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Silibinin-induced autophagy mediated by PPARα-sirt1-AMPK pathway participated in the regulation of type I collagen-enhanced migration in murine 3T3-L1 preadipocytes

Overview of attention for article published in Molecular and Cellular Biochemistry, June 2018
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Title
Silibinin-induced autophagy mediated by PPARα-sirt1-AMPK pathway participated in the regulation of type I collagen-enhanced migration in murine 3T3-L1 preadipocytes
Published in
Molecular and Cellular Biochemistry, June 2018
DOI 10.1007/s11010-018-3368-y
Pubmed ID
Authors

Xiaoling Liu, Qian Xu, Xinyu Long, Weiwei Liu, Yeli Zhao, Toshihiko Hayashi, Shunji Hattori, Hitomi Fujisaki, Takaaki Ogura, Shin-ichi Tashiro, Satoshi Onodera, Masayuki Yamato, Takashi Ikejima

Abstract

Preadipocyte migration is a fundamental and important process for the development of tissue organization, especially in the development of primitive adipose tissue and adipocyte tissue wound healing. However, excessive migration may result in abnormal development and fibrosis-related diseases such as hypertrophic scar. We previously reported that type I collagen (collagen I) enhanced migration of 3T3-L1 preadipocytes via phosphorylation and/or acetylation of NF-κB p65, and the enhanced cell migration is repressed by silibinin treatment through sirt1. It is known that sirt1 has an ability to deacetylate acetylated NF-κB p65, but little is known about the effect of sirt1 on phosphorylated NF-κB p65. This study aims to examine the potential effect of sirt1 on the regulation of phosphorylated NF-κB p65 and the underlying mechanism. Autophagy is involved in many physiological and pathological processes, including regulation of cell migration as well as in cellular homeostasis. The present study demonstrates that silibinin induces autophagy in a dose-dependent manner in 3T3-L1 cells. Autophagy is under the regulation of sirt1/AMPK pathway, and inhibits collagen I-enhanced migration of 3T3-L1 cells through negative regulation of NF-κB p65 phosphorylation but not acetylation. The expression of peroxisome proliferator-activated receptor α (PPARα) is up-regulated with silibinin accompanying up-regulation of autophagy through activating sirt1 in 3T3-L1 cells. Taken together, these findings indicate that silibinin-induced autophagy is mediated by up-regulation of PPARα-sirt1-AMPK, contributing to repression of type I collagen-enhanced migration in murine 3T3-L1 preadipocytes through down-regulation of phosphorylated NF-κB p65.

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Mendeley readers

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Geographical breakdown

Country Count As %
Unknown 24 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 25%
Unspecified 3 13%
Researcher 3 13%
Professor 2 8%
Student > Doctoral Student 1 4%
Other 2 8%
Unknown 7 29%
Readers by discipline Count As %
Pharmacology, Toxicology and Pharmaceutical Science 4 17%
Biochemistry, Genetics and Molecular Biology 4 17%
Unspecified 3 13%
Medicine and Dentistry 2 8%
Agricultural and Biological Sciences 1 4%
Other 2 8%
Unknown 8 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 June 2018.
All research outputs
#18,640,437
of 23,092,602 outputs
Outputs from Molecular and Cellular Biochemistry
#1,580
of 2,327 outputs
Outputs of similar age
#253,015
of 328,114 outputs
Outputs of similar age from Molecular and Cellular Biochemistry
#11
of 24 outputs
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