SILAC-MS Based Characterization of LPS and Resveratrol Induced Changes in Adipocyte Proteomics - Resveratrol as Ameliorating Factor on LPS Induced Changes
Adipose tissue inflammation is believed to play a pivotal role in the development obesity-related morbidities such as insulin resistance. However, it is not known how this (low-grade) inflammatory state develops. It has been proposed that the leakage of lipopolysaccharides (LPS), originating from th...
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| description | Adipose tissue inflammation is believed to play a pivotal role in the development obesity-related morbidities such as insulin resistance. However, it is not known how this (low-grade) inflammatory state develops. It has been proposed that the leakage of lipopolysaccharides (LPS), originating from the gut microbiota, through the gut epithelium could drive initiation of inflammation. To get a better understanding of which proteins and intracellular pathways are affected by LPS in adipocytes, we performed SILAC proteomic analysis and identified proteins that were altered in expression. Furthermore, we tested the anti-inflammatory compound resveratrol. A total of 927 proteins were quantified by the SILAC method and of these 57- and 64 were significantly up- and downregulated by LPS, respectively. Bioinformatic analysis (GO analysis) revealed that the upregulated proteins were especially involved in the pathways of respiratory electron transport chain and inflammation. The downregulated proteins were especially involved in protein glycosylation. One of the latter proteins, GALNT2, has previously been described to regulate the expression of liver lipases such as ANGPTL3 and apoC-III affecting lipid metabolism. Furthermore, LPS treatment reduced the protein levels of the insulin sensitizing adipokine, adiponectin, and proteins participating in the final steps of triglyceride- and cholesterol synthesis. Generally, resveratrol opposed the effect induced by LPS and, as such, functioning as an ameliorating factor in disease state. Using an unbiased proteomic approach, we present novel insight of how the proteome is altered in adipocytes in response to LPS as seen in obesity. We suggest that LPS partly exerts its detrimental effects by altering glycosylation processes of the cell, which is starting to emerge as important posttranscriptional regulators of protein expression. Furthermore, resveratrol could be a prime candidate in ameliorating dysfunctioning adipose tissue induced by inflammatory stimulation. |
| doi_str_mv | 10.1371/journal.pone.0159747 |
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However, it is not known how this (low-grade) inflammatory state develops. It has been proposed that the leakage of lipopolysaccharides (LPS), originating from the gut microbiota, through the gut epithelium could drive initiation of inflammation. To get a better understanding of which proteins and intracellular pathways are affected by LPS in adipocytes, we performed SILAC proteomic analysis and identified proteins that were altered in expression. Furthermore, we tested the anti-inflammatory compound resveratrol. A total of 927 proteins were quantified by the SILAC method and of these 57- and 64 were significantly up- and downregulated by LPS, respectively. Bioinformatic analysis (GO analysis) revealed that the upregulated proteins were especially involved in the pathways of respiratory electron transport chain and inflammation. The downregulated proteins were especially involved in protein glycosylation. One of the latter proteins, GALNT2, has previously been described to regulate the expression of liver lipases such as ANGPTL3 and apoC-III affecting lipid metabolism. Furthermore, LPS treatment reduced the protein levels of the insulin sensitizing adipokine, adiponectin, and proteins participating in the final steps of triglyceride- and cholesterol synthesis. Generally, resveratrol opposed the effect induced by LPS and, as such, functioning as an ameliorating factor in disease state. Using an unbiased proteomic approach, we present novel insight of how the proteome is altered in adipocytes in response to LPS as seen in obesity. We suggest that LPS partly exerts its detrimental effects by altering glycosylation processes of the cell, which is starting to emerge as important posttranscriptional regulators of protein expression. Furthermore, resveratrol could be a prime candidate in ameliorating dysfunctioning adipose tissue induced by inflammatory stimulation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0159747</identifier><identifier>PMID: 27438462</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipocytes ; Adipocytes - metabolism ; Adipocytes - pathology ; Adiponectin ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Amino acids ; Analysis ; Angiopoietin-Like Protein 3 ; Angiopoietin-like Proteins ; Angiopoietins - biosynthesis ; Biology and life sciences ; Chemical properties ; Cholesterol ; Clinical medicine ; Cytokines ; Diabetes ; Electron transport ; Electron transport chain ; Endocrinology ; Epithelium ; Gastrointestinal Microbiome - drug effects ; Gastrointestinal Microbiome - genetics ; Gene expression ; Gene Expression Regulation - drug effects ; Glycosylation ; Glycosylation - drug effects ; Health aspects ; Humans ; Inflammation ; Inflammation - drug therapy ; Inflammation - genetics ; Inflammation - pathology ; Insulin ; Insulin - metabolism ; Insulin resistance ; Insulin Resistance - genetics ; Internal medicine ; Intestinal microflora ; Laboratories ; Lipid Metabolism ; Lipogenesis - drug effects ; Lipopolysaccharides ; Lipopolysaccharides - metabolism ; Liver ; Medicine ; Medicine and Health Sciences ; Metabolism ; Microbiota ; Molecular biology ; N-Acetylgalactosaminyltransferases - biosynthesis ; Obesity ; Obesity - drug therapy ; Obesity - genetics ; Obesity - pathology ; Physiological aspects ; Polypeptide N-acetylgalactosaminyltransferase ; Post-transcription ; Protein expression ; Protein turnover ; Proteins ; Proteome - genetics ; Proteomics ; Regulators ; Research and Analysis Methods ; Resveratrol ; Risk factors ; Rodents ; Sensitizing ; Sterols ; Stilbenes - administration & dosage</subject><ispartof>PloS one, 2016-07, Vol.11 (7), p.e0159747</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Nøhr et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Nøhr et al 2016 Nøhr et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-e8f90b20a56b61e62eaa1f0c518f66cf4fc97372d926a001d44c313d25a4318d3</citedby><cites>FETCH-LOGICAL-c725t-e8f90b20a56b61e62eaa1f0c518f66cf4fc97372d926a001d44c313d25a4318d3</cites><orcidid>0000-0002-5536-654X</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/PMC4954707/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4954707/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27438462$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Eckel, Juergen</contributor><creatorcontrib>Nøhr, Mark K</creatorcontrib><creatorcontrib>Kroager, Toke P</creatorcontrib><creatorcontrib>Sanggaard, Kristian W</creatorcontrib><creatorcontrib>Knudsen, Anders D</creatorcontrib><creatorcontrib>Stensballe, Allan</creatorcontrib><creatorcontrib>Enghild, Jan J</creatorcontrib><creatorcontrib>Ølholm, Jens</creatorcontrib><creatorcontrib>Richelsen, Bjørn</creatorcontrib><creatorcontrib>Pedersen, Steen B</creatorcontrib><title>SILAC-MS Based Characterization of LPS and Resveratrol Induced Changes in Adipocyte Proteomics - Resveratrol as Ameliorating Factor on LPS Induced Changes</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Adipose tissue inflammation is believed to play a pivotal role in the development obesity-related morbidities such as insulin resistance. However, it is not known how this (low-grade) inflammatory state develops. It has been proposed that the leakage of lipopolysaccharides (LPS), originating from the gut microbiota, through the gut epithelium could drive initiation of inflammation. To get a better understanding of which proteins and intracellular pathways are affected by LPS in adipocytes, we performed SILAC proteomic analysis and identified proteins that were altered in expression. Furthermore, we tested the anti-inflammatory compound resveratrol. A total of 927 proteins were quantified by the SILAC method and of these 57- and 64 were significantly up- and downregulated by LPS, respectively. Bioinformatic analysis (GO analysis) revealed that the upregulated proteins were especially involved in the pathways of respiratory electron transport chain and inflammation. The downregulated proteins were especially involved in protein glycosylation. One of the latter proteins, GALNT2, has previously been described to regulate the expression of liver lipases such as ANGPTL3 and apoC-III affecting lipid metabolism. Furthermore, LPS treatment reduced the protein levels of the insulin sensitizing adipokine, adiponectin, and proteins participating in the final steps of triglyceride- and cholesterol synthesis. Generally, resveratrol opposed the effect induced by LPS and, as such, functioning as an ameliorating factor in disease state. Using an unbiased proteomic approach, we present novel insight of how the proteome is altered in adipocytes in response to LPS as seen in obesity. We suggest that LPS partly exerts its detrimental effects by altering glycosylation processes of the cell, which is starting to emerge as important posttranscriptional regulators of protein expression. Furthermore, resveratrol could be a prime candidate in ameliorating dysfunctioning adipose tissue induced by inflammatory stimulation.</description><subject>Adipocytes</subject><subject>Adipocytes - metabolism</subject><subject>Adipocytes - pathology</subject><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Amino acids</subject><subject>Analysis</subject><subject>Angiopoietin-Like Protein 3</subject><subject>Angiopoietin-like Proteins</subject><subject>Angiopoietins - biosynthesis</subject><subject>Biology and life sciences</subject><subject>Chemical properties</subject><subject>Cholesterol</subject><subject>Clinical medicine</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Electron transport</subject><subject>Electron transport chain</subject><subject>Endocrinology</subject><subject>Epithelium</subject><subject>Gastrointestinal Microbiome - drug effects</subject><subject>Gastrointestinal Microbiome - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glycosylation</subject><subject>Glycosylation - drug effects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - genetics</subject><subject>Inflammation - pathology</subject><subject>Insulin</subject><subject>Insulin - metabolism</subject><subject>Insulin resistance</subject><subject>Insulin Resistance - genetics</subject><subject>Internal medicine</subject><subject>Intestinal microflora</subject><subject>Laboratories</subject><subject>Lipid Metabolism</subject><subject>Lipogenesis - drug effects</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - metabolism</subject><subject>Liver</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Microbiota</subject><subject>Molecular