Chaperone-Mediated Autophagy after Spinal Cord Injury
| Autor: | Takehiro Sugaya, Michiharu Matsuda, Kyoichi Handa, Hiroshi Ozawa, Haruo Kanno, Eiji Itoi, Taishi Murakami, Maria Prudnikova |
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| Rok vydání: | 2020 |
| Předmět: |
030506 rehabilitation
Chaperone-Mediated Autophagy Thoracic Vertebrae Mice 03 medical and health sciences 0302 clinical medicine Chaperone-mediated autophagy Lysosomal-Associated Membrane Protein 2 Lysosome medicine Animals Degradation process Spinal cord injury Spinal Cord Injuries Chemistry Autophagy medicine.disease Cell biology Mice Inbred C57BL medicine.anatomical_structure Female Neurology (clinical) 0305 other medical science 030217 neurology & neurosurgery Function (biology) Intracellular |
| Zdroj: | Journal of Neurotrauma. 37:1687-1695 |
| ISSN: | 1557-9042 0897-7151 |
| Popis: | Autophagy is the degradation process of dysfunctional intracellular components and has a crucial function in various human diseases. There are three different types of autophagy: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). CMA is a major route for the elimination of cellular aberrant proteins and can provide a cytoprotective effect. The present study investigated the expression of lysosome-associated membrane protein type 2A (LAMP2A), which is the hallmark of CMA activity, in damaged neural tissue after spinal cord injury (SCI) in mice. The number of LAMP2A-expressing cells was significantly increased at the lesion following SCI. The increased number of LAMP2A-positive cells was observed from 24 h and peaked at 3 days after injury. A western blot analysis confirmed that the level of LAMP2A protein was significantly increased in the injured spinal cord compared with the uninjured cord. On double staining for LAMP2A and different neural cell type markers, the increased expression of LAMP2A was observed in neurons, astrocytes, oligodendrocytes, and microglia/macrophages following injury. An electron microscopic analysis showed that secondary lysosomes were increased in damaged neurons at the lesion site. Immunoelectron microscopy revealed that the gold particles with anti-LAMP2A antibody were frequently localized at the secondary lysosomes in the injured site. These findings indicated that CMA was clearly activated in damaged neural tissue after SCI. The activation of CMA may contribute to the elimination of intracellular aberrant proteins and exert a neuroprotective effect following SCI. |
| Databáze: | OpenAIRE |
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