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Prolonged oxygen exposure causes the mobilization and functional damage of stem or progenitor cells and exacerbates cardiac ischemia or reperfusion injury in healthy mice
Author(s) -
Li Yu,
Luo NaChuan,
Zhang Xu,
Hara Tetsuya,
Inadomi Chiaki,
Li TaoSheng
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30317
Subject(s) - progenitor cell , chemokine , stem cell , reactive oxygen species , ischemia , cytokine , endothelial progenitor cell , oxygen , immunology , inflammation , andrology , medicine , endocrinology , biology , chemistry , biochemistry , microbiology and biotechnology , organic chemistry
Oxygen is often administered to patients and occasionally to healthy individuals as well; however, the cellular toxicity of oxygen, especially following prolonged exposure, is widely known. To evaluate the potential effect of oxygen exposure on circulating stem/progenitor cells and cardiac ischemia/reperfusion (I/R) injury, we exposed healthy adult mice to 100% oxygen for 20 or 60 min. We then examined the c‐kit‐positive stem/progenitor cells and colony‐forming cells and measured the cytokine/chemokine levels in peripheral blood. We also induced cardiac I/R injury in mice at 3 h after 60 min of oxygen exposure and examined the recruitment of inflammatory cells and the fibrotic area in the heart. The proportion of c‐kit‐positive stem/progenitor cells significantly increased in peripheral blood at 3 and 24 h after oxygen exposure for either 20 or 60 min ( p < .01 vs. control). However, the abundance of colony‐forming cells in peripheral blood conversely decreased at 3 and 24 h after oxygen exposure for only 60 min ( p < .05 vs. control). Oxygen exposure for either 20 or 60 min resulted in significantly decreased plasma vascular endothelial growth factor levels at 3 h, whereas oxygen exposure for only 60 min reduced plasma insulin‐like growth factor 1 levels at 24 h ( p < .05 vs. control). Protein array indicated the increase in the levels of some cytokines/chemokines, such as CXCL6 (GCP‐2) at 24 h after 60 min of oxygen exposure. Moreover, oxygen exposure for 60 min enhanced the recruitment of Ly6g‐ and CD11c‐positive inflammatory cells at 3 days ( p < .05 vs. control) and increased the fibrotic area at 14 days in the heart after I/R injury ( p < .05 vs. control). Prolonged oxygen exposure induced the mobilization and functional impairment of stem/progenitor cells and likely enhanced inflammatory responses to exacerbate cardiac I/R injury in healthy mice.