Publication details
SMALL PROLINE-RICH REPEAT PROTEIN 1A IS EXPRESSED BY THE SATELLITE GLIAL CELLS SURROUNDING RAT AXOTOMIZED DORSAL ROOT GANGLION NEURONS
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| Year of publication | 2017 |
| Type | Conference abstract |
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| Description | SMALL PROLINE-RICH REPEAT PROTEIN 1A IS EXPRESSED BY THE SATELLITE GLIAL CELLS SURROUNDING RAT AXOTOMIZED DORSAL ROOT GANGLION NEURONS Dubový P., Klusáková I., Joukal M., Hradilová-Svíženská I. Department of Anatomy, Cellular and Molecular Neurobiology Group, Faculty of Medicine, Masaryk University, Kamenice 3, 62500 Brno, Czech Republic The neuronal regeneration program includes production of growth-specific proteins such as the actin-modulating small proline-rich repeat protein 1A (SPRR1A) and growth associated protein 43 (GAP43). SPRR1A is increased in the mouse primary sensory neurons following a peripheral nerve injury, and its overexpression induces significant increase of neurite outgrowth in vitro (1). We used constriction and transection of the sciatic nerve for 7 days to test expression of SPRR1A in the dorsal root ganglia (DRG) neurons of adult Wistar rats in comparison to the same nerve injury of adult mice. Single immunostaining for SPRR1A or double immunofluorescence for SPRR1A and GAP43, NeuN (neuronal marker) or glutamine synthetase (GC, satellite glial cell marker) were used to detect cellular expression of SPRR1A protein in the rat and mouse model of axotomized DRG neurons. We found no or very weak SPRR1 immunostaining in DRG of L4-L5 segments from naive (n=3) and sham-operated (n=3) rats and mice. A weak SPRR1A immunofluorescence was observed only in the satellite glial cells, but no SPRR1A protein was detected in the DRG neurons of all populations. A sciatic nerve injury induced a higher intensity of SPRR1A immunostaining in DRG neurons of mice, but only in the satellite glial cells of rat DRG, while the rat neuronal bodies displayed only a small increase of SPRR1A immunofluorescence. The mouse satellite glial cells surrounding large neuronal bodies were also immunostained for SPRR1A. In contrast, a nerve injury induced a higher intensity of GAP43 immunofluorescence in DRG neurons of large and medium sizes. Our results indicate that SPRR1A protein is not upregulated by nerve injury in DRG neurons, but only in the satellite glial cells of rat DRG. This is in contrast to published results obtained in mouse model. The results suggested that SPRR1A is involved also in actin modulation of satellite glial cells. 1. Bonilla et al. 2002. J. Neurosci. 22, 1303–1315. Acknowledgements. The work was supported by grant 16-08508S of The Czech Science Foundation (GACR). We thank Bc. Jitka Mikulášková, Ms. Dana Kutějová and Ms. Marta Lněníčková for their skillful technical assistance. |
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