biology</subject><subject>N-Acetylgalactosaminyltransferases - 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biosynthesis</topic><topic>Obesity</topic><topic>Obesity - drug therapy</topic><topic>Obesity - genetics</topic><topic>Obesity - pathology</topic><topic>Physiological aspects</topic><topic>Polypeptide N-acetylgalactosaminyltransferase</topic><topic>Post-transcription</topic><topic>Protein expression</topic><topic>Protein turnover</topic><topic>Proteins</topic><topic>Proteome - genetics</topic><topic>Proteomics</topic><topic>Regulators</topic><topic>Research and Analysis Methods</topic><topic>Resveratrol</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>Sensitizing</topic><topic>Sterols</topic><topic>Stilbenes - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nøhr, Mark K</creatorcontrib><creatorcontrib>Kroager, Toke P</creatorcontrib><creatorcontrib>Sanggaard, Kristian W</creatorcontrib><creatorcontrib>Knudsen, Anders D</creatorcontrib><creatorcontrib>Stensballe, Allan</creatorcontrib><creatorcontrib>Enghild, Jan J</creatorcontrib><creatorcontrib>Ølholm, Jens</creatorcontrib><creatorcontrib>Richelsen, Bjørn</creatorcontrib><creatorcontrib>Pedersen, Steen B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Resveratrol as Ameliorating Factor on LPS Induced Changes</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-07-20</date><risdate>2016</risdate><volume>11</volume><issue>7</issue><spage>e0159747</spage><pages>e0159747-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Adipose tissue inflammation is believed to play a pivotal role in the development obesity-related morbidities such as insulin resistance. However, it is not known how this (low-grade) inflammatory state develops. It has been proposed that the leakage of lipopolysaccharides (LPS), originating from the gut microbiota, through the gut epithelium could drive initiation of inflammation. To get a better understanding of which proteins and intracellular pathways are affected by LPS in adipocytes, we performed SILAC proteomic analysis and identified proteins that were altered in expression. Furthermore, we tested the anti-inflammatory compound resveratrol. A total of 927 proteins were quantified by the SILAC method and of these 57- and 64 were significantly up- and downregulated by LPS, respectively. Bioinformatic analysis (GO analysis) revealed that the upregulated proteins were especially involved in the pathways of respiratory electron transport chain and inflammation. The downregulated proteins were especially involved in protein glycosylation. One of the latter proteins, GALNT2, has previously been described to regulate the expression of liver lipases such as ANGPTL3 and apoC-III affecting lipid metabolism. Furthermore, LPS treatment reduced the protein levels of the insulin sensitizing adipokine, adiponectin, and proteins participating in the final steps of triglyceride- and cholesterol synthesis. Generally, resveratrol opposed the effect induced by LPS and, as such, functioning as an ameliorating factor in disease state. Using an unbiased proteomic approach, we present novel insight of how the proteome is altered in adipocytes in response to LPS as seen in obesity. We suggest that LPS partly exerts its detrimental effects by altering glycosylation processes of the cell, which is starting to emerge as important posttranscriptional regulators of protein expression. Furthermore, resveratrol could be a prime candidate in ameliorating dysfunctioning adipose tissue induced by inflammatory stimulation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27438462</pmid><doi>10.1371/journal.pone.0159747</doi><tpages>e0159747</tpages><orcidid>https://orcid.org/0000-0002-5536-654X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-07, Vol.11 (7), p.e0159747 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1805755995 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adipocytes Adipocytes - metabolism Adipocytes - pathology Adiponectin Adipose tissue Adipose Tissue - metabolism Adipose Tissue - pathology Amino acids Analysis Angiopoietin-Like Protein 3 Angiopoietin-like Proteins Angiopoietins - biosynthesis Biology and life sciences Chemical properties Cholesterol Clinical medicine Cytokines Diabetes Electron transport Electron transport chain Endocrinology Epithelium Gastrointestinal Microbiome - drug effects Gastrointestinal Microbiome - genetics Gene expression Gene Expression Regulation - drug effects Glycosylation Glycosylation - drug effects Health aspects Humans Inflammation Inflammation - drug therapy Inflammation - genetics Inflammation - pathology Insulin Insulin - metabolism Insulin resistance Insulin Resistance - genetics Internal medicine Intestinal microflora Laboratories Lipid Metabolism Lipogenesis - drug effects Lipopolysaccharides Lipopolysaccharides - metabolism Liver Medicine Medicine and Health Sciences Metabolism Microbiota Molecular biology N-Acetylgalactosaminyltransferases - biosynthesis Obesity Obesity - drug therapy Obesity - genetics Obesity - pathology Physiological aspects Polypeptide N-acetylgalactosaminyltransferase Post-transcription Protein expression Protein turnover Proteins Proteome - genetics Proteomics Regulators Research and Analysis Methods Resveratrol Risk factors Rodents Sensitizing Sterols Stilbenes - administration & dosage |
| title | SILAC-MS Based Characterization of LPS and Resveratrol Induced Changes in Adipocyte Proteomics - Resveratrol as Ameliorating Factor on LPS Induced Changes |
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