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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
31
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pubmed:dateCreated |
2010-8-4
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pubmed:abstractText |
Regulation of apoptosis and cell cycle progression plays an essential role in the maintenance of B-cell homeostasis, because a fine balance of survival and expansion is critical for preventing lymphocytic disorders. Although remarkable progress in understanding B-cell development has been achieved, much less is known concerning niches that are critical to the maintenance of B-cell homeostasis. Leptin has recently been recognized to be important for modulating the immune responses, but it has remained unclear how leptin signaling influences B-cell physiology. A variety of lymphocytic malignancies have been reported to be linked to leptin, and therefore it is necessary to elucidate the mechanisms involved. Here we demonstrate that leptin promotes B-cell homeostasis by inhibiting apoptosis and by inducing cell cycle entry through the activation of expressions of B-cell CLL/lymphoma 2 (Bcl-2) and cyclin D1. We further show that leptin can induce Bcl-2 and cyclin D1 expression by two pathways, including the direct activation of their promoters and suppression of microRNAs (miRNAs) that target their putative 3'untranslated regions. Amplification of these leptin-modulated miRNAs inhibited B lymphoma cell growth. These findings provide insights into mechanisms for leptin regulation of the humoral immune system and suggest new therapeutic strategies for leptin receptor expressing malignancies.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-11777985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-11937559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-11983156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-12414721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-12575997,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-12615201,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-12637767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-15159310,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-15284443,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-16825489,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17060474,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17080020,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17125143,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17349207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17644328,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-17660512,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-19259271,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-19594439,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-19887048,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-19917778,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-20018552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-2649247,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-7519826,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-8187765,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-8402909,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-8710878,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20643953-9652725
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/3' Untranslated Regions,
http://linkedlifedata.com/resource/pubmed/chemical/Ccnd1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/MicroRNAs,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/leptin receptor, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1091-6490
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
3
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13812-7
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pubmed:dateRevised |
2011-7-22
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pubmed:meshHeading |
pubmed-meshheading:20643953-3' Untranslated Regions,
pubmed-meshheading:20643953-Animals,
pubmed-meshheading:20643953-B-Lymphocytes,
pubmed-meshheading:20643953-Cell Line,
pubmed-meshheading:20643953-Cell Proliferation,
pubmed-meshheading:20643953-Cyclin D1,
pubmed-meshheading:20643953-Gene Expression Regulation,
pubmed-meshheading:20643953-Homeostasis,
pubmed-meshheading:20643953-Humans,
pubmed-meshheading:20643953-Leptin,
pubmed-meshheading:20643953-Male,
pubmed-meshheading:20643953-Mice,
pubmed-meshheading:20643953-Mice, Inbred C57BL,
pubmed-meshheading:20643953-MicroRNAs,
pubmed-meshheading:20643953-Promoter Regions, Genetic,
pubmed-meshheading:20643953-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:20643953-Receptors, Leptin,
pubmed-meshheading:20643953-Signal Transduction
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pubmed:year |
2010
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pubmed:articleTitle |
Leptin signaling maintains B-cell homeostasis via induction of Bcl-2 and Cyclin D1.
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pubmed:affiliation |
Department of Pathology and Centre of Infection and Immunology, University of Hong Kong, Hong Kong, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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