Elevation of glycoprotein nonmetastatic melanoma protein B in type 1 Gaucher disease patients and mouse models
Gaucher disease is caused by inherited deficiency of lysosomal glucocerebrosidase. Proteome analysis of laser‐dissected splenic Gaucher cells revealed increased amounts of glycoprotein nonmetastatic melanoma protein B (gpNMB). Plasma gpNMB was also elevated, correlating with chitotriosidase and CCL1...
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| Veröffentlicht in: | FEBS open bio 2016-09, Vol.6 (9), p.902-913 |
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| creator | Kramer, Gertjan Wegdam, Wouter Donker‐Koopman, Wilma Ottenhoff, Roelof Gaspar, Paulo Verhoek, Marri Nelson, Jessica Gabriel, Tanit Kallemeijn, Wouter Boot, Rolf G. Laman, Jon D. Vissers, Johannes P.C. Cox, Timothy Pavlova, Elena Moran, Mary Teresa Aerts, Johannes M. Eijk, Marco |
| description | Gaucher disease is caused by inherited deficiency of lysosomal glucocerebrosidase. Proteome analysis of laser‐dissected splenic Gaucher cells revealed increased amounts of glycoprotein nonmetastatic melanoma protein B (gpNMB). Plasma gpNMB was also elevated, correlating with chitotriosidase and CCL18, which are established markers for human Gaucher cells. In Gaucher mice, gpNMB is also produced by Gaucher cells. Correction of glucocerebrosidase deficiency in mice by gene transfer or pharmacological substrate reduction reverses gpNMB abnormalities. In conclusion, gpNMB acts as a marker for glucosylceramide‐laden macrophages in man and mouse and gpNMB should be considered as candidate biomarker for Gaucher disease in treatment monitoring.
Gaucher disease (GD) is caused by an inherited deficiency of lysosomal glucocerebrosidase (GBA1), leading to endo‐lysosomal glucosylceramide (GlcCer) accumulation, causing endo‐lysosomal stress. This drives glycoprotein nonmetastatic melanoma protein B (gpNMB) induction in macrophages (Gaucher cells), which is shed and enters the circulation of both GD mice and patients. gpNMB goes down upon therapeutic intervention, and should be viewed as candidate biomarker for Gaucher disease. |
| doi_str_mv | 10.1002/2211-5463.12078 |
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Gaucher disease (GD) is caused by an inherited deficiency of lysosomal glucocerebrosidase (GBA1), leading to endo‐lysosomal glucosylceramide (GlcCer) accumulation, causing endo‐lysosomal stress. This drives glycoprotein nonmetastatic melanoma protein B (gpNMB) induction in macrophages (Gaucher cells), which is shed and enters the circulation of both GD mice and patients. gpNMB goes down upon therapeutic intervention, and should be viewed as candidate biomarker for Gaucher disease.</description><identifier>ISSN: 2211-5463</identifier><identifier>EISSN: 2211-5463</identifier><identifier>DOI: 10.1002/2211-5463.12078</identifier><identifier>PMID: 27642553</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Animal models ; Biomarkers ; Blood ; Bone marrow ; CCL18 protein ; Chemokines ; chitotriosidase ; DC‐HIL ; Enzymes ; Gaucher's disease ; Gene transfer ; Glucosylceramidase ; glucosylceramide ; Glycoproteins ; Heparan sulfate ; Lipids ; lysosome ; Macrophages ; Melanoma ; Mutation ; osteoactivin ; Patients ; Protein B ; Proteomes ; R&D ; Research & development ; Spleen ; storage disease</subject><ispartof>FEBS open bio, 2016-09, Vol.6 (9), p.902-913</ispartof><rights>2016 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.</rights><rights>2016. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5348-cecefc27538ec170a0c99cd05bb7679cd5117a0b041a0dd5a8eec44dcab2bcfb3</citedby><cites>FETCH-LOGICAL-c5348-cecefc27538ec170a0c99cd05bb7679cd5117a0b041a0dd5a8eec44dcab2bcfb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011488/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011488/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27642553$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kramer, Gertjan</creatorcontrib><creatorcontrib>Wegdam, Wouter</creatorcontrib><creatorcontrib>Donker‐Koopman, Wilma</creatorcontrib><creatorcontrib>Ottenhoff, Roelof</creatorcontrib><creatorcontrib>Gaspar, Paulo</creatorcontrib><creatorcontrib>Verhoek, Marri</creatorcontrib><creatorcontrib>Nelson, Jessica</creatorcontrib><creatorcontrib>Gabriel, Tanit</creatorcontrib><creatorcontrib>Kallemeijn, Wouter</creatorcontrib><creatorcontrib>Boot, Rolf G.</creatorcontrib><creatorcontrib>Laman, Jon D.</creatorcontrib><creatorcontrib>Vissers, Johannes P.C.</creatorcontrib><creatorcontrib>Cox, Timothy</creatorcontrib><creatorcontrib>Pavlova, Elena</creatorcontrib><creatorcontrib>Moran, Mary Teresa</creatorcontrib><creatorcontrib>Aerts, Johannes M.</creatorcontrib><creatorcontrib>Eijk, Marco</creatorcontrib><title>Elevation of glycoprotein nonmetastatic melanoma protein B in type 1 Gaucher disease patients and mouse models</title><title>FEBS open bio</title><addtitle>FEBS Open Bio</addtitle><description>Gaucher disease is caused by inherited deficiency of lysosomal glucocerebrosidase. Proteome analysis of laser‐dissected splenic Gaucher cells revealed increased amounts of glycoprotein nonmetastatic melanoma protein B (gpNMB). Plasma gpNMB was also elevated, correlating with chitotriosidase and CCL18, which are established markers for human Gaucher cells. In Gaucher mice, gpNMB is also produced by Gaucher cells. Correction of glucocerebrosidase deficiency in mice by gene transfer or pharmacological substrate reduction reverses gpNMB abnormalities. In conclusion, gpNMB acts as a marker for glucosylceramide‐laden macrophages in man and mouse and gpNMB should be considered as candidate biomarker for Gaucher disease in treatment monitoring.
