The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in Neurodegeneration
Identifieur interne : 000003 ( Main/Exploration ); précédent : 000002; suivant : 000004The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in Neurodegeneration
Auteurs : Emma Perri [Australie] ; Colleen Thomas [Australie] ; Sonam Parakh [Australie] ; Damian Spencer [Australie] ; Julie Atkin [Australie]Source :
- Frontiers in Cell and Developmental Biology ; 2016.
Abstract
The maintenance and regulation of proteostasis is a critical function for post-mitotic neurons and its dysregulation is increasingly implicated in neurodegenerative diseases. Despite having different clinical manifestations, these disorders share similar pathology; an accumulation of misfolded proteins in neurons and subsequent disruption to cellular proteostasis. The endoplasmic reticulum (ER) is an important component of proteostasis, and when the accumulation of misfolded proteins occurs within the ER, this disturbs ER homeostasis, giving rise to ER stress. This triggers the unfolded protein response (UPR), distinct signaling pathways that whilst initially protective, are pro-apoptotic if ER stress is prolonged. ER stress is increasingly implicated in neurodegenerative diseases, and emerging evidence highlights the complexity of the UPR in these disorders, with both protective and detrimental components being described. Protein Disulfide Isomerase (PDI) is an ER chaperone induced during ER stress that is responsible for the formation of disulfide bonds in proteins. Whilst initially considered to be protective, recent studies have revealed unconventional roles for PDI in neurodegenerative diseases, distinct from its normal function in the UPR and the ER, although these mechanisms remain poorly defined. However, specific aspects of PDI function may offer the potential to be exploited therapeutically in the future. This review will focus on the evidence linking ER stress and the UPR to neurodegenerative diseases, with particular emphasis on the emerging functions ascribed to PDI in these conditions.
Url:
DOI: 10.3389/fcell.2015.00080
PubMed: 26779479
PubMed Central: 4705227
Affiliations:
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and Microbiology, School of Life Sciences, La Trobe University</institution><country>Melbourne, VIC, Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Parakh, Sonam" sort="Parakh, Sonam" uniqKey="Parakh S" first="Sonam" last="Parakh">Sonam Parakh</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Biomedical Sciences, Faculty of Medicine and Human Science, Macquarie University</institution><country>Sydney, NSW, Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Spencer, Damian M" sort="Spencer, Damian M" uniqKey="Spencer D" first="Damian" last="Spencer">Damian Spencer</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University</institution><country>Melbourne, VIC, Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Atkin, Julie D" sort="Atkin, Julie D" uniqKey="Atkin J" first="Julie" last="Atkin">Julie Atkin</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University</institution><country>Melbourne, VIC, Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Biomedical Sciences, Faculty of Medicine and Human Science, Macquarie University</institution><country>Sydney, NSW, Australia</country></nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Cell and Developmental Biology</title><idno type="e-ISSN">2296-634X</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The maintenance and regulation of proteostasis is a critical function for post-mitotic neurons and its dysregulation is increasingly implicated in neurodegenerative diseases. Despite having different clinical manifestations, these disorders share similar pathology; an accumulation of misfolded proteins in neurons and subsequent disruption to cellular proteostasis. The endoplasmic reticulum (ER) is an important component of proteostasis, and when the accumulation of misfolded proteins occurs within the ER, this disturbs ER homeostasis, giving rise to ER stress. This triggers the unfolded protein response (UPR), distinct signaling pathways that whilst initially protective, are pro-apoptotic if ER stress is prolonged. ER stress is increasingly implicated in neurodegenerative diseases, and emerging evidence highlights the complexity of the UPR in these disorders, with both protective and detrimental components being described. Protein Disulfide Isomerase (PDI) is an ER chaperone induced during ER stress that is responsible for the formation of disulfide bonds in proteins. Whilst initially considered to be protective, recent studies have revealed unconventional roles for PDI in neurodegenerative diseases, distinct from its normal function in the UPR and the ER, although these mechanisms remain poorly defined. However, specific aspects of PDI function may offer the potential to be exploited therapeutically in the future. This review will focus on the evidence linking ER stress and the UPR to neurodegenerative diseases, with particular emphasis on the emerging functions ascribed to PDI in these conditions.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Atkin, J D" uniqKey="Atkin J">J. D. Atkin</name></author><author><name sortKey="Farg, M A" uniqKey="Farg M">M. A. Farg</name></author><author><name sortKey="Soo, K Y" uniqKey="Soo K">K. Y. Soo</name></author><author><name sortKey="Walker, A K" uniqKey="Walker A">A. K. Walker</name></author><author><name sortKey="Halloran, M" uniqKey="Halloran M">M. 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Lin</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Perri, Emma R" sort="Perri, Emma R" uniqKey="Perri E" first="Emma" last="Perri">Emma Perri</name></noRegion><name sortKey="Atkin, Julie D" sort="Atkin, Julie D" uniqKey="Atkin J" first="Julie" last="Atkin">Julie Atkin</name><name sortKey="Atkin, Julie D" sort="Atkin, Julie D" uniqKey="Atkin J" first="Julie" last="Atkin">Julie Atkin</name><name sortKey="Parakh, Sonam" sort="Parakh, Sonam" uniqKey="Parakh S" first="Sonam" last="Parakh">Sonam Parakh</name><name sortKey="Spencer, Damian M" sort="Spencer, Damian M" uniqKey="Spencer D" first="Damian" last="Spencer">Damian Spencer</name><name sortKey="Thomas, Colleen J" sort="Thomas, Colleen J" uniqKey="Thomas C" first="Colleen" last="Thomas">Colleen Thomas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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