Transcriptomic profiling and regulatory pathways of cardiac resident macrophages in aging
Cardiovascular diseases are an array of age-related disorders, and accumulating evidence suggests a link between cardiac resident macrophages (CRMs) and the age-related disorders. However, how does CRMs alter with aging remains elusive. In the present study, aged mice (20 months old) have been emplo...
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2024-12, Vol.81 (1), p.220-220, Article 220 |
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| creator | Xia, Guofang Zhu, Simeng Liu, Yujia Pan, Jingwei Wang, Xiaoqing Shen, Chengxing Du, Ailian Xu, Congfeng |
| description | Cardiovascular diseases are an array of age-related disorders, and accumulating evidence suggests a link between cardiac resident macrophages (CRMs) and the age-related disorders. However, how does CRMs alter with aging remains elusive. In the present study, aged mice (20 months old) have been employed to check for their cardiac structural and functional alterations, and the changes in the proportion of CRM subsets as well, followed by sorting of CRMs, including C-C Motif Chemokine Receptor 2 (CCR2)
+
and CCR2
–
CRMs, which were subjected to Smart-Seq. Integrated analysis of the Smart-Seq data with three publicly available single-cell RNA-seq datasets revealed that inflammatory genes were drastic upregulated for both CCR2
+
and CCR2
–
CRMs with aging, but genes germane to wound healing were downregulated for CCR2
–
CRMs, suggesting the differential functions of these two subsets. More importantly, inflammatory genes involved in damage sensing, complement cascades, and phagocytosis were largely upregulated in CCR2
–
CRMs, implying the imbalance of inflammatory response upon aging. Our work provides a comprehensive framework and transcriptional resource for assessing the impact of aging on CRMs with a potential for further understanding cardiac aging. |
| doi_str_mv | 10.1007/s00018-024-05235-x |
| format | Article |
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+
and CCR2
–
CRMs, which were subjected to Smart-Seq. Integrated analysis of the Smart-Seq data with three publicly available single-cell RNA-seq datasets revealed that inflammatory genes were drastic upregulated for both CCR2
+
and CCR2
–
CRMs with aging, but genes germane to wound healing were downregulated for CCR2
–
CRMs, suggesting the differential functions of these two subsets. More importantly, inflammatory genes involved in damage sensing, complement cascades, and phagocytosis were largely upregulated in CCR2
–
CRMs, implying the imbalance of inflammatory response upon aging. Our work provides a comprehensive framework and transcriptional resource for assessing the impact of aging on CRMs with a potential for further understanding cardiac aging.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-024-05235-x</identifier><identifier>PMID: 38763956</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Age related diseases ; Aging ; Aging - genetics ; Aging - metabolism ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cardiovascular diseases ; CC chemokine receptors ; Cell Biology ; Chemokine receptors ; Down-regulation ; Gene Expression Profiling ; Genes ; Inflammation ; Inflammation - genetics ; Inflammation - metabolism ; Inflammation - pathology ; Inflammatory response ; Life Sciences ; Macrophages ; Macrophages - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium - metabolism ; Original ; Original Article ; Phagocytosis ; Receptors, CCR2 - genetics ; Receptors, CCR2 - metabolism ; Signal Transduction ; Single-Cell Analysis ; Structure-function relationships ; Transcriptome ; Transcriptomics ; Wound healing</subject><ispartof>Cellular and molecular life sciences : CMLS, 2024-12, Vol.81 (1), p.220-220, Article 220</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. 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-c475t-80a3f602423f531a499ed82dfd7c5946fb6eac0f3faced459a791627e7ec18183</citedby><cites>FETCH-LOGICAL-c475t-80a3f602423f531a499ed82dfd7c5946fb6eac0f3faced459a791627e7ec18183</cites><orcidid>0000-0002-8009-4865</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/PMC11102896/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11102896/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,41120,41488,42189,42557,51319,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38763956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xia, Guofang</creatorcontrib><creatorcontrib>Zhu, Simeng</creatorcontrib><creatorcontrib>Liu, Yujia</creatorcontrib><creatorcontrib>Pan, Jingwei</creatorcontrib><creatorcontrib>Wang, Xiaoqing</creatorcontrib><creatorcontrib>Shen, Chengxing</creatorcontrib><creatorcontrib>Du, Ailian</creatorcontrib><creatorcontrib>Xu, Congfeng</creatorcontrib><title>Transcriptomic profiling and regulatory pathways of cardiac resident macrophages in aging</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>Cardiovascular diseases are an array of age-related disorders, and accumulating evidence suggests a link between cardiac resident macrophages (CRMs) and the age-related disorders. However, how does CRMs alter with aging remains elusive. In the present study, aged mice (20 months old) have been employed to check for their cardiac structural and functional alterations, and the changes in the proportion of CRM subsets as well, followed by sorting of CRMs, including C-C Motif Chemokine Receptor 2 (CCR2)
+
and CCR2
