Clusterin/ApoJ enhances central leptin signaling through Lrp2-mediated endocytosis
- Authors
- Byun, Kyunghee; Gil, So Young; Namkoong, Churl; Youn, Byung-Soo; Huang, Hu; Shin, Mi-Seon; Kang, Gil Myoung; Kim, Hyun-Kyong; Lee, Bonghee; Kim, Young-Bum; Kim, Min-Seon
- Issue Date
- Jul-2014
- Publisher
- WILEY-BLACKWELL
- Keywords
- clusterin; endocytosis; leptin; Lrp2; Stat3
- Citation
- EMBO REPORTS, v.15, no.7, pp.801 - 808
- Journal Title
- EMBO REPORTS
- Volume
- 15
- Number
- 7
- Start Page
- 801
- End Page
- 808
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12488
- DOI
- 10.15252/embr.201338317
- ISSN
- 1469-221X
- Abstract
- Hypothalamic leptin signaling plays a central role in maintaining body weight homeostasis. Here, we show that clusterin/ApoJ, recently identified as an anorexigenic neuropeptide, is an important regulator in the hypothalamic leptin signaling pathway. Coadministration of clusterin potentiates the anorexigenic effect of leptin and boosts leptin-induced hypothalamic Stat3 activation. In cultured neurons, clusterin enhances receptor binding and subsequent endocytosis of leptin. These effects are mainly mediated through the LDL receptor-related protein-2 (Lrp2). Notably, inhibition of hypothalamic clusterin, Lrp2 or endocytosis abrogates anorexia and hypothalamic Stat3 activation caused by leptin. These findings propose a novel regulatory mechanism in central leptin signaling pathways.
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