation, leading to the altered expression of certain cellular adhesion molecules (such as VCAM-1 or ICAM-1) on the cell surface. This activation can influence leukocyte tethering and migration dynamics. Additionally, investigators look at how localized or systemic variations in angiogenic factors, such as vascular endothelial growth factor (VEGF), interact with these cells, observing how chronic, compartmentalized pulmonary diseases might subtly influence wider vascular homeostasis and permeability.
In laboratory settings, HAOEC-AS serve as a unique in vitro platform to explore the debated links between chronic respiratory diseases, systemic inflammation, and cardiovascular disease. Researchers utilize these cells alongside established animal models, including asthmatic mice, to cross-reference localized respiratory findings—such as airway inflammation markers in bronchoalveolar lavage fluid or tissue-specific eosinophil count metrics—with human macrovascular cell behavior. By monitoring altered gene expression profiles under controlled conditions, scientists can evaluate how endothelial responses differ among asthma patients, healthy controls, or individuals with chronic obstructive pulmonary disease (COPD). Furthermore, HAOEC-AS can be used in translational assays to support target validation and airway drug development. Due to the inherent heterogeneity of primary tissue, utilizing these cells effectively in drug-discovery screens requires careful experimental validation, strict passage control, and meticulous donor-matching to account for confounding shared risk factors and treatments.
- Demonstrate that increased glucose flux leads to endothelial dysfunction in diabetes via activating Egr1-mediated proinflammatory and prothrombotic responses
- Study apoptosis, oxidative stress and inflammation associated with atherosclerosis and demonstrate the beneficial effects of anthocyanin on endothelial cells damaged by exposure to oxidized sterols
- Demonstrate that upregulation of thioredoxin via AMPK-FOXO3 pathway protects endothelial cells from oxidative stress and may prevent cardiovascular diseases in patients with metabolic syndrome and diabetes and further elucidate the involvement of AMPK cascade in mediating beneficial cardiovascular effects of green tea
- Test anti-inflammatory and vasodilating properties of a synthetic rutaecarpine derivative
- Show that glycated albumin, associated with diabetic complications, decreases endothelial miR-146a expression which leads to increased IL-6 production, and that angiotensin protects endothelial cells by preventing miR-146a downregulation
- Demonstrate that air pollutants can directly affect ZO-1 function leading to increased endothelial permeability, inflammatory cell transmigration and initiation of atherosclerosis
- Discover the involvement of stress signaling JNK and p38 pathways in pathological suppression of thrombomodulin, a vascular protective molecule, downregulated in many thrombotic and vascular diseases
- Link uremic toxins (in particular, PAA) in patients with chronic liver disease to increased ROS production and stimulation of TNF-a in endothelial cells leading to atherosclerosis and vascular calcification
- Demonstrate that in diabetes, advanced glycation end products lead to ROS generation in endothelia via sustained NF-kB activation, contributing to progression of atherosclerosis
- Discover that CD40 ligand promotes monocyte adhesion to endothelial cells via PKCa, NF-kB and VCAM-1 signaling cascade, explaining the role of CD40L in atherogenesis
- Show that monocytes activated by endothelial cells, produce CD80 signaling that leads to allogenic immune response, indicating the need for specific therapy to prevent monocyte activation during allograft transplantation
- Identify tetraspanin CD82 as the recognition sensor responsible for rejection of xenotransplants
- Develop 3d endothelialized engineered tissues, as well as new technology based on novel material surfaces and drugs (such as paclitaxel, sirolimus, vitamin C, C6-ceramide and 17β-estradiol) to inhibit smooth muscle cell proliferation at the same time allowing endothelial cells adhesion and proliferation in order to reduce risk associated with vascular implants
Details
| Tissue | Normal healthy human aorta |
|---|---|
| QC | No bacteria, yeast, fungi, mycoplasma |
| Character | Factor VIII-related Ag, DiI-Ac-LDL uptake. S-HAOEC are select HAOEC lots that have been tested positive for VEGFR2 pathway activation following stimulation by VEGF. |
| Bioassay | Attach, spread, proliferate in Growth Med |
| Cryovial | 500,000 HAOEC-AS (2nd passage) frozen in Basal Medium w/10% FBS, 10% DMSO |
| Kit | Cryovial frozen HAOEC-AS (304AS-05a), Growth Medium (211-500), Subculture Rgnt Kit (090K) |
| Proliferating | Shipped in Tsfr Med, 3rd psg (flasks or plates) |
| Doublings | At least 16 |
| Applications | Laboratory research use only (RUO). Not for human, clinical, diagnostic or veterinary use. |
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