Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice
The mechanisms driving atherothrombotic risk in individuals with JAK2 ( Jak2 ) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood. The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2 expr...
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| Veröffentlicht in: | Circulation research 2018-11, Vol.123 (11), p.e35-e47 |
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| creator | Wang, Wei Liu, Wenli Fidler, Trevor Wang, Ying Tang, Yang Woods, Brittany Welch, Carrie Cai, Bishuang Silvestre-Roig, Carlos Ai, Ding Yang, Yong-Guang Hidalgo, Andres Soehnlein, Oliver Tabas, Ira Levine, Ross L Tall, Alan R Wang, Nan |
| description | The mechanisms driving atherothrombotic risk in individuals with JAK2
( Jak2
) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood.
The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2
expression.
Irradiated low-density lipoprotein receptor knockout ( Ldlr
) mice were transplanted with bone marrow from wild-type or Jak2
mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2
mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2
lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2
erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a "don't-eat-me" signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2
macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis.
Hematopoietic Jak2
expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2
caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability. |
| doi_str_mv | 10.1161/CIRCRESAHA.118.313283 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_483260</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2159987868</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3413-7001d5b8e418aeef4e2de73327743f05d21944e744b6e8949648c0bbf6b948c53</originalsourceid><addsrcrecordid>eNp1kU1PwkAQhjdGI4j-BE2PHijuV7e7R0JAMBAT_Liu23YqlX5gt8Tw711SkJOX3Znd95mZzIvQLcEDQgR5GM2Wo-X4ZTgdulwOGGFUsjPUJQHlPg9Cco66GGPlh4zhDrqy9gtjwhlVl6jDsBNwgbvoY2HiutqszCd4szLNTVGYJqvKvjeud82q_ariXVPZzPY9UybeMI4hh9o04OJmBXVl43x_ZtbLSu_JrKn3Lkg48RZZDNfoIjW5hZvD3UNvk_HraOrPnx9no-HcjxknzA_dcEkQSeBEGoCUA03AjU7DkLMUBwklinMIOY8ESMWV4DLGUZSKSLkoYD3kt3XtD2y2kd7UWWHqna5Mpg9PaxeB5pJRgZ1e_avf1FVygo4gYSoQUlHm2PuWdcLvLdhGF5l1S8lNCdXWakoCpWQohXTSoJW6LVtbQ_rXiGC9N1KfjHS51K2Rjrs7tNhGBSR_1NE59gv7XpqA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2159987868</pqid></control><display><type>article</type><title>Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>SWEPUB Freely available online</source><source>Journals@Ovid Ovid Autoload</source><creator>Wang, Wei ; Liu, Wenli ; Fidler, Trevor ; Wang, Ying ; Tang, Yang ; Woods, Brittany ; Welch, Carrie ; Cai, Bishuang ; Silvestre-Roig, Carlos ; Ai, Ding ; Yang, Yong-Guang ; Hidalgo, Andres ; Soehnlein, Oliver ; Tabas, Ira ; Levine, Ross L ; Tall, Alan R ; Wang, Nan</creator><creatorcontrib>Wang, Wei ; Liu, Wenli ; Fidler, Trevor ; Wang, Ying ; Tang, Yang ; Woods, Brittany ; Welch, Carrie ; Cai, Bishuang ; Silvestre-Roig, Carlos ; Ai, Ding ; Yang, Yong-Guang ; Hidalgo, Andres ; Soehnlein, Oliver ; Tabas, Ira ; Levine, Ross L ; Tall, Alan R ; Wang, Nan</creatorcontrib><description>The mechanisms driving atherothrombotic risk in individuals with JAK2
( Jak2
) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood.
The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2
expression.
Irradiated low-density lipoprotein receptor knockout ( Ldlr
) mice were transplanted with bone marrow from wild-type or Jak2
mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2
mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2
lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2
erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a "don't-eat-me" signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2
macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis.
