Alpha-2-Macroglobulin, a Hypochlorite-Regulated Chaperone and Immune System Modulator
Alpha-macroglobulins are ancient proteins that include monomeric, dimeric, and tetrameric family members. In humans, and many other mammals, the predominant alpha-macroglobulin is alpha-2-macroglobulin (α2M), a tetrameric protein that is constitutively abundant in biological fluids (e.g., blood plas...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-9 |
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| creator | Cater, Jordan H. Wyatt, Amy R. Wilson, Mark R. |
| description | Alpha-macroglobulins are ancient proteins that include monomeric, dimeric, and tetrameric family members. In humans, and many other mammals, the predominant alpha-macroglobulin is alpha-2-macroglobulin (α2M), a tetrameric protein that is constitutively abundant in biological fluids (e.g., blood plasma, cerebral spinal fluid, synovial fluid, ocular fluid, and interstitial fluid). α2M is best known for its remarkable ability to inhibit a broad spectrum of proteases, but the full gamut of its activities affects diverse biological processes. For example, α2M can stabilise and facilitate the clearance of the Alzheimer’s disease-associated amyloid beta (Aβ) peptide. Additionally, α2M can influence the signalling of cytokines and growth factors including neurotrophins. The results of several studies support the idea that the functions of α2M are uniquely regulated by hypochlorite, an oxidant that is generated during inflammation, which induces the native α2M tetramer to dissociate into dimers. This review will discuss the evidence for hypochlorite-induced regulation of α2M and the possible implications of this in neuroinflammation and neurodegeneration. |
| doi_str_mv | 10.1155/2019/5410657 |
| format | Article |
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In humans, and many other mammals, the predominant alpha-macroglobulin is alpha-2-macroglobulin (α2M), a tetrameric protein that is constitutively abundant in biological fluids (e.g., blood plasma, cerebral spinal fluid, synovial fluid, ocular fluid, and interstitial fluid). α2M is best known for its remarkable ability to inhibit a broad spectrum of proteases, but the full gamut of its activities affects diverse biological processes. For example, α2M can stabilise and facilitate the clearance of the Alzheimer’s disease-associated amyloid beta (Aβ) peptide. Additionally, α2M can influence the signalling of cytokines and growth factors including neurotrophins. The results of several studies support the idea that the functions of α2M are uniquely regulated by hypochlorite, an oxidant that is generated during inflammation, which induces the native α2M tetramer to dissociate into dimers. This review will discuss the evidence for hypochlorite-induced regulation of α2M and the possible implications of this in neuroinflammation and neurodegeneration.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/5410657</identifier><identifier>PMID: 31428227</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Alzheimer's disease ; Amyloid beta-Peptides - metabolism ; Animals ; Arthritis ; Binding sites ; Cytokines ; Disease ; Glycoproteins ; Humans ; Hypochlorous Acid - metabolism ; Immune System - metabolism ; Insulin-like growth factors ; Ligands ; Neurodegenerative Diseases - metabolism ; Neurodegenerative Diseases - pathology ; Peptide Hydrolases - metabolism ; Peptides ; Pregnancy ; Pregnancy-Associated alpha 2-Macroglobulins - chemistry ; Pregnancy-Associated alpha 2-Macroglobulins - metabolism ; Proteases ; Protein Binding ; Proteins ; Review ; Signal Transduction ; Tumor necrosis factor-TNF</subject><ispartof>Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-9</ispartof><rights>Copyright © 2019 Jordan H. Cater et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Jordan H. Cater et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Jordan H. Cater et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-af111a4802129713be6e644605924e5e846e0910c9a7d55686ad64435efb116c3</citedby><cites>FETCH-LOGICAL-c499t-af111a4802129713be6e644605924e5e846e0910c9a7d55686ad64435efb116c3</cites><orcidid>0000-0002-3650-2438</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679887/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679887/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,4010,27904,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31428227$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bekeschus, Sander</contributor><contributor>Sander Bekeschus</contributor><creatorcontrib>Cater, Jordan H.</creatorcontrib><creatorcontrib>Wyatt, Amy R.</creatorcontrib><creatorcontrib>Wilson, Mark R.</creatorcontrib><title>Alpha-2-Macroglobulin, a Hypochlorite-Regulated Chaperone and Immune System Modulator</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Alpha-macroglobulins are ancient proteins that include monomeric, dimeric, and tetrameric family members. In humans, and many other mammals, the predominant alpha-macroglobulin is alpha-2-macroglobulin (α2M), a tetrameric protein that is constitutively abundant in biological fluids (e.g., blood plasma, cerebral spinal fluid, synovial fluid, ocular fluid, and interstitial fluid). α2M is best known for its remarkable ability to inhibit a broad spectrum of proteases, but the full gamut of its activities affects diverse biological processes. For example, α2M can stabilise and facilitate the clearance of the Alzheimer’s disease-associated amyloid beta (Aβ) peptide. Additionally, α2M can influence the signalling of cytokines and growth factors including neurotrophins. The results of several studies support the idea that the functions of α2M are uniquely regulated by hypochlorite, an oxidant that is generated during inflammation, which induces the native α2M tetramer to dissociate into dimers. This review will discuss the evidence for hypochlorite-induced regulation of α2M and the possible implications of this in neuroinflammation and neurodegeneration.