Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood
Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective because of UCP1 (uncoupling protein 1)-dependent thermogenesis. We sought to determine the differential effects of ambient envir...
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Veröffentlicht in: | Circulation research 2017-09, Vol.121 (6), p.662-676 |
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creator | Williams, Jesse W Elvington, Andrew Ivanov, Stoyan Kessler, Skyler Luehmann, Hannah Baba, Osamu Saunders, Brian T Kim, Ki-Wook Johnson, Michael W Craft, Clarissa S Choi, Jae-Hoon Sorci-Thomas, Mary G Zinselmeyer, Bernd H Brestoff, Jonathan R Liu, Yongjian Randolph, Gwendalyn J |
description | Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective because of UCP1 (uncoupling protein 1)-dependent thermogenesis.
We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression.
Using mouse models of atherosclerosis housed at 3 different ambient temperatures, we observed that cold temperature enhanced, whereas thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1. However, whereas UCP1 deficiency promoted poor glucose tolerance, thermoneutral housing enhanced glucose tolerance, and this effect held even in the context of UCP1 deficiency. In conditions of thermoneutrality, but not UCP1 deficiency, circulating monocyte counts were reduced, likely accounting for fewer monocytes entering plaques. Reductions in circulating blood monocytes were also found in a large human cohort in correlation with environmental temperature. By contrast, reduced plaque growth in mice lacking UCP1 was linked to lower cholesterol. Through application of a positron emission tomographic tracer to track CCR2
cell localization and intravital 2-photon imaging of bone marrow, we associated thermoneutrality with an increased monocyte retention in bone marrow. Pharmacological activation of β3-adrenergic receptors applied to mice housed at thermoneutrality induced UCP1 in beige fat pads but failed to promote monocyte egress from the marrow.
Warm ambient temperature is, like UCP1 deficiency, atheroprotective, but the mechanisms of action differ. Thermoneutrality associates with reduced monocyte egress from the bone marrow in a UCP1-dependent manner in mice and likewise may also suppress blood monocyte counts in man. |
doi_str_mv | 10.1161/CIRCRESAHA.117.311519 |
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We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression.
Using mouse models of atherosclerosis housed at 3 different ambient temperatures, we observed that cold temperature enhanced, whereas thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1. However, whereas UCP1 deficiency promoted poor glucose tolerance, thermoneutral housing enhanced glucose tolerance, and this effect held even in the context of UCP1 deficiency. In conditions of thermoneutrality, but not UCP1 deficiency, circulating monocyte counts were reduced, likely accounting for fewer monocytes entering plaques. Reductions in circulating blood monocytes were also found in a large human cohort in correlation with environmental temperature. By contrast, reduced plaque growth in mice lacking UCP1 was linked to lower cholesterol. Through application of a positron emission tomographic tracer to track CCR2
cell localization and intravital 2-photon imaging of bone marrow, we associated thermoneutrality with an increased monocyte retention in bone marrow. Pharmacological activation of β3-adrenergic receptors applied to mice housed at thermoneutrality induced UCP1 in beige fat pads but failed to promote monocyte egress from the marrow.
