Abstract

Background:Acute lung injury is characterized by infiltration of mixed inflammatory cells and diffuse destruction of the alveolar–capillary barrier.  Although some stem cells populations are reported to regulate lung homeostasis in lung tissues, vascular adventitial fibroblasts involve mesenchymal stem/progenitor cells. In a recent study, a newly defined MSCs marker A was identified as a regulator of their undifferentiated state in fibroblasts. However, the roles of the marker A in the development of acute lung injury have not been investigated.

Objectives:We examined the expression of the marker A in the lung and its involvement in acute lung injury.

Methods and Results:In a model of bleomycin (BLM)-induced acute lung injury, the expression of the marker A in whole lung elevated on day 7 and peaked on day 14 in BLM group. Histological analysis revealed that whereas the marker A-positive cell located slightly at peribronchiolar and perivascular lesion in control group, they located robustly at fibrotic lesion in BLM group. The gene A knock out (KO) mice exhibited a drastic loss of body weight and a shorter survival after BLM administration than did WT mice. Histological analysis showed abnormal infiltration of inflammatory cells in the BLM-treated gene A KO mice. Analysis of bronchoalveolar lavage fluid (BALF) revealed an increase in the numbers of neutrophils and total protein concentration in the BLM-treated gene A KO mice.

Conclusion:These data suggested that the newly defined MSCs marker A may have a protective role in the development of acute lung injury.