Mitophagy regulates macrophage phenotype in diabetic nephropathy rats
Imbalance of M1/M2 macrophages phenotype activation is a key point in diabetic nephropathy (DN). Macrophages mainly exhibit M1 phenotype, which contributes to the inflammation and fibrosis in DN. Studies indicate that autophage plays an important role in M1/M2 activation. However, the effect of mito...
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Veröffentlicht in: | Biochemical and biophysical research communications 2017-12, Vol.494 (1-2), p.42-50 |
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description | Imbalance of M1/M2 macrophages phenotype activation is a key point in diabetic nephropathy (DN). Macrophages mainly exhibit M1 phenotype, which contributes to the inflammation and fibrosis in DN. Studies indicate that autophage plays an important role in M1/M2 activation. However, the effect of mitophage on M1/M2 macrophage phenotype transformation in DN is unknown. This study investigates the role of mitophage on macrophage polarization in DN. In vivo experiments show that macrophages are exhibited to M1 phenotype and display a lower level of mitophagy in the kidney of streptozocin (STZ)-induced diabetic rats. Additionally, inducible nitric oxide synthase (iNOS) expression is positive correlated with the P62 expression, while negative correlated with LC3. Electronic microscope analysis shows mitochondria swelling, crista decrease and lysosome reduction in DN rats compared with NC rats. In vitro, RAW264.7 macrophages switch to M1 phenotype under high glucose conditions. Mitophagy is downregulated in such high glucose induced M1 macrophages. Furthermore, macrophages tend to switch to the M1 phenotype, expressing higher iNOS and TNF-α when impair mitophagy by 3-MA. Rapamycin, an activator of mitophagy, signifcantly blocks high-glucose induced M1 makers (iNOS and TNF-α) expression, meanwhile enhances M2 makers (MR and Arg-1) expression. These results demonstrate that mitophage participates in the regulation of M1/M2 macrophage phenotype in diabetic nephropathy.
•A novel link between autophagy and macrophage M1 phenotype in DN rats.•RAW264.7 macrophages switched to M1 phenotype and mitophagy downregulated under high glucose conditions.•Regulation of mitophagy changes RAW264.7 macrophage M1/M2 phenotype in high glucose condition. |
doi_str_mv | 10.1016/j.bbrc.2017.10.088 |
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•A novel link between autophagy and macrophage M1 phenotype in DN rats.•RAW264.7 macrophages switched to M1 phenotype and mitophagy downregulated under high glucose conditions.•Regulation of mitophagy changes RAW264.7 macrophage M1/M2 phenotype in high glucose condition.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2017.10.088</identifier><identifier>PMID: 29061302</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Autophagy - physiology ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Diabetic nephropathy ; Glucose - metabolism ; Kidney - metabolism ; Kidney - pathology ; M1/M2 phenotype ; Macrophage ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Mice ; Microscopy, Electron, Transmission ; Mitochondria - ultrastructure ; Mitochondrial Degradation - physiology ; Mitophage ; Nitric Oxide Synthase Type II - metabolism ; Phenotype ; Rats ; Rats, Sprague-Dawley ; RAW 264.7 Cells ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2017-12, Vol.494 (1-2), p.42-50</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c356t-4178d4d3f6cd824ab1884e973e2d679f1f5dc7e907475a75214f85c3cdeb75503</citedby><cites>FETCH-LOGICAL-c356t-4178d4d3f6cd824ab1884e973e2d679f1f5dc7e907475a75214f85c3cdeb75503</cites><orcidid>0000-0003-3295-7379</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2017.10.088$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29061302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Yu</creatorcontrib><creatorcontrib>Guo, Yinfeng</creatorcontrib><creatorcontrib>Jiang, Yuteng</creatorcontrib><creatorcontrib>Zhu, Xiaodong</creatorcontrib><creatorcontrib>Liu, Yuqiu</creatorcontrib><creatorcontrib>Zhang, Xiaoliang</creatorcontrib><title>Mitophagy