Regulation of protease nexin-1 and angiotensin II receptor subtype 1 expression: Inverse relationship in experimental models of nerve injury
| Autor: | D. Monard, A. Bleuel |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Serine Proteinase Inhibitors
medicine.medical_treatment Nerve guidance conduit Down-Regulation Receptors Cell Surface Biology Rats Sprague-Dawley Amyloid beta-Protein Precursor Cellular and Molecular Neuroscience Dorsal root ganglion Ganglia Spinal medicine Animals Cells Cultured Neurons Receptors Angiotensin Angiotensin II receptor type 1 Nerve injury Sciatic Nerve Angiotensin II Axons Rats Ganglion Cell biology Protease Nexins medicine.anatomical_structure nervous system Schwann Cells Sciatic nerve medicine.symptom Axotomy Carrier Proteins Neuroscience |
| Zdroj: | Journal of Neuroscience Research. 42:562-570 |
| ISSN: | 1097-4547 0360-4012 |
| Popis: | The up-regulation of PN-1 following nerve lesion has been investigated in vitro in cultures of dorsal root ganglion (DRG) explants, sciatic nerve segments, and isolated Schwann cells. In the first culture model, Schwann cells associated with neuronal processes synthesized small amounts of PN-1. Injury of the neurites emerging from the DRGs led to enhanced levels of PN-1 in Schwann cells located distal to the lesion site where degeneration of neuronal processes took place. In cultured sciatic nerve segments, PN-1 synthesis increased with a time-course comparable to that in ganglion explants following lesion. In the third model, PN-1 levels gradually rose in isolated Schwann cells during the first 3-8 days in culture. Dissociation of Schwann cells from the sciatic nerve therefore causes an effect similar to nerve damage. Impairment of Schwann cell-neuron interactions was followed by a reduction in the expression levels of the angiotensin II (Ang II) receptor subtype AT1 in all three systems studied. Since the neuropeptide Ang II is able to repress PN-1 synthesis in cultured Schwann cells, loss of neuronal contact might decrease their responsiveness to Ang II, thus resulting in PN-1 upregulation by default. © 1995 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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