Gaucher disease (GD) is caused by an inherited deficiency of lysosomal glucocerebrosidase (GBA1), leading to endo‐lysosomal glucosylceramide (GlcCer) accumulation, causing endo‐lysosomal stress. This drives glycoprotein nonmetastatic melanoma protein B (gpNMB) induction in macrophages (Gaucher cells), which is shed and enters the circulation of both GD mice and patients. gpNMB goes down upon therapeutic intervention, and should be viewed as candidate biomarker for Gaucher disease.</description><subject>Animal models</subject><subject>Biomarkers</subject><subject>Blood</subject><subject>Bone marrow</subject><subject>CCL18 protein</subject><subject>Chemokines</subject><subject>chitotriosidase</subject><subject>DC‐HIL</subject><subject>Enzymes</subject><subject>Gaucher's disease</subject><subject>Gene transfer</subject><subject>Glucosylceramidase</subject><subject>glucosylceramide</subject><subject>Glycoproteins</subject><subject>Heparan sulfate</subject><subject>Lipids</subject><subject>lysosome</subject><subject>Macrophages</subject><subject>Melanoma</subject><subject>Mutation</subject><subject>osteoactivin</subject><subject>Patients</subject><subject>Protein B</subject><subject>Proteomes</subject><subject>R&D</subject><subject>Research & development</subject><subject>Spleen</subject><subject>storage disease</subject><issn>2211-5463</issn><issn>2211-5463</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkUFP3DAQhS3UChDlzK2y1EsvCzNOHDuXSgUttBJSL-VsOc4EghI7tRPQ_vt6u7CivdQHezTzzdOMH2NnCOcIIC6EQFzJsirOUYDSB-x4n3n3Jj5ipyk9Qj4VYAVwyI6EqkohZXHM_HqgJzv3wfPQ8fth48IUw0y95z74kWab5lx2fKTB-jBa_lq-5PmaNxNx5Dd2cQ8Uedsnson4lFvIz4lb3_IxLDk1hpaG9IG97-yQ6PTlPWF31-ufV99Wtz9uvl99vV05WZR65chR54SShSaHCiy4unYtyKZRlcqRRFQWGijRQttKq4lcWbbONqJxXVOcsC873WlpRmpdHibawUyxH23cmGB783fF9w_mPjwZCYil1lng84tADL8WSrMZ--RoyJ9AeR-DWqDSdY11Rj_9gz6GJfq8nhGihvzXoFWmLnaUiyGlSN1-GASztdNsDTNbw8wfO3PHx7c77PlX8zJQ7YDnfqDN__TM9fqy3Cn_BiojrHY</recordid><startdate>201609</startdate><enddate>201609</enddate><creator>Kramer, Gertjan</creator><creator>Wegdam, Wouter</creator><creator>Donker‐Koopman, Wilma</creator><creator>Ottenhoff, Roelof</creator><creator>Gaspar, Paulo</creator><creator>Verhoek, Marri</creator><creator>Nelson, Jessica</creator><creator>Gabriel, Tanit</creator><creator>Kallemeijn, Wouter</creator><creator>Boot, Rolf G.</creator><creator>Laman, Jon D.</creator><creator>Vissers, Johannes P.C.</creator><creator>Cox, Timothy</creator><creator>Pavlova, Elena</creator><creator>Moran, Mary Teresa</creator><creator>Aerts, Johannes M.</creator><creator>Eijk, Marco</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201609</creationdate><title>Elevation of glycoprotein nonmetastatic melanoma protein B in type 1 Gaucher disease patients and mouse models</title><author>Kramer, Gertjan ; Wegdam, Wouter ; Donker‐Koopman, Wilma ; Ottenhoff, Roelof ; Gaspar, Paulo ; Verhoek, Marri ; Nelson, Jessica ; Gabriel, Tanit ; Kallemeijn, Wouter ; Boot, Rolf G. ; Laman, Jon D. ; Vissers, Johannes P.C. ; Cox, Timothy ; Pavlova, Elena ; Moran, Mary Teresa ; Aerts, Johannes M. ; Eijk, Marco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5348-cecefc27538ec170a0c99cd05bb7679cd5117a0b041a0dd5a8eec44dcab2bcfb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animal models</topic><topic>Biomarkers</topic><topic>Blood</topic><topic>Bone marrow</topic><topic>CCL18 protein</topic><topic>Chemokines</topic><topic>chitotriosidase</topic><topic>DC‐HIL</topic><topic>Enzymes</topic><topic>Gaucher's disease</topic><topic>Gene transfer</topic><topic>Glucosylceramidase</topic><topic>glucosylceramide</topic><topic>Glycoproteins</topic><topic>Heparan sulfate</topic><topic>Lipids</topic><topic>lysosome</topic><topic>Macrophages</topic><topic>Melanoma</topic><topic>Mutation</topic><topic>osteoactivin</topic><topic>Patients</topic><topic>Protein