Hematopoietic Jak2
expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2
caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability.</description><identifier>ISSN: 0009-7330</identifier><identifier>ISSN: 1524-4571</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.118.313283</identifier><identifier>PMID: 30571460</identifier><language>eng</language><publisher>United States</publisher><subject>Adult ; Aged ; Animals ; Atherosclerosis - blood ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; c-Mer Tyrosine Kinase - metabolism ; CD47 Antigen - genetics ; CD47 Antigen - metabolism ; Cytokines - genetics ; Cytokines - metabolism ; Erythrocytes - metabolism ; Female ; Hematopoiesis ; Humans ; Iron - metabolism ; Janus Kinase 2 - genetics ; Macrophages - metabolism ; Male ; Medicin och hälsovetenskap ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Neutrophils - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phagocytosis</subject><ispartof>Circulation research, 2018-11, Vol.123 (11), p.e35-e47</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3413-7001d5b8e418aeef4e2de73327743f05d21944e744b6e8949648c0bbf6b948c53</citedby><cites>FETCH-LOGICAL-c3413-7001d5b8e418aeef4e2de73327743f05d21944e744b6e8949648c0bbf6b948c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,552,780,784,885,3687,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30571460$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:139568923$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Liu, Wenli</creatorcontrib><creatorcontrib>Fidler, Trevor</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Tang, Yang</creatorcontrib><creatorcontrib>Woods, Brittany</creatorcontrib><creatorcontrib>Welch, Carrie</creatorcontrib><creatorcontrib>Cai, Bishuang</creatorcontrib><creatorcontrib>Silvestre-Roig, Carlos</creatorcontrib><creatorcontrib>Ai, Ding</creatorcontrib><creatorcontrib>Yang, Yong-Guang</creatorcontrib><creatorcontrib>Hidalgo, Andres</creatorcontrib><creatorcontrib>Soehnlein, Oliver</creatorcontrib><creatorcontrib>Tabas, Ira</creatorcontrib><creatorcontrib>Levine, Ross L</creatorcontrib><creatorcontrib>Tall, Alan R</creatorcontrib><creatorcontrib>Wang, Nan</creatorcontrib><title>Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>The mechanisms driving atherothrombotic risk in individuals with JAK2
( Jak2
) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood.
The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2
expression.
Irradiated low-density lipoprotein receptor knockout ( Ldlr
) mice were transplanted with bone marrow from wild-type or Jak2
mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2
mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2
lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2
erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a "don't-eat-me" signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2
macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis.
Hematopoietic Jak2
expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2
caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability.</description><subject>Adult</subject><subject>Aged</subject><subject>Animals</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - metabolism</subject><subject>c-Mer Tyrosine Kinase - metabolism</subject><subject>CD47 Antigen - genetics</subject><subject>CD47 Antigen - metabolism</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Erythrocytes - metabolism</subject><subject>Female</subject><subject>Hematopoiesis</subject><subject>Humans</subject><subject>Iron - metabolism</subject><subject>Janus Kinase 2 - genetics</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medicin och hälsovetenskap</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Middle Aged</subject><subject>Neutrophils - metabolism</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phagocytosis</subject><issn>0009-7330</issn><issn>1524-4571</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNp1kU1PwkAQhjdGI4j-BE2PHijuV7e7R0JAMBAT_Liu23YqlX5gt8Tw711SkJOX3Znd95mZzIvQLcEDQgR5GM2Wo-X4ZTgdulwOGGFUsjPUJQHlPg9Cco66GGPlh4zhDrqy9gtjwhlVl6jDsBNwgbvoY2HiutqszCd4szLNTVGYJqvKvjeud82q_ariXVPZzPY9UybeMI4hh9o04OJmBXVl43x_ZtbLSu_JrKn3Lkg48RZZDNfoIjW5hZvD3UNvk_HraOrPnx9no-HcjxknzA_dcEkQSeBEGoCUA03AjU7DkLMUBwklinMIOY8ESMWV4DLGUZSKSLkoYD3kt3XtD2y2kd7UWWHqna5Mpg9PaxeB5pJRgZ1e_avf1FVygo4gYSoQUlHm2PuWdcLvLdhGF5l1S8lNCdXWakoCpWQohXTSoJW6LVtbQ_rXiGC9N1KfjHS51K2Rjrs7tNhGBSR_1NE59gv7XpqA</recordid><startdate>20181109</startdate><enddate>20181109</enddate><creator>Wang, Wei</creator><creator>Liu, Wenli</creator><creator>Fidler, Trevor</creator><creator>Wang, Ying</creator><creator>Tang, Yang</creator><creator>Woods, Brittany</creator><creator>Welch, Carrie</creator><creator>Cai, Bishuang</creator><creator>Silvestre-Roig, Carlos</creator><creator>Ai, Ding</creator><creator>Yang, Yong-Guang</creator><creator>Hidalgo, Andres</creator><creator>Soehnlein, Oliver</creator><creator>Tabas, Ira</creator><creator>Levine, Ross L</creator><creator>Tall, Alan R</creator><creator>Wang, Nan</creator><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><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>20181109</creationdate><title>Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice</title><author>Wang, Wei ; Liu, Wenli ; Fidler, Trevor ; Wang, Ying ; Tang, Yang ; Woods, Brittany ; Welch, Carrie ; Cai, Bishuang ; Silvestre-Roig, Carlos ; Ai, Ding ; Yang, Yong-Guang ; Hidalgo, Andres ; Soehnlein, Oliver ; Tabas, Ira ; Levine, Ross L ; Tall, Alan R ; Wang, Nan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3413-7001d5b8e418aeef4e2de73327743f05d21944e744b6e8949648c0bbf6b948c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Animals</topic><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - metabolism</topic><topic>c-Mer Tyrosine Kinase - metabolism</topic><topic>CD47 Antigen - genetics</topic><topic>CD47 Antigen - metabolism</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Erythrocytes - metabolism</topic><topic>Female</topic><topic>Hematopoiesis</topic><topic>Humans</topic><topic>Iron - metabolism</topic><topic>Janus Kinase 2 - genetics</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medicin och hälsovetenskap</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Middle Aged</topic><topic>Neutrophils - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phagocytosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Liu, Wenli</creatorcontrib><creatorcontrib>Fidler, Trevor</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Tang, Yang</creatorcontrib><creatorcontrib>Woods, Brittany</creatorcontrib><creatorcontrib>Welch, Carrie</creatorcontrib><creatorcontrib>Cai, Bishuang</creatorcontrib><creatorcontrib>Silvestre-Roig, Carlos</creatorcontrib><creatorcontrib>Ai, Ding</creatorcontrib><creatorcontrib>Yang, Yong-Guang</creatorcontrib><creatorcontrib>Hidalgo, Andres</creatorcontrib><creatorcontrib>Soehnlein, Oliver</creatorcontrib><creatorcontrib>Tabas, Ira</creatorcontrib><creatorcontrib>Levine, Ross L</creatorcontrib><creatorcontrib>Tall, Alan R</creatorcontrib><creatorcontrib>Wang, Nan</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><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Wei</au><au>Liu, Wenli</au><au>Fidler, Trevor</au><au>Wang, Ying</au><au>Tang, Yang</au><au>Woods, Brittany</au><au>Welch, Carrie</au><au>Cai, Bishuang</au><au>Silvestre-Roig, Carlos</au><au>Ai, Ding</au><au>Yang, Yong-Guang</au><au>Hidalgo, Andres</au><au>Soehnlein, Oliver</au><au>Tabas, Ira</au><au>Levine, Ross L</au><au>Tall, Alan R</au><au>Wang, Nan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2018-11-09</date><risdate>2018</risdate><volume>123</volume><issue>11</issue><spage>e35</spage><epage>e47</epage><pages>e35-e47</pages><issn>0009-7330</issn><issn>1524-4571</issn><eissn>1524-4571</eissn><abstract>The mechanisms driving atherothrombotic risk in individuals with JAK2
( Jak2
) positive clonal hematopoiesis or myeloproliferative neoplasms are poorly understood.
The goal of this study was to assess atherosclerosis and underlying mechanisms in hypercholesterolemic mice with hematopoietic Jak2
expression.
Irradiated low-density lipoprotein receptor knockout ( Ldlr
) mice were transplanted with bone marrow from wild-type or Jak2
mice and fed a high-fat high-cholesterol Western diet. Hematopoietic functions and atherosclerosis were characterized. After 7 weeks of Western diet, Jak2
mice showed increased atherosclerosis. Early atherosclerotic lesions showed increased neutrophil adhesion and content, correlating with lesion size. After 12 weeks of Western diet, Jak2
lesions showed increased complexity, with larger necrotic cores, defective efferocytosis, prominent iron deposition, and costaining of erythrocytes and macrophages, suggesting erythrophagocytosis. Jak2
erythrocytes were more susceptible to phagocytosis by wild-type macrophages and showed decreased surface expression of CD47, a "don't-eat-me" signal. Human JAK2VF erythrocytes were also more susceptible to erythrophagocytosis. Jak2
macrophages displayed increased expression and production of proinflammatory cytokines and chemokines, prominent inflammasome activation, increased p38 MAPK (mitogen-activated protein kinase) signaling, and reduced levels of MerTK (c-Mer tyrosine kinase), a key molecule mediating efferocytosis. Increased erythrophagocytosis also suppressed efferocytosis.
Hematopoietic Jak2
expression promotes early lesion formation and increased complexity in advanced atherosclerosis. In addition to increasing hematopoiesis and neutrophil infiltration in early lesions, Jak2
caused cellular defects in erythrocytes and macrophages, leading to increased erythrophagocytosis but defective efferocytosis. These changes promote accumulation of iron in plaques and increased necrotic core formation which, together with exacerbated proinflammatory responses, likely contribute to plaque instability.</abstract><cop>United States</cop><pmid>30571460</pmid><doi>10.1161/CIRCRESAHA.118.313283</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; SWEPUB Freely available online; Journals@Ovid Ovid Autoload |
| subjects | Adult Aged Animals Atherosclerosis - blood Atherosclerosis - genetics Atherosclerosis - metabolism c-Mer Tyrosine Kinase - metabolism CD47 Antigen - genetics CD47 Antigen - metabolism Cytokines - genetics Cytokines - metabolism Erythrocytes - metabolism Female Hematopoiesis Humans Iron - metabolism Janus Kinase 2 - genetics Macrophages - metabolism Male Medicin och hälsovetenskap Mice Mice, Inbred C57BL Middle Aged Neutrophils - metabolism p38 Mitogen-Activated Protein Kinases - metabolism Phagocytosis |
| title | Macrophage Inflammation, Erythrophagocytosis, and Accelerated Atherosclerosis in Jak2 V617F Mice |
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