| Literature DB >> 34135312 |
Nunzio Vicario1,2, Federica M Spitale3, Daniele Tibullo4, Cesarina Giallongo5, Angela M Amorini4, Grazia Scandura3,5, Graziana Spoto3, Miriam W Saab4, Simona D'Aprile3, Cristiana Alberghina3, Renata Mangione4,6, Joshua D Bernstock7, Cirino Botta8, Massimo Gulisano9,10, Emanuele Buratti11, Giampiero Leanza9,10, Robert Zorec12,13, Michele Vecchio14,15, Michelino Di Rosa16, Giovanni Li Volti4, Giuseppe Lazzarino4, Rosalba Parenti17,18, Rosario Gulino19,20.
Abstract
Motoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and supporting spinal plasticity. These effects were coupled with reduced pro-inflammatory microglia and reactive astrogliosis, reduced muscle atrophy, and support of mitochondrial integrity and metabolism. Our results suggest that clobetasol stimulates a series of compensatory processes and therefore represents a translational approach for intractable denervating and neurodegenerative disorders.Entities:
Year: 2021 PMID: 34135312 DOI: 10.1038/s41419-021-03907-1
Source DB: PubMed Journal: Cell Death Dis Impact factor: 8.469