Analysis of Stratifin Expression and Proteome Variation in a Rat Model of Acute Lung Injury.

Summary

In an oleic acid-induced rat ARDS/ALI model, stratifin (14-3-3σ) increased in BALF and serum and localized to proliferating type II pneumocytes with p53 activation. Proteomics showed early inflammatory/HIF-1 signals (peaking at 3 h) and sustained cell cycle/p53 pathway activation (peaking at 48 h), positioning SFN as a biomarker of alveolar remodeling during repair.

Key Findings

• BALF and serum SFN levels increased after OA-induced lung injury and persisted through the repair phase.
• Proteomics showed early upregulation of inflammatory and HIF-1 signaling proteins at 3 h, followed by decline.
• Cell cycle and p53 pathway proteins, including SFN, rose from 3 h and peaked at 48 h.
• SFN localized to a subset of proliferating alveolar type II cells with p53 activation, supporting a role in remodeling.

Clinical Implications

SFN may serve as a dynamic biomarker indicating progression from injury to repair, informing timing of therapies and monitoring recovery in ARDS.

Limitations

• Animal OA model may not fully recapitulate human ARDS heterogeneity
• No interventional manipulation of SFN to establish causality
• Sample size not reported; no human validation in this study

Future Directions

Validate SFN kinetics in human ARDS cohorts and test whether SFN-guided stratification improves trial design or therapy timing.