@article{800aeeb1d0924753b14a2d2af93c9f13,
title = "Schwann cell-specific Pten inactivation reveals essential role of the sympathetic nervous system activity in adipose tissue development",
abstract = "There is increasing evidence that the sympathetic nervous system (SNS) plays an important role in adipose tissue development. However, the underlying molecular mechanism(s) associated with this remains unclear. SNS innervation of white adipose tissue (WAT) is believed to be necessary and sufficient to elicit WAT lipolysis. In this current study, mice with Schwann cell (SC)-specific inactivation of phosphatase and tensin homolog (Pten) displayed enlarged inguinal white adipose tissue (iWAT). This serendipitous observation implicates the role of SCs in mediating SNS activity associated with mouse adipose tissue development. Mice with SC-specific Pten inactivation displayed enlarged iWAT. Interestingly, the SNS activity in iWAT of SC-specific Pten-deficient mice was reduced as demonstrated by decreased tyrosine hydroxylase (TH) expression level and neurotransmitters, such as norepinephrine (NE) and histamine (H). The lipolysis related protein, phosphorylated hormone sensitive lipase (pHSL), was also decreased. As expected, AKT-associated signaling pathway was hyperactivated and hypothesized to induce enlarged iWAT in SC-specific Pten-deficient mice. Moreover, preliminary experiments using AKT inhibitor AZD5363 treatment ameliorated the enlarged iWAT condition in SC-specific Pten-deficient mice. Taken together, SCs play an essential role in the regulation of SNS activity in iWAT development via the AKT signaling pathway. This novel role of SCs in SNS function allows for better understanding into the genetic mechanisms of peripheral neuropathy associated obesity.",
keywords = "Pten, Schwann cell, Sympathetic nervous system, White adipose tissue",
author = "Li, {Xiao Xiao} and Zhang, {Shi Jie} and Man, {Ka Yi} and Chiu, {Amy P.} and Lo, {Lilian H.} and To, {Jeffrey C.} and Chiu, {Cynthia H.} and Chan, {Chi On} and Mok, {Daniel K.W.} and Rowlands, {Dewi K.} and Keng, {Vincent W.}",
note = "Funding Information: V.W.K. is supported by Collaborative Research Fund Equipment Grant ( C5012-15E ) and Research Impact Fund ( R5050-18 ) from the Research Grant Council, Hong Kong Government ; NSFC/RGC Joint Research Scheme (N-PolyU 503/16). State Key Laboratory of Chemical Biology and Drug Discovery, and Research Project Grants ( ZE19 , ZVLC , UA94 , YBTA ) funded by the Department of Applied and Chemical Technology, The Hong Kong Polytechnic University . Funding Information: V.W.K. is supported by Collaborative Research Fund Equipment Grant (C5012-15E) and Research Impact Fund (R5050-18) from the Research Grant Council, Hong Kong Government; NSFC/RGC Joint Research Scheme (N-PolyU 503/16). State Key Laboratory of Chemical Biology and Drug Discovery, and Research Project Grants (ZE19, ZVLC, UA94, YBTA) funded by the Department of Applied and Chemical Technology, The Hong Kong Polytechnic University. D.K.W.M. is supported by 153027/18P from the Research Grant Council of the Hong Kong Government; Hong Kong Chinese Materia Medica Standards Project, an internal grant (YBU0) and the Large Equipment Funds and University Research Facility in Chemical and Environmental Analysis of the Hong Kong Polytechnic University. Funding Information: D.K.W.M. is supported by 153027/18P from the Research Grant Council of the Hong Kong Government ; Hong Kong Chinese Materia Medica Standards Project , an internal grant (YBU0) and the Large Equipment Funds and University Research Facility in Chemical and Environmental Analysis of the Hong Kong Polytechnic University . Publisher Copyright: {\textcopyright} 2020 Elsevier Inc.",
year = "2020",
month = oct,
day = "15",
doi = "10.1016/j.bbrc.2020.07.050",
language = "English",
volume = "531",
pages = "118--124",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier B.V.",
number = "2",
}
