AI Article Synopsis

  • * Research indicates that autophagy, a cellular process for degrading and recycling components, is crucial for the maturation of LBs, with LBs developing from autophagic vacuoles during early development.
  • * Disruptions in autophagic activity, whether through genetic knockouts or targeted reductions in AT2 cells, lead to problems in LB maturation and surfactant protein B production, highlighting the importance of autophagy for maintaining lung health.

Article Abstract

The lamellar body (LB), a concentric structure loaded with surfactant proteins and phospholipids, is an organelle specific to type 2 alveolar epithelial cells (AT2). However, the origin of LBs has not been fully elucidated. We have previously reported that autophagy regulates Weibel-Palade bodies (WPBs) formation, and here we demonstrated that autophagy is involved in LB maturation, another lysosome-related organelle. We found that during development, LBs were transformed from autophagic vacuoles containing cytoplasmic contents such as glycogen. Fusion between LBs and autophagosomes was observed in wild-type neonate mice. Moreover, the markers of autophagic activity, microtubule-associated protein 1 light chain 3B (LC3B), largely co-localized on the limiting membrane of the LB. Both () global knockout and conditional knockdown in AT2 cells in mice led to defects in LB maturation and surfactant protein B production. Additionally, changes in autophagic activity altered LB formation and surfactant protein B production. Taken together, these results suggest that autophagy plays a critical role in the regulation of LB formation during development and the maintenance of LB homeostasis during adulthood.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8771840PMC
http://dx.doi.org/10.7150/ijbs.64285DOI Listing

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