Key result
Periostin deficiency increases early lethality and pulmonary leakage in bleomycin-exposed mice.
Why the study?
The role of the extracellular matrix, specifically periostin, in preventing pulmonary capillary leakage and progression of acute lung injury was not addressed.
Does periostin deficiency increase lethality in mice with bleomycin-induced lung injury?
Does periostin deficiency increase lethality in mice with bleomycin-induced lung injury?
Periostin in the extracellular matrix architecture plays a protective role in preventing pulmonary leakage and increasing survival in acute lung injury.
Periostin-organized ECM may limit alveolar fluid influx in experimental ALI; leaves open clinical relevance or therapeutic targeting.
Pulmonary capillary leakage followed by influx of blood fluid into the air space of lung alveoli is a crucial step in the progression of acute lung injury (ALI). This influx is due to increased permeability of the alveolar-capillary barrier. The extracellular matrix (ECM) between the capillary and the epithelium would be expected to be involved in prevention of the influx; however, the role of the ECM remains to be addressed. Here, we show that the ECM architecture organized by periostin, a matricellular protein, plays a pivotal role in the survival of bleomycin-exposed mice. Periostin was localized in the alveolar walls. Although periostin-null mice displayed no significant difference in lung histology and air-blood permeability, they exhibited early lethality in a model of bleomycin-induced lung injury, compared with their wild-type counterparts. This early lethality may have been due to increased pulmonary leakage of blood fluid into the air space in the bleomycin-exposed periostin-null mice. These results suggest that periostin in the ECM architecture prevents pulmonary leakage of blood fluid, thus increasing the survival rate in mice with ALI. Thus, this study provides an evidence for the protective role of the ECM architecture in the lung alveoli.
No takes yet. Share an insight, caveat, or question.
Kondoh et al. (2016) studied Bleomycin-induced acute lung injury. Periostin deficiency vs. Wild-type was evaluated on Lethality / survival. Periostin deficiency in mice caused early lethality and increased pulmonary leakage of blood fluid following bleomycin administration compared with wild-type counterparts.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: