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Role of Heat Shock Proteins in Glaucoma

Glaucoma, one of the most common causes of blindness worldwide, is a multifactorial neurodegenerative disease characterized by damage of retinal ganglion cells and optic nerve degeneration. However, the exact mechanism leading to glaucoma is still not understood. Evidences suggest an immunological i...

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Detalles Bibliográficos
Autores principales: Tsai, Teresa, Grotegut, Pia, Reinehr, Sabrina, Joachim, Stephanie C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834184/
https://www.ncbi.nlm.nih.gov/pubmed/31635205
http://dx.doi.org/10.3390/ijms20205160
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author Tsai, Teresa
Grotegut, Pia
Reinehr, Sabrina
Joachim, Stephanie C.
author_facet Tsai, Teresa
Grotegut, Pia
Reinehr, Sabrina
Joachim, Stephanie C.
author_sort Tsai, Teresa
collection PubMed
description Glaucoma, one of the most common causes of blindness worldwide, is a multifactorial neurodegenerative disease characterized by damage of retinal ganglion cells and optic nerve degeneration. However, the exact mechanism leading to glaucoma is still not understood. Evidences suggest an immunological involvement in the pathogenesis. Among other immune responses, altered autoantibody patterns were found in glaucoma patients. Especially elevated antibody levels against heat shock proteins (HSPs), like HSP27 or HSP60, were identified. In an animal model, an immunization with these HSPs induced a pressure-independent retinal ganglion cell degeneration and axon loss, hence mimicking glaucoma-like damage. In addition, development of autoreactive antibodies, as well as a glia and T-cell activation, were described in these animals. Recently, we noted that intravitreal HSP27 injection likewise led to a degeneration of retinal ganglion cells and their axons. Therefore, HSP27 might have a direct damaging effect on retinal cells, and might play a key role in glaucoma.
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spelling pubmed-68341842019-11-25 Role of Heat Shock Proteins in Glaucoma Tsai, Teresa Grotegut, Pia Reinehr, Sabrina Joachim, Stephanie C. Int J Mol Sci Review Glaucoma, one of the most common causes of blindness worldwide, is a multifactorial neurodegenerative disease characterized by damage of retinal ganglion cells and optic nerve degeneration. However, the exact mechanism leading to glaucoma is still not understood. Evidences suggest an immunological involvement in the pathogenesis. Among other immune responses, altered autoantibody patterns were found in glaucoma patients. Especially elevated antibody levels against heat shock proteins (HSPs), like HSP27 or HSP60, were identified. In an animal model, an immunization with these HSPs induced a pressure-independent retinal ganglion cell degeneration and axon loss, hence mimicking glaucoma-like damage. In addition, development of autoreactive antibodies, as well as a glia and T-cell activation, were described in these animals. Recently, we noted that intravitreal HSP27 injection likewise led to a degeneration of retinal ganglion cells and their axons. Therefore, HSP27 might have a direct damaging effect on retinal cells, and might play a key role in glaucoma. MDPI 2019-10-18 /pmc/articles/PMC6834184/ /pubmed/31635205 http://dx.doi.org/10.3390/ijms20205160 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Tsai, Teresa
Grotegut, Pia
Reinehr, Sabrina
Joachim, Stephanie C.
Role of Heat Shock Proteins in Glaucoma
title Role of Heat Shock Proteins in Glaucoma
title_full Role of Heat Shock Proteins in Glaucoma
title_fullStr Role of Heat Shock Proteins in Glaucoma
title_full_unstemmed Role of Heat Shock Proteins in Glaucoma
title_short Role of Heat Shock Proteins in Glaucoma
title_sort role of heat shock proteins in glaucoma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834184/
https://www.ncbi.nlm.nih.gov/pubmed/31635205
http://dx.doi.org/10.3390/ijms20205160
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