–
CRMs, which were subjected to Smart-Seq. Integrated analysis of the Smart-Seq data with three publicly available single-cell RNA-seq datasets revealed that inflammatory genes were drastic upregulated for both CCR2
+
and CCR2
–
CRMs with aging, but genes germane to wound healing were downregulated for CCR2
–
CRMs, suggesting the differential functions of these two subsets. More importantly, inflammatory genes involved in damage sensing, complement cascades, and phagocytosis were largely upregulated in CCR2
–
CRMs, implying the imbalance of inflammatory response upon aging. Our work provides a comprehensive framework and transcriptional resource for assessing the impact of aging on CRMs with a potential for further understanding cardiac aging.</description><subject>Age related diseases</subject><subject>Aging</subject><subject>Aging - genetics</subject><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cardiovascular diseases</subject><subject>CC chemokine receptors</subject><subject>Cell Biology</subject><subject>Chemokine receptors</subject><subject>Down-regulation</subject><subject>Gene Expression Profiling</subject><subject>Genes</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammatory response</subject><subject>Life Sciences</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardium - metabolism</subject><subject>Original</subject><subject>Original Article</subject><subject>Phagocytosis</subject><subject>Receptors, CCR2 - genetics</subject><subject>Receptors, CCR2 - metabolism</subject><subject>Signal Transduction</subject><subject>Single-Cell Analysis</subject><subject>Structure-function relationships</subject><subject>Transcriptome</subject><subject>Transcriptomics</subject><subject>Wound healing</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp9kUtv1DAUhS1ERUvhD7BAltiwCfgRP7JCqOIlVWJTJFhZt46dcZXYwU5K59_j6QwtZcHKls53j-_xQegFJW8oIeptIYRQ3RDWNkQwLpqbR-iEtow0HVH08eEuNft-jJ6WclVpoZl8go65VpJ3Qp6gHxcZYrE5zEuagsVzTj6MIQ4YYo-zG9YRlpS3eIZl8wu2BSePLeQ-gK1yCb2LC57A5jRvYHAFh4hhqAbP0JGHsbjnh_MUffv44eLsc3P-9dOXs_fnjW2VWBpNgHtZMzDuBafQdp3rNet9r6zoWukvpQNLPPdgXd-KDlRHJVNOOUs11fwUvdv7zuvl5Hpb98kwmjmHCfLWJAjmoRLDxgzp2lBKCdOdrA6vDw45_VxdWcwUinXjCNGltRhOhCJK6I5V9NU_6FVac6z5dpQUTBO2M2R7qv5KKdn5u20oMbvqzL46U2Ob2-rMTR16-XeOu5E_XVWA74FSpTi4fP_2f2x_A1Popws</recordid><startdate>20241201</startdate><enddate>20241201</enddate><creator>Xia, Guofang</creator><creator>Zhu, Simeng</creator><creator>Liu, Yujia</creator><creator>Pan, Jingwei</creator><creator>Wang, Xiaoqing</creator><creator>Shen, Chengxing</creator><creator>Du, Ailian</creator><creator>Xu, Congfeng</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8009-4865</orcidid></search><sort><creationdate>20241201</creationdate><title>Transcriptomic profiling and regulatory pathways of cardiac resident macrophages in aging</title><author>Xia, Guofang ; 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Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2024-12-01</date><risdate>2024</risdate><volume>81</volume><issue>1</issue><spage>220</spage><epage>220</epage><pages>220-220</pages><artnum>220</artnum><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Cardiovascular diseases are an array of age-related disorders, and accumulating evidence suggests a link between cardiac resident macrophages (CRMs) and the age-related disorders. However, how does CRMs alter with aging remains elusive. In the present study, aged mice (20 months old) have been employed to check for their cardiac structural and functional alterations, and the changes in the proportion of CRM subsets as well, followed by sorting of CRMs, including C-C Motif Chemokine Receptor 2 (CCR2)
+
and CCR2
–
CRMs, which were subjected to Smart-Seq. Integrated analysis of the Smart-Seq data with three publicly available single-cell RNA-seq datasets revealed that inflammatory genes were drastic upregulated for both CCR2
+
and CCR2
–
CRMs with aging, but genes germane to wound healing were downregulated for CCR2
–
CRMs, suggesting the differential functions of these two subsets. More importantly, inflammatory genes involved in damage sensing, complement cascades, and phagocytosis were largely upregulated in CCR2
–
CRMs, implying the imbalance of inflammatory response upon aging. Our work provides a comprehensive framework and transcriptional resource for assessing the impact of aging on CRMs with a potential for further understanding cardiac aging.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>38763956</pmid><doi>10.1007/s00018-024-05235-x</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-8009-4865</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Age related diseases Aging Aging - genetics Aging - metabolism Animals Biochemistry Biomedical and Life Sciences Biomedicine Cardiovascular diseases CC chemokine receptors Cell Biology Chemokine receptors Down-regulation Gene Expression Profiling Genes Inflammation Inflammation - genetics Inflammation - metabolism Inflammation - pathology Inflammatory response Life Sciences Macrophages Macrophages - metabolism Male Mice Mice, Inbred C57BL Myocardium - metabolism Original Original Article Phagocytosis Receptors, CCR2 - genetics Receptors, CCR2 - metabolism Signal Transduction Single-Cell Analysis Structure-function relationships Transcriptome Transcriptomics Wound healing |
| title | Transcriptomic profiling and regulatory pathways of cardiac resident macrophages in aging |
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