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Basal Lamina Layering in Diabetes Mellitus: Evidence for Accelerated Rate of Cell Death and Cell Regeneration
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Excessive deposition of basal lamina in capillaries and othei structures of individuals with diabetes mellitus is characterized by formation of multiple layers of basal lamina and accumulation of cell debris between the layers. In capillaries with multiple BL layers, between pericytes and endothelial cells, only a single layer is generally present These and other features suggest that basal lamina formation is a quantified event and that excessive accumulation could be the result of (1) cell death and cell replacement, (2) discrete turning on and off of basal lamina production or (3) defective resorption of old basal lamina layers. Evidence indicating that the major component in the pathogenesis of basal lamina accumulation is cell death and cell regeneration is presented. Whether interrupted production or impaired resorption also contribute to this process is unknown.
The common presence of BL layering in patients with diabetes mellitus indicates that diabetics' cells are different from nondiabetics', the difference manifesting itself by increased rate of cell death. The focal nature of this process suggests further that injurious events in the cells' environment contribute to the pathogenesis of this lesion.
Whatever the cause, the BL characteristics discussed, like rings on cross-sections of tree trunks, give some indication of the number of cell generations which have occurred at that particular site.
Title: Basal Lamina Layering in Diabetes Mellitus: Evidence for Accelerated Rate of Cell Death and Cell Regeneration
Description:
Excessive deposition of basal lamina in capillaries and othei structures of individuals with diabetes mellitus is characterized by formation of multiple layers of basal lamina and accumulation of cell debris between the layers.
In capillaries with multiple BL layers, between pericytes and endothelial cells, only a single layer is generally present These and other features suggest that basal lamina formation is a quantified event and that excessive accumulation could be the result of (1) cell death and cell replacement, (2) discrete turning on and off of basal lamina production or (3) defective resorption of old basal lamina layers.
Evidence indicating that the major component in the pathogenesis of basal lamina accumulation is cell death and cell regeneration is presented.
Whether interrupted production or impaired resorption also contribute to this process is unknown.
The common presence of BL layering in patients with diabetes mellitus indicates that diabetics' cells are different from nondiabetics', the difference manifesting itself by increased rate of cell death.
The focal nature of this process suggests further that injurious events in the cells' environment contribute to the pathogenesis of this lesion.
Whatever the cause, the BL characteristics discussed, like rings on cross-sections of tree trunks, give some indication of the number of cell generations which have occurred at that particular site.
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