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Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood. | LitMetric

Thermoneutrality but Not UCP1 Deficiency Suppresses Monocyte Mobilization Into Blood.

Circ Res

From the Department of Pathology and Immunology (J.W.W., A.E., S.I., S.K., O.B., B.T.S., K.-W.K., M.W.J., J.-H.C., B.H.Z., J.R.B., G.J.R.), Department of Radiology (H.L., Y.L.), and Department of Medicine, Division of Bone and Mineral Diseases (C.S.C.), Washington University School of Medicine, St. Louis, MO; Division of Health and Sport Sciences, Missouri Baptist University, St. Louis (A.E.); Department of Life Science, College of Natural Sciences, Research Institute for Natural Sciences, Hanyang University, Seoul, South Korea (J.-H.C.); and Department of Medicine, Division of Endocrinology, Medical College of Wisconsin, Milwaukee (M.G.S.-T.).

Published: September 2017

AI Article Synopsis

  • Cold weather increases cardiovascular events, yet exposure to cold can be metabolically protective due to UCP1 (uncoupling protein 1)-dependent thermogenesis.
  • Research on mouse models reveals that cold temperatures promote atherosclerotic plaque growth, while thermoneutral conditions inhibit it, regardless of UCP1 levels.
  • Warm temperatures, similar to UCP1 deficiency, provide protection against atherosclerosis by decreasing circulating monocytes and their entry into plaques, indicating that environmental temperature influences cardiovascular health.

Article Abstract

Rationale: 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.

Objective: We sought to determine the differential effects of ambient environmental temperature challenge and UCP1 activation in relation to cardiovascular disease progression.

Methods And Results: 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.

Conclusions: 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5718914PMC
http://dx.doi.org/10.1161/CIRCRESAHA.117.311519DOI Listing

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