</description><subject>Alzheimer's disease</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Binding sites</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Hypochlorous Acid - metabolism</subject><subject>Immune System - metabolism</subject><subject>Insulin-like growth factors</subject><subject>Ligands</subject><subject>Neurodegenerative Diseases - metabolism</subject><subject>Neurodegenerative Diseases - pathology</subject><subject>Peptide Hydrolases - metabolism</subject><subject>Peptides</subject><subject>Pregnancy</subject><subject>Pregnancy-Associated alpha 2-Macroglobulins - chemistry</subject><subject>Pregnancy-Associated alpha 2-Macroglobulins - metabolism</subject><subject>Proteases</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Tumor necrosis factor-TNF</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc1r3DAQxU1padK0t56LoZdC40SjL0uXwrKkTSCh0DZnobXHawXZcmU7Yf_7aNntpu0ppxmYH2_mzcuy90DOAIQ4pwT0ueBApChfZMegOS2I1vzloSfkKHszjneESEY5vM6OGHCqKC2Ps9uFH1pb0OLGVjGsfVjN3vWnuc0vN0OoWh-im7D4gevZ2wnrfNnaAWPoMbd9nV913Zzan5txwi6_CfWWCvFt9qqxfsR3-3qS3X69-LW8LK6_f7taLq6Lims9FbYBAMsVoUB1CWyFEiXnkghNOQpUXCLRQCpty1oIqaSt05wJbFYAsmIn2Zed7jCvOqwr7KdovRmi62zcmGCd-XfSu9asw72RstRKlUng014ght8zjpPp3Fih97bHMI-GMsYk4QAqoR__Q-_CHPtkz6RPaiWpUOSJWluPxvVNSHurrahZSAKEKsUgUac7Kv18HCM2h5OBmG2qZpuq2aea8A9_2zzAf2JMwOcd0Lq-tg_umXKYGGzsE02TVUbYI2umsSs</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Cater, Jordan H.</creator><creator>Wyatt, Amy R.</creator><creator>Wilson, Mark R.</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3650-2438</orcidid></search><sort><creationdate>2019</creationdate><title>Alpha-2-Macroglobulin, a Hypochlorite-Regulated Chaperone and Immune System Modulator</title><author>Cater, Jordan H. ; Wyatt, Amy R. ; Wilson, Mark R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-af111a4802129713be6e644605924e5e846e0910c9a7d55686ad64435efb116c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alzheimer's disease</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animals</topic><topic>Arthritis</topic><topic>Binding sites</topic><topic>Cytokines</topic><topic>Disease</topic><topic>Glycoproteins</topic><topic>Humans</topic><topic>Hypochlorous Acid - metabolism</topic><topic>Immune System - metabolism</topic><topic>Insulin-like growth factors</topic><topic>Ligands</topic><topic>Neurodegenerative Diseases - metabolism</topic><topic>Neurodegenerative Diseases - pathology</topic><topic>Peptide Hydrolases - metabolism</topic><topic>Peptides</topic><topic>Pregnancy</topic><topic>Pregnancy-Associated alpha 2-Macroglobulins - chemistry</topic><topic>Pregnancy-Associated alpha 2-Macroglobulins - metabolism</topic><topic>Proteases</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cater, Jordan H.</creatorcontrib><creatorcontrib>Wyatt, Amy R.</creatorcontrib><creatorcontrib>Wilson, Mark R.</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cater, Jordan H.</au><au>Wyatt, Amy R.</au><au>Wilson, Mark R.</au><au>Bekeschus, Sander</au><au>Sander Bekeschus</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alpha-2-Macroglobulin, a Hypochlorite-Regulated Chaperone and Immune System Modulator</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2019</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Alpha-macroglobulins are ancient proteins that include monomeric, dimeric, and tetrameric family members. In humans, and many other mammals, the predominant alpha-macroglobulin is alpha-2-macroglobulin (α2M), a tetrameric protein that is constitutively abundant in biological fluids (e.g., blood plasma, cerebral spinal fluid, synovial fluid, ocular fluid, and interstitial fluid). α2M is best known for its remarkable ability to inhibit a broad spectrum of proteases, but the full gamut of its activities affects diverse biological processes. For example, α2M can stabilise and facilitate the clearance of the Alzheimer’s disease-associated amyloid beta (Aβ) peptide. Additionally, α2M can influence the signalling of cytokines and growth factors including neurotrophins. The results of several studies support the idea that the functions of α2M are uniquely regulated by hypochlorite, an oxidant that is generated during inflammation, which induces the native α2M tetramer to dissociate into dimers. This review will discuss the evidence for hypochlorite-induced regulation of α2M and the possible implications of this in neuroinflammation and neurodegeneration.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31428227</pmid><doi>10.1155/2019/5410657</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3650-2438</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Alzheimer's disease Amyloid beta-Peptides - metabolism Animals Arthritis Binding sites Cytokines Disease Glycoproteins Humans Hypochlorous Acid - metabolism Immune System - metabolism Insulin-like growth factors Ligands Neurodegenerative Diseases - metabolism Neurodegenerative Diseases - pathology Peptide Hydrolases - metabolism Peptides Pregnancy Pregnancy-Associated alpha 2-Macroglobulins - chemistry Pregnancy-Associated alpha 2-Macroglobulins - metabolism Proteases Protein Binding Proteins Review Signal Transduction Tumor necrosis factor-TNF |
| title | Alpha-2-Macroglobulin, a Hypochlorite-Regulated Chaperone and Immune System Modulator |
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