XXMD Reduced
Autolysosome Formation in the Penumbra of the Ischemic Cortex.
Additionally, MSCs promote autophagosome and
autolysosome formation and thereby protect the islet cells [141].
Impaired
autolysosome formation correlates with Lamp-2 depletion: Role of apoptosis, autophagy, and necrosis in pancreatitis.
In the end, cargo degradation is dependent on the interplay between lysosomes and autophagosomes, the so-called
autolysosome. One key participant in the transport of autophagic vacuoles is FYCO1 protein [46-47].
Autophagy is a dynamic process in which damaged organelles and long-lived proteins are delivered to the lysosome for degradation and recycling.[7] During this dynamic process, a double-membrane vesicle called autophagosome fuses with lysosomal to form an
autolysosome. Light chain 3 type II (LC3II) and p62 are two major proteins in autophagy.
Fusion of the autophagosome with a lysosome to form the
autolysosome is a prerequisite for complete degradation of cargo content, which ensures proper disposal of damaged cellular biomolecules or organelles.
Examination with TEM showed these inclusions to be a continuum of phagolysosome profiles (which we have termed accumulation bodies) - from phagolysosomes containing possible
autolysosome and other dinoflagellate debris, to those filled with densely flocculent material, to residual bodies containing haphazardly arranged, laminated, dense bundles of fibers with both loose and condensed appearances [ILLUSTRATION FOR FIGURES 4B and 4C OMITTED].