regulates macrophage phenotype in diabetic nephropathy rats</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Imbalance of M1/M2 macrophages phenotype activation is a key point in diabetic nephropathy (DN). Macrophages mainly exhibit M1 phenotype, which contributes to the inflammation and fibrosis in DN. Studies indicate that autophage plays an important role in M1/M2 activation. However, the effect of mitophage on M1/M2 macrophage phenotype transformation in DN is unknown. This study investigates the role of mitophage on macrophage polarization in DN. In vivo experiments show that macrophages are exhibited to M1 phenotype and display a lower level of mitophagy in the kidney of streptozocin (STZ)-induced diabetic rats. Additionally, inducible nitric oxide synthase (iNOS) expression is positive correlated with the P62 expression, while negative correlated with LC3. Electronic microscope analysis shows mitochondria swelling, crista decrease and lysosome reduction in DN rats compared with NC rats. In vitro, RAW264.7 macrophages switch to M1 phenotype under high glucose conditions. Mitophagy is downregulated in such high glucose induced M1 macrophages. Furthermore, macrophages tend to switch to the M1 phenotype, expressing higher iNOS and TNF-α when impair mitophagy by 3-MA. Rapamycin, an activator of mitophagy, signifcantly blocks high-glucose induced M1 makers (iNOS and TNF-α) expression, meanwhile enhances M2 makers (MR and Arg-1) expression. These results demonstrate that mitophage participates in the regulation of M1/M2 macrophage phenotype in diabetic nephropathy.
•A novel link between autophagy and macrophage M1 phenotype in DN rats.•RAW264.7 macrophages switched to M1 phenotype and mitophagy downregulated under high glucose conditions.•Regulation of mitophagy changes RAW264.7 macrophage M1/M2 phenotype in high glucose condition.</description><subject>Animals</subject><subject>Autophagy - physiology</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic nephropathy</subject><subject>Glucose - metabolism</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>M1/M2 phenotype</subject><subject>Macrophage</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Microscopy, Electron, Transmission</subject><subject>Mitochondria - ultrastructure</subject><subject>Mitochondrial Degradation - physiology</subject><subject>Mitophage</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Phenotype</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RAW 264.7 Cells</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEFr3DAQhUVpaDZp_0APwcdevJ2RbcmCXkLYJoGUXhLITcjSOKtl13YkbWD_feXuNseeBh7fezAfY18Rlggovm-WXRfskgPKHCyhbT-wBYKCkiPUH9kCAETJFT6fs4sYNwCItVCf2DlXILACvmCrXz6N09q8HIpAL_utSRSLnbHhb0jFtKZhTIeJCj8UzpuOkrfFQNM6Eyatc82k-Jmd9WYb6cvpXrKnn6vHm7vy4fft_c31Q2mrRqSyRtm62lW9sK7ltemwbWtSsiLuhFQ99o2zkhTIWjZGNhzrvm1sZR11smmgumTfjrtTGF_3FJPe-WhpuzUDjfuoUWVKSIEqo_yI5ldiDNTrKfidCQeNoGd9eqNnfXrWN2dZXy5dnfb33Y7ce-Wfrwz8OAKUv3zzFHS0ngZLzgeySbvR_2__D8wEgRc</recordid><startdate>20171209</startdate><enddate>20171209</enddate><creator>Zhao, Yu</creator><creator>Guo, Yinfeng</creator><creator>Jiang, Yuteng</creator><creator>Zhu, Xiaodong</creator><creator>Liu, Yuqiu</creator><creator>Zhang, Xiaoliang</creator><general>Elsevier Inc</general><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>7X8</scope><orcidid>https://orcid.org/0000-0003-3295-7379</orcidid></search><sort><creationdate>20171209</creationdate><title>Mitophagy regulates macrophage phenotype in diabetic nephropathy rats</title><author>Zhao, Yu ; Guo, Yinfeng ; Jiang, Yuteng ; Zhu, Xiaodong ; Liu, Yuqiu ; Zhang, Xiaoliang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-4178d4d3f6cd824ab1884e973e2d679f1f5dc7e907475a75214f85c3cdeb75503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Autophagy - physiology</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic nephropathy</topic><topic>Glucose - metabolism</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>M1/M2 phenotype</topic><topic>Macrophage</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Microscopy, Electron, Transmission</topic><topic>Mitochondria - ultrastructure</topic><topic>Mitochondrial Degradation - physiology</topic><topic>Mitophage</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Phenotype</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RAW 264.7 Cells</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Yu</creatorcontrib><creatorcontrib>Guo, Yinfeng</creatorcontrib><creatorcontrib>Jiang, Yuteng</creatorcontrib><creatorcontrib>Zhu, Xiaodong</creatorcontrib><creatorcontrib>Liu, Yuqiu</creatorcontrib><creatorcontrib>Zhang, Xiaoliang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Yu</au><au>Guo, Yinfeng</au><au>Jiang, Yuteng</au><au>Zhu, Xiaodong</au><au>Liu, Yuqiu</au><au>Zhang, Xiaoliang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitophagy regulates macrophage phenotype in diabetic nephropathy rats</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2017-12-09</date><risdate>2017</risdate><volume>494</volume><issue>1-2</issue><spage>42</spage><epage>50</epage><pages>42-50</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Imbalance of M1/M2 macrophages phenotype activation is a key point in diabetic nephropathy (DN). Macrophages mainly exhibit M1 phenotype, which contributes to the inflammation and fibrosis in DN. Studies indicate that autophage plays an important role in M1/M2 activation. However, the effect of mitophage on M1/M2 macrophage phenotype transformation in DN is unknown. This study investigates the role of mitophage on macrophage polarization in DN. In vivo experiments show that macrophages are exhibited to M1 phenotype and display a lower level of mitophagy in the kidney of streptozocin (STZ)-induced diabetic rats. Additionally, inducible nitric oxide synthase (iNOS) expression is positive correlated with the P62 expression, while negative correlated with LC3. Electronic microscope analysis shows mitochondria swelling, crista decrease and lysosome reduction in DN rats compared with NC rats. In vitro, RAW264.7 macrophages switch to M1 phenotype under high glucose conditions. Mitophagy is downregulated in such high glucose induced M1 macrophages. Furthermore, macrophages tend to switch to the M1 phenotype, expressing higher iNOS and TNF-α when impair mitophagy by 3-MA. Rapamycin, an activator of mitophagy, signifcantly blocks high-glucose induced M1 makers (iNOS and TNF-α) expression, meanwhile enhances M2 makers (MR and Arg-1) expression. These results demonstrate that mitophage participates in the regulation of M1/M2 macrophage phenotype in diabetic nephropathy.
•A novel link between autophagy and macrophage M1 phenotype in DN rats.•RAW264.7 macrophages switched to M1 phenotype and mitophagy downregulated under high glucose conditions.•Regulation of mitophagy changes RAW264.7 macrophage M1/M2 phenotype in high glucose condition.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>29061302</pmid><doi>10.1016/j.bbrc.2017.10.088</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-3295-7379</orcidid></addata></record> |
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subjects | Animals Autophagy - physiology Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy Glucose - metabolism Kidney - metabolism Kidney - pathology M1/M2 phenotype Macrophage Macrophages - metabolism Macrophages - pathology Male Mice Microscopy, Electron, Transmission Mitochondria - ultrastructure Mitochondrial Degradation - physiology Mitophage Nitric Oxide Synthase Type II - metabolism Phenotype Rats Rats, Sprague-Dawley RAW 264.7 Cells Tumor Necrosis Factor-alpha - metabolism |
title | Mitophagy regulates macrophage phenotype in diabetic nephropathy rats |
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