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Article: The FGF21-CCL11 Axis Mediates Beiging of White Adipose Tissues by Coupling Sympathetic Nervous System to Type 2 Immunity

TitleThe FGF21-CCL11 Axis Mediates Beiging of White Adipose Tissues by Coupling Sympathetic Nervous System to Type 2 Immunity
Authors
Issue Date2017
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellmet
Citation
Cell Metabolism, 2017, v. 26 n. 3, p. 493-508.e4 How to Cite?
AbstractType 2 cytokines are important signals triggering biogenesis of thermogenic beige adipocytes in white adipose tissue (WAT) during cold acclimation. However, how cold activates type 2 immunity in WAT remains obscure. Here we show that cold-induced type 2 immune responses and beiging in subcutaneous WAT (scWAT) are abrogated in mice with adipose-selective ablation of FGF21 or its co-receptor β-Klotho, whereas such impairments are reversed by replenishment with chemokine CCL11. Mechanistically, FGF21 acts on adipocytes in an autocrine manner to promote the expression and secretion of CCL11 via activation of ERK1/2, which drives recruitment of eosinophils into scWAT, leading to increases in accumulation of M2 macrophages, and proliferation and commitment of adipocyte precursors into beige adipocytes. These FGF21-elicited type 2 immune responses and beiging are blocked by CCL11 neutralization. Thus, the adipose-derived FGF21-CCL11 axis triggers cold-induced beiging and thermogenesis by coupling sympathetic nervous system to activation of type 2 immunity in scWAT.
Persistent Identifierhttp://hdl.handle.net/10722/245110
ISSN
2019 Impact Factor: 21.567
2015 SCImago Journal Rankings: 11.842
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHuang, Z-
dc.contributor.authorZhong, L-
dc.contributor.authorLEE, THJ-
dc.contributor.authorZhang, J-
dc.contributor.authorGENG, L-
dc.contributor.authorWang, Y-
dc.contributor.authorWong, CM-
dc.contributor.authorXu, A-
dc.date.accessioned2017-09-18T02:04:47Z-
dc.date.available2017-09-18T02:04:47Z-
dc.date.issued2017-
dc.identifier.citationCell Metabolism, 2017, v. 26 n. 3, p. 493-508.e4-
dc.identifier.issn1550-4131-
dc.identifier.urihttp://hdl.handle.net/10722/245110-
dc.description.abstractType 2 cytokines are important signals triggering biogenesis of thermogenic beige adipocytes in white adipose tissue (WAT) during cold acclimation. However, how cold activates type 2 immunity in WAT remains obscure. Here we show that cold-induced type 2 immune responses and beiging in subcutaneous WAT (scWAT) are abrogated in mice with adipose-selective ablation of FGF21 or its co-receptor β-Klotho, whereas such impairments are reversed by replenishment with chemokine CCL11. Mechanistically, FGF21 acts on adipocytes in an autocrine manner to promote the expression and secretion of CCL11 via activation of ERK1/2, which drives recruitment of eosinophils into scWAT, leading to increases in accumulation of M2 macrophages, and proliferation and commitment of adipocyte precursors into beige adipocytes. These FGF21-elicited type 2 immune responses and beiging are blocked by CCL11 neutralization. Thus, the adipose-derived FGF21-CCL11 axis triggers cold-induced beiging and thermogenesis by coupling sympathetic nervous system to activation of type 2 immunity in scWAT.-
dc.languageeng-
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellmet-
dc.relation.ispartofCell Metabolism-
dc.titleThe FGF21-CCL11 Axis Mediates Beiging of White Adipose Tissues by Coupling Sympathetic Nervous System to Type 2 Immunity-
dc.typeArticle-
dc.identifier.emailHuang, Z: zhehuang@hku.hk-
dc.identifier.emailZhong, L: kelsey@hku.hk-
dc.identifier.emailZhang, J: hjzhang@hkucc.hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.emailWong, CM: wispwong@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.authorityWang, Y=rp00239-
dc.identifier.authorityWong, CM=rp01489-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.doi10.1016/j.cmet.2017.08.003-
dc.identifier.hkuros277828-
dc.identifier.volume26-
dc.identifier.issue3-
dc.identifier.spage493-
dc.identifier.epage508.e4-
dc.identifier.isiWOS:000409244000006-
dc.publisher.placeUnited States-

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