Warm ambient temperature is, like UCP1 deficiency, atheroprotective, but the mechanisms of action differ. Thermoneutrality associates with reduced monocyte egress from the bone marrow in a UCP1-dependent manner in mice and likewise may also suppress blood monocyte counts in man.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.117.311519</identifier><identifier>PMID: 28696252</identifier><language>eng</language><publisher>United States: Lippincott Williams & Wilkins Ovid Technologies</publisher><subject>Adrenergic receptors ; Animal models ; Animals ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - blood ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Atherosclerosis - physiopathology ; Blood ; Bone imaging ; Bone marrow ; Cardiovascular disease ; Cardiovascular diseases ; CC chemokine receptors ; CCR2 protein ; Cell activation ; Cell Movement ; Cholesterol ; Cholesterol - metabolism ; Cold Temperature ; Glucose tolerance ; Humans ; Localization ; Mice ; Mice, Inbred C57BL ; Monocyte chemoattractant protein 1 ; Monocytes ; Monocytes - metabolism ; Monocytes - physiology ; Plaque, Atherosclerotic - blood ; Plaque, Atherosclerotic - metabolism ; Plaques ; Receptors, CCR2 - genetics ; Receptors, CCR2 - metabolism ; Temperature ; Temperature effects ; Thermogenesis ; Uncoupling protein 1 ; Uncoupling Protein 1 - deficiency ; Uncoupling Protein 1 - genetics ; Uncoupling Protein 1 - metabolism</subject><ispartof>Circulation research, 2017-09, Vol.121 (6), p.662-676</ispartof><rights>2017 American Heart Association, Inc.</rights><rights>Copyright Lippincott Williams & Wilkins Ovid Technologies Sep 1, 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-d49df72d42722b1a75dcf1cabc12bd9667208855c4794856b22cc6277489fe043</citedby><cites>FETCH-LOGICAL-c439t-d49df72d42722b1a75dcf1cabc12bd9667208855c4794856b22cc6277489fe043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28696252$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Williams, Jesse W</creatorcontrib><creatorcontrib>Elvington, Andrew</creatorcontrib><creatorcontrib>Ivanov, Stoyan</creatorcontrib><creatorcontrib>Kessler, Skyler</creatorcontrib><creatorcontrib>Luehmann, Hannah</creatorcontrib><creatorcontrib>Baba, Osamu</creatorcontrib><creatorcontrib>Saunders, Brian T</creatorcontrib><creatorcontrib>Kim, Ki-Wook</creatorcontrib><creatorcontrib>Johnson, Michael W</creatorcontrib><creatorcontrib>Craft, Clarissa S</creatorcontrib><creatorcontrib>Choi, Jae-Hoon</creatorcontrib><creatorcontrib>Sorci-Thomas, Mary G</creatorcontrib><creatorcontrib>Zinselmeyer, Bernd H</creatorcontrib><creatorcontrib>Brestoff, Jonathan R</creatorcontrib><creatorcontrib>Liu, Yongjian</creatorcontrib><creatorcontrib>Randolph, Gwendalyn J</creatorcontrib><title>Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective because of UCP1 (uncoupling protein 1)-dependent thermogenesis.
We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression.
Using mouse models of atherosclerosis housed at 3 different ambient temperatures, we observed that cold temperature enhanced, whereas thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1. However, whereas UCP1 deficiency promoted poor glucose tolerance, thermoneutral housing enhanced glucose tolerance, and this effect held even in the context of UCP1 deficiency. In conditions of thermoneutrality, but not UCP1 deficiency, circulating monocyte counts were reduced, likely accounting for fewer monocytes entering plaques. Reductions in circulating blood monocytes were also found in a large human cohort in correlation with environmental temperature. By contrast, reduced plaque growth in mice lacking UCP1 was linked to lower cholesterol. Through application of a positron emission tomographic tracer to track CCR2
cell localization and intravital 2-photon imaging of bone marrow, we associated thermoneutrality with an increased monocyte retention in bone marrow. Pharmacological activation of β3-adrenergic receptors applied to mice housed at thermoneutrality induced UCP1 in beige fat pads but failed to promote monocyte egress from the marrow.
