Involvement of 9-O-Acetyl GD3 ganglioside in Mycobacterium leprae infection of Schwann cells
Autor: | Maria Cristina Vidal Pessolani, Lucineia Alves, Michelle Lopes Ribeiro-Guimarães, Robertha Mariana Rodrigues Lemes, Isis C. Nascimento, Victor T. Ribeiro-Resende, Rosalia Mendez-Otero, Flávio Alves Lara |
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Rok vydání: | 2010 |
Předmět: |
MAPK/ERK pathway
Male media_common.quotation_subject Cell Population Mice Nude Apoptosis Biochemistry Models Biological Microbiology Mice Gangliosides Leprosy medicine Animals Humans education Internalization Molecular Biology Mycobacterium leprae Myelin Sheath media_common Neurons education.field_of_study Ganglioside biology Integrin beta1 Cell Biology biology.organism_classification Molecular biology medicine.anatomical_structure nervous system Cell culture Immunology Schwann Cells Signal Transduction |
Zdroj: | The Journal of biological chemistry. 285(44) |
ISSN: | 1083-351X |
Popis: | Mycobacterium leprae (ML), the etiologic agent of leprosy, mainly affects the skin and peripheral nerves, leading to demyelization and loss of axonal conductance. Schwann cells (SCs) are the main cell population infected by ML in the nerves, and infection triggers changes in the SC phenotype from a myelinated to a nonmyelinated state. In the present study, we show that expression of 9-O-acetyl GD3, a ganglioside involved in cellular anti-apoptotic signaling and nerve regeneration, increases in SCs following infection with ML. Observation by confocal microscopy together with coimmunoprecipitation suggested that this ganglioside participates in ML attachment and internalization by SC. Immunoblockage of 9-O-acetyl GD3 in vitro significantly reduced adhesion of ML to SC surfaces. Finally, we show that activation of the MAPK (ERK 1/2) pathway and SC proliferation, two known effects of ML on SCs that result in demyelization, are significantly reduced when the 9-O-acetyl GD3 ganglioside is immunoblocked. Taken together, these data suggest the involvement of 9-O-acetyl GD3 in ML infection on SCs. |
Databáze: | OpenAIRE |
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