Actin Fence Therapy for Acute Lung Injury
Abstract
F-actin is known to be a major regulator of molecular trafficking between intracellular organelles (e.g. the Golgi) and the cell membrane. However, very little is known regarding f-actin regulation in the AE, the major site of the severe alveolar inflammation that causes lung injury. Our findings indicate that enrichment of the lungs epithelial lining with an f-actin stabilizing biologic blocked the surface display of a proinflammatory receptor, abrogating both the inflammatory response to LPS as well as the associated mortality. By contrast, in the absence of the biologic, receptor-medicated signaling leading to loss of the actin fence resulted in a major surge of proinflammatory receptor display. As proof-of-principle, we addressed these f-actin dependent responses in terms of TNFR1 expression. Strengthening of the fence by f-actin stabilization was we believe, a major factor in abating receptor expression, hence accounting for better mouse survival.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 01, 2020
- Accession Number
- AD1168855
Entities
People
- Galina Gusarova
- Jahar Bhattacharya
Organizations
- Columbia University