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
Hauptverfasser: 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
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container_end_page 676
container_issue 6
container_start_page 662
container_title Circulation research
container_volume 121
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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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. 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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. 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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 &amp; 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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