The Effect of Race and Shear Stress on CRP-Induced Responses in Endothelial Cells

Autor:	Maitha Aldokhayyil, Heather Grimm, Chenyi Ling, Michael F. Brown, Dulce H. Gomez, Marc D. Cook
Rok vydání:	2021
Předmět:	medicine.medical_specialty Article Subject Nitric Oxide Synthase Type III Endothelium Receptor expression Immunology Systemic inflammation White People Umbilical vein Nitric oxide chemistry.chemical_compound Enos Internal medicine Human Umbilical Vein Endothelial Cells Pathology medicine Humans RB1-214 Receptor Cells Cultured biology Cell adhesion molecule Receptors IgG Cell Biology biology.organism_classification Black or African American C-Reactive Protein Endocrinology medicine.anatomical_structure chemistry Cardiovascular Diseases Stress Mechanical medicine.symptom Research Article
Zdroj:	Mediators of Inflammation, Vol 2021 (2021) Mediators of Inflammation
ISSN:	1466-1861 0962-9351
DOI:	10.1155/2021/6687250
Popis:	Background. C-reactive protein (CRP) is an independent biomarker of systemic inflammation and a predictor of future cardiovascular disease (CVD). More than just a pure bystander, CRP directly interacts with endothelial cells to decrease endothelial nitric oxide synthase (eNOS) expression and bioactivity, decrease nitric oxide (NO) production, and increase the release of vasoconstrictors and adhesion molecules. Race is significantly associated with CRP levels and CVD risks. With aerobic exercise, the vessel wall is exposed to chronic high laminar shear stress (HiLSS) that shifts the endothelium phenotype towards an anti-inflammatory, antioxidant, antiapoptotic, and antiproliferative environment. Thus, the purpose of this study was to assess the racial differences concerning the CRP-induced effects in endothelial cells and the potential role of HiLSS in mitigating these differences. Methods. Human umbilical vein endothelial cells (HUVECs) from four African American (AA) and four Caucasian (CA) donors were cultured and incubated under the following conditions: (1) static control, (2) CRP (10 μg/mL, 24 hours), (3) CRP receptor (FcγRIIB) inhibitor followed by CRP stimulation, (4) HiLSS (20 dyne/cm2, 24 hours), and (5) HiLSS followed by CRP stimulation. Results. AA HUVECs had significantly higher FcγRIIB receptor expression under both basal and CRP incubation conditions. Blocking FcγRIIB receptor significantly attenuated the CRP-induced decrements in eNOS expression only in AA HUVECs. Finally, HiLSS significantly counteracted CRP-induced effects. Conclusion. Understanding potential racial differences in endothelial function is important to improve CVD prevention. Our results shed light on FcγRIIB receptor as a potential contributor to racial differences in endothelial function in AA.
Databáze:	OpenAIRE
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