Warm ambient temperature is, like UCP1 deficiency, atheroprotective, but the mechanisms of action differ. Thermoneutrality associates with reduced monocyte egress from the bone marrow in a UCP1-dependent manner in mice and likewise may also suppress blood monocyte counts in man.</description><subject>Adrenergic receptors</subject><subject>Animal models</subject><subject>Animals</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - pathology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Blood</subject><subject>Bone imaging</subject><subject>Bone marrow</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>CC chemokine receptors</subject><subject>CCR2 protein</subject><subject>Cell activation</subject><subject>Cell Movement</subject><subject>Cholesterol</subject><subject>Cholesterol - metabolism</subject><subject>Cold Temperature</subject><subject>Glucose tolerance</subject><subject>Humans</subject><subject>Localization</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - physiology</subject><subject>Plaque, Atherosclerotic - blood</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Plaques</subject><subject>Receptors, CCR2 - genetics</subject><subject>Receptors, CCR2 - metabolism</subject><subject>Temperature</subject><subject>Temperature effects</subject><subject>Thermogenesis</subject><subject>Uncoupling protein 1</subject><subject>Uncoupling Protein 1 - deficiency</subject><subject>Uncoupling Protein 1 - genetics</subject><subject>Uncoupling Protein 1 - metabolism</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUU1P3DAQtapWZaH9CVSReuES6nH8eam0BCgr0Q_BcrYSxylGWXuxHaTl15PVUmh7mhnNe0_z5iF0CPgYgMOXenFVX51dzy_m0yyOKwAG6g2aASO0pEzAWzTDGKtSVBXeQ_sp3WEMtCLqPdojkitOGJmh5fLWxlXwdsyxGVzeFO2Yix8hFzf1LyhObe-Ms95siutxvY42JZuK78EHs8l2alo3uMcmu-CLhc-hOBlC6D6gd30zJPvxuR6gm_OzZX1RXv78tqjnl6WhlcplR1XXC9JRIghpoRGsMz2YpjVA2k5xLgiWkjFDhaKS8ZYQYzgRgkrVW0yrA_R1p7se25XtjPVbE3od3aqJGx0ap__deHerf4cHPb1HKtgKHD0LxHA_2pT1yiVjh6HxNoxJgwKhOHBeTdDP_0Hvwhj9ZE8TjLmUUmAxodgOZWJIKdr-5RjAepubfs1tmoXe5TbxPv3t5IX1J6jqCSLxlOQ</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Williams, Jesse W</creator><creator>Elvington, Andrew</creator><creator>Ivanov, Stoyan</creator><creator>Kessler, Skyler</creator><creator>Luehmann, Hannah</creator><creator>Baba, Osamu</creator><creator>Saunders, Brian T</creator><creator>Kim, Ki-Wook</creator><creator>Johnson, Michael W</creator><creator>Craft, Clarissa S</creator><creator>Choi, Jae-Hoon</creator><creator>Sorci-Thomas, Mary G</creator><creator>Zinselmeyer, Bernd H</creator><creator>Brestoff, Jonathan R</creator><creator>Liu, Yongjian</creator><creator>Randolph, Gwendalyn J</creator><general>Lippincott Williams & Wilkins Ovid Technologies</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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170901</creationdate><title>Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood</title><author>Williams, Jesse W ; Elvington, Andrew ; Ivanov, Stoyan ; Kessler, Skyler ; Luehmann, Hannah ; Baba, Osamu ; Saunders, Brian T ; Kim, Ki-Wook ; Johnson, Michael W ; Craft, Clarissa S ; Choi, Jae-Hoon ; Sorci-Thomas, Mary G ; Zinselmeyer, Bernd H ; Brestoff, Jonathan R ; Liu, Yongjian ; Randolph, Gwendalyn J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-d49df72d42722b1a75dcf1cabc12bd9667208855c4794856b22cc6277489fe043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adrenergic receptors</topic><topic>Animal models</topic><topic>Animals</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - pathology</topic><topic>Atherosclerosis - physiopathology</topic><topic>Blood</topic><topic>Bone imaging</topic><topic>Bone marrow</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>CC chemokine receptors</topic><topic>CCR2 protein</topic><topic>Cell activation</topic><topic>Cell Movement</topic><topic>Cholesterol</topic><topic>Cholesterol - metabolism</topic><topic>Cold Temperature</topic><topic>Glucose tolerance</topic><topic>Humans</topic><topic>Localization</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>Monocytes - metabolism</topic><topic>Monocytes - physiology</topic><topic>Plaque, Atherosclerotic - blood</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Plaques</topic><topic>Receptors, CCR2 - genetics</topic><topic>Receptors, CCR2 - metabolism</topic><topic>Temperature</topic><topic>Temperature effects</topic><topic>Thermogenesis</topic><topic>Uncoupling protein 1</topic><topic>Uncoupling Protein 1 - deficiency</topic><topic>Uncoupling Protein 1 - genetics</topic><topic>Uncoupling Protein 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Williams, Jesse W</creatorcontrib><creatorcontrib>Elvington, Andrew</creatorcontrib><creatorcontrib>Ivanov, Stoyan</creatorcontrib><creatorcontrib>Kessler, Skyler</creatorcontrib><creatorcontrib>Luehmann, Hannah</creatorcontrib><creatorcontrib>Baba, Osamu</creatorcontrib><creatorcontrib>Saunders, Brian T</creatorcontrib><creatorcontrib>Kim, Ki-Wook</creatorcontrib><creatorcontrib>Johnson, Michael W</creatorcontrib><creatorcontrib>Craft, Clarissa S</creatorcontrib><creatorcontrib>Choi, Jae-Hoon</creatorcontrib><creatorcontrib>Sorci-Thomas, Mary G</creatorcontrib><creatorcontrib>Zinselmeyer, Bernd H</creatorcontrib><creatorcontrib>Brestoff, Jonathan R</creatorcontrib><creatorcontrib>Liu, Yongjian</creatorcontrib><creatorcontrib>Randolph, Gwendalyn J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Williams, Jesse W</au><au>Elvington, Andrew</au><au>Ivanov, Stoyan</au><au>Kessler, Skyler</au><au>Luehmann, Hannah</au><au>Baba, Osamu</au><au>Saunders, Brian T</au><au>Kim, Ki-Wook</au><au>Johnson, Michael W</au><au>Craft, Clarissa S</au><au>Choi, Jae-Hoon</au><au>Sorci-Thomas, Mary G</au><au>Zinselmeyer, Bernd H</au><au>Brestoff, Jonathan R</au><au>Liu, Yongjian</au><au>Randolph, Gwendalyn J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>121</volume><issue>6</issue><spage>662</spage><epage>676</epage><pages>662-676</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><abstract>Ambient temperature is a risk factor for cardiovascular disease. Cold weather increases cardiovascular events, but paradoxically, cold exposure is metabolically protective because of UCP1 (uncoupling protein 1)-dependent thermogenesis.
We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression.
Using mouse models of atherosclerosis housed at 3 different ambient temperatures, we observed that cold temperature enhanced, whereas thermoneutral housing temperature inhibited atherosclerotic plaque growth, as did deficiency in UCP1. However, whereas UCP1 deficiency promoted poor glucose tolerance, thermoneutral housing enhanced glucose tolerance, and this effect held even in the context of UCP1 deficiency. In conditions of thermoneutrality, but not UCP1 deficiency, circulating monocyte counts were reduced, likely accounting for fewer monocytes entering plaques. Reductions in circulating blood monocytes were also found in a large human cohort in correlation with environmental temperature. By contrast, reduced plaque growth in mice lacking UCP1 was linked to lower cholesterol. Through application of a positron emission tomographic tracer to track CCR2
cell localization and intravital 2-photon imaging of bone marrow, we associated thermoneutrality with an increased monocyte retention in bone marrow. Pharmacological activation of β3-adrenergic receptors applied to mice housed at thermoneutrality induced UCP1 in beige fat pads but failed to promote monocyte egress from the marrow.
Warm ambient temperature is, like UCP1 deficiency, atheroprotective, but the mechanisms of action differ. Thermoneutrality associates with reduced monocyte egress from the bone marrow in a UCP1-dependent manner in mice and likewise may also suppress blood monocyte counts in man.</abstract><cop>United States</cop><pub>Lippincott Williams & Wilkins Ovid Technologies</pub><pmid>28696252</pmid><doi>10.1161/CIRCRESAHA.117.311519</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adrenergic receptors Animal models Animals Arteriosclerosis Atherosclerosis Atherosclerosis - blood Atherosclerosis - metabolism Atherosclerosis - pathology Atherosclerosis - physiopathology Blood Bone imaging Bone marrow Cardiovascular disease Cardiovascular diseases CC chemokine receptors CCR2 protein Cell activation Cell Movement Cholesterol Cholesterol - metabolism Cold Temperature Glucose tolerance Humans Localization Mice Mice, Inbred C57BL Monocyte chemoattractant protein 1 Monocytes Monocytes - metabolism Monocytes - physiology Plaque, Atherosclerotic - blood Plaque, Atherosclerotic - metabolism Plaques Receptors, CCR2 - genetics Receptors, CCR2 - metabolism Temperature Temperature effects Thermogenesis Uncoupling protein 1 Uncoupling Protein 1 - deficiency Uncoupling Protein 1 - genetics Uncoupling Protein 1 - metabolism |
title | Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood |
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