Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition

Obesity is associated with energy metabolic disturbance and is caused by long-term excessive energy storage in white adipose tissue (WAT). The WAT browning potentially reduces excessive energy accumulation, contributing an attractive target to combat obesity. As a pivotal regulator of cell growth, t...

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Autores principales:	Mingchen Xiong, Weijie Hu, Yufang Tan, Honghao Yu, Qi Zhang, Chongru Zhao, Yi Yi, Yichen Wang, Yiping Wu, Min Wu
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	E2F1 transcription factor obesity white adipose tissue (WAT) browning autophagy Physiology QP1-981
Acceso en línea:	https://doaj.org/article/dada8bef8de04a20adf8b4bcd5ffdc3a
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spelling	oai:doaj.org-article:dada8bef8de04a20adf8b4bcd5ffdc3a2021-11-08T05:18:57ZTranscription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition1664-042X10.3389/fphys.2021.748040https://doaj.org/article/dada8bef8de04a20adf8b4bcd5ffdc3a2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphys.2021.748040/fullhttps://doaj.org/toc/1664-042XObesity is associated with energy metabolic disturbance and is caused by long-term excessive energy storage in white adipose tissue (WAT). The WAT browning potentially reduces excessive energy accumulation, contributing an attractive target to combat obesity. As a pivotal regulator of cell growth, the transcription factor E2F1 activity dysregulation leads to metabolic complications. The regulatory effect and underlying mechanism of E2F1 knockout on WAT browning, have not been fully elucidated. To address this issue, in this study, the in vivo adipose morphology, mitochondria quantities, uncoupling protein 1 (UCP-1), autophagy-related genes in WAT of wild-type (WT) and E2F1–/– mice were detected. Furthermore, we evaluated the UCP-1, and autophagy-related gene expression in WT and E2F1–/– adipocyte in vitro. The results demonstrated that E2F1 knockout could increase mitochondria and UCP-1 expression in WAT through autophagy suppression in mice, thus promoting WAT browning. Besides, adipocytes lacking E2F1 showed upregulated UCP-1 and downregulated autophagy-related genes expression in vitro. These results verified that E2F1 knockout exerted effects on inducing mice WAT browning through autophagy inhibition in vivo and in vitro. These findings regarding the molecular mechanism of E2F1-modulated autophagy in controlling WAT plasticity, provide a novel insight into the functional network with the potential therapeutic application against obesity.Mingchen XiongWeijie HuYufang TanHonghao YuQi ZhangChongru ZhaoYi YiYichen WangYiping WuMin WuFrontiers Media S.A.articleE2F1 transcription factorobesitywhite adipose tissue (WAT)browningautophagyPhysiologyQP1-981ENFrontiers in Physiology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	E2F1 transcription factor obesity white adipose tissue (WAT) browning autophagy Physiology QP1-981
spellingShingle	E2F1 transcription factor obesity white adipose tissue (WAT) browning autophagy Physiology QP1-981 Mingchen Xiong Weijie Hu Yufang Tan Honghao Yu Qi Zhang Chongru Zhao Yi Yi Yichen Wang Yiping Wu Min Wu Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
description	Obesity is associated with energy metabolic disturbance and is caused by long-term excessive energy storage in white adipose tissue (WAT). The WAT browning potentially reduces excessive energy accumulation, contributing an attractive target to combat obesity. As a pivotal regulator of cell growth, the transcription factor E2F1 activity dysregulation leads to metabolic complications. The regulatory effect and underlying mechanism of E2F1 knockout on WAT browning, have not been fully elucidated. To address this issue, in this study, the in vivo adipose morphology, mitochondria quantities, uncoupling protein 1 (UCP-1), autophagy-related genes in WAT of wild-type (WT) and E2F1–/– mice were detected. Furthermore, we evaluated the UCP-1, and autophagy-related gene expression in WT and E2F1–/– adipocyte in vitro. The results demonstrated that E2F1 knockout could increase mitochondria and UCP-1 expression in WAT through autophagy suppression in mice, thus promoting WAT browning. Besides, adipocytes lacking E2F1 showed upregulated UCP-1 and downregulated autophagy-related genes expression in vitro. These results verified that E2F1 knockout exerted effects on inducing mice WAT browning through autophagy inhibition in vivo and in vitro. These findings regarding the molecular mechanism of E2F1-modulated autophagy in controlling WAT plasticity, provide a novel insight into the functional network with the potential therapeutic application against obesity.
format	article
author	Mingchen Xiong Weijie Hu Yufang Tan Honghao Yu Qi Zhang Chongru Zhao Yi Yi Yichen Wang Yiping Wu Min Wu
author_facet	Mingchen Xiong Weijie Hu Yufang Tan Honghao Yu Qi Zhang Chongru Zhao Yi Yi Yichen Wang Yiping Wu Min Wu
author_sort	Mingchen Xiong
title	Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
title_short	Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
title_full	Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
title_fullStr	Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
title_full_unstemmed	Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition
title_sort	transcription factor e2f1 knockout promotes mice white adipose tissue browning through autophagy inhibition
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/dada8bef8de04a20adf8b4bcd5ffdc3a
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Transcription Factor E2F1 Knockout Promotes Mice White Adipose Tissue Browning Through Autophagy Inhibition

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