Hypoxia‐induced endothelial cell responses – possible roles during periodontal disease
Autor: | Daniel Nguyen, Reila Tainá Mendes, Hatice Hasturk, Danielle Stephens, Alpdogan Kantarci, Thomas E. Van Dyke, Daniel Fernandes, Ferda Pamuk |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
CD31 Angiogenesis Inflammation Nitric oxide Andrology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine periodontitis General Dentistry Fusobacterium nucleatum biology Chemistry Original Articles Hypoxia (medical) biology.organism_classification endothelial cells Endothelial stem cell 030104 developmental biology inflammation 030220 oncology & carcinogenesis Original Article Tumor necrosis factor alpha medicine.symptom oxygen |
Zdroj: | Clinical and Experimental Dental Research |
ISSN: | 2057-4347 |
DOI: | 10.1002/cre2.135 |
Popis: | Background and objective Inflammatory periodontal pockets are known to be hypoxic. Hypoxia influences vascular response to periodontal inflammation, including angiogenesis, which is critical for oxygen and nutrient delivery to periodontal tissues and granulation tissue formation. Our previous work suggests that periodontal bacteria may actively contribute to pocket hypoxia. Herein, we test the hypothesis that Fusobacterium nucleatum actively induces low oxygen tension, which modulates angiogenesis and endothelial cell activity. HUVEC cells were incubated in 1.5% oxygen for (Folkman & Shing, 1992)48 hours. Cell proliferation was measured by MTT; surface expression of CD31, CD34 and VEGF receptors (VEGFR1, VEGFR2) were analyzed by FACS. mRNA expression of HIF isoforms, iNOS, eNOS, COX‐2, and VEGF was measured by quantitative PCR. Supernatants were analyzed for the release of IL‐1α, TNF‐α, and VEGF by ELISA or multiplex immunoassays and nitric oxide was measured by colorimetric assay. F. nucleatum actively depleted oxygen. Hypoxia resulted in a significant increase of HIF isoforms. iNOS was increased while nitric oxide was unchanged. VEGF release was increased at 4 hours followed by an increase in VEGFR1 at 12 hours, but not VEGFR2. CD31 expression was reduced and CD34 was increased after 48 hours (p |
Databáze: | OpenAIRE |
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