B</topic><topic>Proteomes</topic><topic>R&D</topic><topic>Research & development</topic><topic>Spleen</topic><topic>storage disease</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kramer, Gertjan</creatorcontrib><creatorcontrib>Wegdam, Wouter</creatorcontrib><creatorcontrib>Donker‐Koopman, Wilma</creatorcontrib><creatorcontrib>Ottenhoff, Roelof</creatorcontrib><creatorcontrib>Gaspar, Paulo</creatorcontrib><creatorcontrib>Verhoek, Marri</creatorcontrib><creatorcontrib>Nelson, Jessica</creatorcontrib><creatorcontrib>Gabriel, Tanit</creatorcontrib><creatorcontrib>Kallemeijn, Wouter</creatorcontrib><creatorcontrib>Boot, Rolf G.</creatorcontrib><creatorcontrib>Laman, Jon D.</creatorcontrib><creatorcontrib>Vissers, Johannes P.C.</creatorcontrib><creatorcontrib>Cox, Timothy</creatorcontrib><creatorcontrib>Pavlova, Elena</creatorcontrib><creatorcontrib>Moran, Mary Teresa</creatorcontrib><creatorcontrib>Aerts, Johannes M.</creatorcontrib><creatorcontrib>Eijk, Marco</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>FEBS open bio</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kramer, Gertjan</au><au>Wegdam, Wouter</au><au>Donker‐Koopman, Wilma</au><au>Ottenhoff, Roelof</au><au>Gaspar, Paulo</au><au>Verhoek, Marri</au><au>Nelson, Jessica</au><au>Gabriel, Tanit</au><au>Kallemeijn, Wouter</au><au>Boot, Rolf G.</au><au>Laman, Jon D.</au><au>Vissers, Johannes P.C.</au><au>Cox, Timothy</au><au>Pavlova, Elena</au><au>Moran, Mary Teresa</au><au>Aerts, Johannes M.</au><au>Eijk, Marco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Elevation of glycoprotein nonmetastatic melanoma protein B in type 1 Gaucher disease patients and mouse models</atitle><jtitle>FEBS open bio</jtitle><addtitle>FEBS Open Bio</addtitle><date>2016-09</date><risdate>2016</risdate><volume>6</volume><issue>9</issue><spage>902</spage><epage>913</epage><pages>902-913</pages><issn>2211-5463</issn><eissn>2211-5463</eissn><abstract>Gaucher disease is caused by inherited deficiency of lysosomal glucocerebrosidase. Proteome analysis of laser‐dissected splenic Gaucher cells revealed increased amounts of glycoprotein nonmetastatic melanoma protein B (gpNMB). Plasma gpNMB was also elevated, correlating with chitotriosidase and CCL18, which are established markers for human Gaucher cells. In Gaucher mice, gpNMB is also produced by Gaucher cells. Correction of glucocerebrosidase deficiency in mice by gene transfer or pharmacological substrate reduction reverses gpNMB abnormalities. In conclusion, gpNMB acts as a marker for glucosylceramide‐laden macrophages in man and mouse and gpNMB should be considered as candidate biomarker for Gaucher disease in treatment monitoring.
Gaucher disease (GD) is caused by an inherited deficiency of lysosomal glucocerebrosidase (GBA1), leading to endo‐lysosomal glucosylceramide (GlcCer) accumulation, causing endo‐lysosomal stress. This drives glycoprotein nonmetastatic melanoma protein B (gpNMB) induction in macrophages (Gaucher cells), which is shed and enters the circulation of both GD mice and patients. gpNMB goes down upon therapeutic intervention, and should be viewed as candidate biomarker for Gaucher disease.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>27642553</pmid><doi>10.1002/2211-5463.12078</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animal models Biomarkers Blood Bone marrow CCL18 protein Chemokines chitotriosidase DC‐HIL Enzymes Gaucher's disease Gene transfer Glucosylceramidase glucosylceramide Glycoproteins Heparan sulfate Lipids lysosome Macrophages Melanoma Mutation osteoactivin Patients Protein B Proteomes R&D Research & development Spleen storage disease |
| title | Elevation of glycoprotein nonmetastatic melanoma protein B in type 1 Gaucher disease patients and mouse models |
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