ArticleCirculation research2017
Regulation of Macrophage Apoptosis and Atherosclerosis by Lipid-Induced PKCδ Isoform Activation.
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Article in Circulation research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 47 citations in OpenAlex.
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- Role and Mechanism of PKC-δ for Cardiovascular Disease: Current Status and Perspective.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
11 authors at 1 institution in 1 country.
Qian LiFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Kyoungmin ParkFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Yu XiaFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Motonobu MatsumotoFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Weier QiFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Jialin FuFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Hisashi YokomizoFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Mogher KhamaisiFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Xuanchun WangFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
Christian Rask-MadsenFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.).
George L KingFrom the Section of Vascular Cell Biology, Dianne Nunnally Hoppes Laboratory for Diabetes Complications, Joslin Diabetes Center, Harvard Medical School, Boston, MA (Q.L., K.P., Y.X., W.Q., J.F., H.Y., M.K., X.W., C.R.-M., G.L.K.); Department of Research and Development, SunStar, Inc, Osaka, Japan (M.M.); and Translational Research and Early Clinical Development, Cardiovascular and Metabolic Research, AstraZeneca, Mölndal, Sweden (W.Q.). george.king@joslin.harvard.edu.
Sunstar (Japan) · JP
Funding
SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5MVanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9MSELECTIVE INSULIN RESISTANCE--DIABETIC VASCULAR DISEASER01DK053105 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 1997 to 2017
$5.0MSpecial BD LSRFortessaS10OD021740 · OD · JOSLIN DIABETES CENTER · PI SERWOLD, THOMAS F · 2016 to 2016
$363kNIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK053105NIDDK NIH HHS U24 DK059637NIH HHS S10 OD021740
Abstract
rationaleActivation of monocytes/macrophages by hyperlipidemia associated with diabetes mellitus and obesity contributes to the development of atherosclerosis. PKCδ (protein kinase C δ) expression and activity in monocytes were increased by hyperlipidemia and diabetes mellitus with unknown consequences to atherosclerosis.
objectiveTo investigate the effect of PKCδ activation in macrophages on the severity of atherosclerosis. METHODS AND
resultsPKCδ expression and activity were increased in Zucker diabetic rats. Mice with selective deletion of PKCδ in macrophages were generated by breeding PKCδ flox/flox mice with LyzM-Cre and ApoE
conclusionsAccelerated development of atherosclerosis induced by insulin resistance and hyperlipidemia may be partially limited by PKCδ isoform activation in the monocytes, which decreased its number and inflammatory responses in the arterial wall.
Indexed as
AnimalsApoptosisAtherosclerosisDiet, High-FatEnzyme ActivationHyperlipidemiasInsulin ResistanceIsoenzymesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutProtein Kinase C-deltaRatsRats, ZuckerIsoenzymesPrkcd protein, mouseProtein Kinase C-deltaapoptosisatherosclerosiscell proliferationmacrophagesprotein kinase C-delta
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