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Regulation of protease nexin‐1 and angiotensin II receptor subtype 1 expression: Inverse relationship in experimental models of nerve injury
Author(s) -
Bleuel A.,
Monard D.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490420414
Subject(s) - sciatic nerve , schwann cell , neurite , dorsal root ganglion , sciatic nerve injury , nerve injury , receptor , microbiology and biotechnology , lesion , biology , neuroscience , endocrinology , chemistry , medicine , in vitro , pathology , anatomy , spinal cord , biochemistry
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 AT 1 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.