Linking in vitro models of endothelial dysfunction with cell senescence
| Autor: | Àngela Vea Badenes, Manel Sabaté Tenas, Joaquim Bobi Gibert, Francisco R. Jimenez Trinidad, Ana Paula Dantas, Marta Arrieta Ruiz, Montserrat Rigol Muxart, Antoni Valera Cañellas, Mercè Roqué Moreno, Olga Tura-Ceide, Xavier Freixa Rofastes, Núria Solanes Batlló |
|---|---|
| Přispěvatelé: | Cardiology, Institut Català de la Salut, [Jimenez Trinidad FR, Arrieta Ruiz M, Solanes Batlló N, Valera Cañellas A, Roqué Moreno M, Freixa Rofastes X, Sabaté Tenas M, Dantas AP] Cardiology Department, Institute Clinic Cardiovascular (ICCV), Hospital Clinic, Institute d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. [Vea Badenes A] Department of Pulmonary Medicine, Servei de Pneumologia, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. [Bobi Gibert J] Department of Cardiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands. [Tura-Ceide O] Department of Pulmonary Medicine, Servei de Pneumologia, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain. Biomedical Research Networking Centre on Respiratory Diseases (CIBERES), CB06/06/0011 Group, Pulmonary Hypertension Programme, Instituto de Salud Carlos III, Madrid, Spain. Department of Pulmonary Medicine, Santa Caterina Hospital de Salt, Biomedical Research Institute (IDIBGI), Hospital Universitari de Girona Doctor Josep Trueta, Institut Català de la Salut (ICS), Girona, Spain. [Rigol Muxart M] Cardiology Department, Institute Clinic Cardiovascular (ICCV), Hospital Clinic, Institute d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain, Hospital Universitari de Girona Dr Josep Trueta |
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Senescence
senescence Science Cell Cell Physiological Phenomena::Cellular Senescence [PHENOMENA AND PROCESSES] Pharmacology Biology medicine.disease_cause Endoteli células::células epiteliales::células endoteliales [ANATOMÍA] Article General Biochemistry Genetics and Molecular Biology Umbilical vein endothelial dysfunction SDG 3 - Good Health and Well-being medicine oxidative stress Endothelial dysfunction Ecology Evolution Behavior and Systematics in vitro models Cells::Epithelial Cells::Endothelial Cells [ANATOMY] cell culture starvation Paleontology medicine.disease Endothelial stem cell medicine.anatomical_structure Space and Planetary Science Cell culture Toxicity fenómenos fisiológicos celulares::senescencia celular [FENÓMENOS Y PROCESOS] Cèl·lules - Envelliment Oxidative stress |
| Zdroj: | Life, 11(12):1323. Multidisciplinary Digital Publishing Institute (MDPI) Life, Vol 11, Iss 1323, p 1323 (2021) Life; Volume 11; Issue 12; Pages: 1323 Scientia Life |
| ISSN: | 2075-1729 |
| Popis: | Disfunció endotelial; Envellliment cel·lular Disfunción endotelial; Envejecimiento celular Endothelial dysfunction; Senescence Endothelial cell dysfunction is the principal cause of several cardiovascular diseases that are increasing in prevalence, healthcare costs, and mortality. Developing a standardized, representative in vitro model of endothelial cell dysfunction is fundamental to a greater understanding of the pathophysiology, and to aiding the development of novel pharmacological therapies. We subjected human umbilical vein endothelial cells (HUVECs) to different periods of nutrient deprivation or increasing doses of H2O2 to represent starvation or elevated oxidative stress, respectively, to investigate changes in cellular function. Both in vitro cellular models of endothelial cell dysfunction-associated senescence developed in this study, starvation and oxidative stress, were validated by markers of cellular senescence (increase in β-galactosidase activity, and changes in senescence gene markers SIRT1 and P21) and endothelial dysfunction as denoted by reductions in angiogenic and migratory capabilities. HUVECs showed a significant H2O2 concentration-dependent reduction in cell viability (p < 0.0001), and a significant increase in oxidative stress (p < 0.0001). Furthermore, HUVECs subjected to 96 h of starvation, or exposed to concentrations of H2O2 of 400 to 1000 μM resulted in impaired angiogenic and migratory potentials. These models will enable improved physiological studies of endothelial cell dysfunction, and the rapid testing of cellular efficacy and toxicity of future novel therapeutic compounds. This research was funded by Beca de Investigacion Basica en Cardiologia from the Sociedad Española de Cardiologia, Fondo de Investigacion en Salud (grants PI18/00277, PI16/00742, PI19/00264, PI18/00960 and PI15/00553) from the Spanish Ministry of Science and Innovation, Instituto de Salud Carlos III–Fondo Europeo de Desarrollo Regional (FEDER), and Spanish Society of Respiratory Medicine (SEPAR) and Catalan Society of Pneumology (SOCAP) grants. FRJT and OTC are the recipients of the Ayudas para la formación de profesorado universitario (FPU19/04925) and Miguel Servet (CP17/00114) grants, respectively, from the Spanish Ministry of Science and Innovation. IDIBAPS belongs to the CERCA Programme, and receives partial funding from the Generalitat de Catalunya. Cofunding was provided by the Fondo Europeo de Desarrollo Regional (FEDER); “Una manera de hacer Europa”. |
| Databáze: | OpenAIRE |
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