Schwann Cell Proliferation during Postnatal Development, Wallerian Degeneration and Axon Regeneration in Trembler Dysmyelinating Mutant

Effect of Aqueous Extract of Phaseolus Vulgaris on the Regulation of Glucose and Lipid Metabolism in Diabetic Rats

“…This extract is capable of restoring the regulation of the glucose metabolism disturbed by the injection of the streptozotocin. Our results confirm those of [14]; [26]; [16] that showed the consequences of glycated hemoglobin on the diabetes by an increase of the level of HbA1c in the diabetic rats; these authors had also noted that the total hemoglobin decreased in the group of the diabetic rats probably due to the increased of the HbA1c formation. This increase of the glycosylated hemoglobin in diabetic rats also shows a change in its affinity for oxygen, which may be a tissue anoxia factor, and promotes the production of free radicals [13].…”

In vivo Proliferative Pattern of Trembler Hypomyelinating Schwann Cells Is Modified in Culture: An Experimental Analysis

“…Recently, we have also found that the proliferative abnormality of Trembler Schwann cells is not genetically programmed [12]; it appears to be a secondary manifes tation of the mutation, as has been previously suggested [17,18].…”

“…In a first step, we show that the age-related increase of Trembler Schwann cell proliferation observed in vivo [12] is not maintained in vitro. Mutant cells divide at a slower rate than normal Schwann cells when they are cultured from sciatic nerves of 15-day-old mice but not from I -and 4-day-old nerves.…”

“…It has been shown that both myelin breakdown prod ucts and contact with regenerating axons stimulate Schwann cell proliferation [5,12,20,21]. In addition, several molecules are found to be mitogenic for Schwann cells, like cyclic AMP [22], acidic and basic fibroblast growth factors (FGFs) [23], platelet-derived growth fac tor [23], transforming growth factors [31 and [32 [24], extracellular matrix molecules, i.e.…”

“…The proliferation of Schwann cells decreases rapidly and stops as soon as myelination starts [3]. However, these cells are capable of resum ing mitosis after nerve injuries, mainly when myelin is degraded, as in Wallerian degeneration [4,5], intoxica tion [6], Charcot-Marie-Tooth's neuropathy [7] and tions and/or a multilayered basal lamina around the Schwann cells [9,10,12].…”