期刊
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
卷 57, 期 6, 页码 651-661出版社
AMER THORACIC SOC
DOI: 10.1165/rcmb.2016-0386OC
关键词
CD34; vascular endothelia; lung injury; bleomycin; influenza
资金
- AllerGen Networks Centres of Excellence of Canada Strategic Initiative grant
- Canadian Institutes of Health Research grant [MOP-84545]
- University of British Columbia Four Year Doctoral Fellowship
- AllerGen Canadian Allergy and Immune Diseases Advanced Training Initiative award
Survival during lung injury requires a coordinated program of damage limitation and rapid repair. CD34 is a cell surface sialomucin expressed by epithelial, vascular, and stromal cells that promotes cell adhesion, coordinates inflammatory cell recruitment, and drives angiogenesis. To test whether CD34 also orchestrates pulmonary damage and repair, we induced acute lung injury in wild-type (WT) and Cd342/2 mice by bleomycin administration. We found that Cd342/2 mice displayed severe weight loss and early mortality compared with WT controls. Despite equivalent early airway inflammation to WT mice, CD34-deficient animals developed interstitial edema and endothelial delamination, suggesting impaired endothelial function. Chimeric Cd342/2mice reconstituted with WT hematopoietic cells exhibited early mortality compared with WT mice reconstituted with Cd342/2 cells, supporting an endothelial defect. CD34-deficient mice were also more sensitive to lung damage caused by influenza infection, showing greater weight loss and more extensive pulmonary remodeling. Together, our data suggest that CD34 plays an essential role in maintaining vascular integrity in the lung in response to chemical-and infection-induced tissue damage.
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