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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Modes of participation of macrophages in the formation of membranocystic lesions.

We investigated the modes of participation of macrophages in the formation of non-specific (i.e., unrelated to membranous lipodystrophy) membranocystic lesions (MCLs). Surgical specimens of atherosclerosis and chronic panniculitis containing MCLs as well as experimentally formed MCLs were examined, using paraffin sections, by Sudan black B (SBB) stain and by immunostaining for CD68, Bax protein and advanced glycation end products (AGEs). In the atherosclerotic lesions, MCLs were formed by a gradual fusion of SBB-positive multivesicular structures in the macrophages, associated with the cell breakdown. MCLs in the panniculitis were formed in the macrophages, as in atherosclerosis, or derived from degenerative fat cells, often with attachment of macrophages. CD68 was demonstrated in some MCLs or around them, and Bax was also present in some MCLs as well as some macrophages in both lesions. On the other hand, macrophages were not involved in the experimental MCLs. AGEs were widely detected in some MCLs, macrophages and degenerative background in all specimens. These results suggest that MCLs share AGEs as common components with various types of fat degeneration, and are formed physicochemically in the event that macrophages cannot dispose of the degenerative fat sufficiently due to their relative functional impairment and/or the physical circumstances.[1]


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