PMID- 30797958
OWN - NLM
STAT- MEDLINE
DCOM- 20200203
LR  - 20200306
IS  - 1879-260X (Electronic)
IS  - 0925-4439 (Linking)
VI  - 1865
IP  - 6
DP  - 2019 Jun 1
TI  - Deficiency of heat shock protein A12A promotes browning of white adipose tissues 
      in mice.
PG  - 1451-1459
LID - S0925-4439(19)30069-9 [pii]
LID - 10.1016/j.bbadis.2019.02.017 [doi]
AB  - Browning of white adipose tissues (WAT) is critical for a variety of 
      physiological and pathophysiological events. Given the limited understanding in 
      molecular control of WAT browning, further research is needed. Heat shock protein 
      A12A (HSPA12A) is a new member of multigene Hsp70 family. This study investigated 
      the effect of HSPA12A on the browning of WAT. WAT Browning in mice was induced by 
      cold exposure for 5 days. We observed that nuclear HSPA12A content was increased 
      in WAT after cold exposure, while deficiency of HSPA12A (Hspa12a(-/-)) promoted 
      the cold-induced browning of WAT in mice compared to wild type (WT) littermates. 
      Accordingly, Hspa12a(-/-) mice showed attenuation of body temperature drop and 
      increase of thermogenic gene expression compared to WT mice after cold exposure. 
      However, in vitro experiments demonstrated that HSPA12A deficiency in primary 
      white adipocytes did not affect their browning and thermogenic gene expression. 
      Further loss- and gain-of-HSPA12A functional studies revealed that HSPA12A 
      deficiency promoted whereas HSPA12A overexpression impeded M2 macrophage 
      polarization. Importantly, the conditioned medium (CM) from Hspa12a(-/-) bone 
      marrow-derived macrophages (BMDMs) enhanced the browning of primary white 
      adipocytes when compared to the CM from WT BMDMs. The data identified macrophage 
      HSPA12A as a novel regulator of WAT browning through a paracrine mechanism. 
      Targeting HSPA12A might provide meaningful advances for the management of 
      browning-associated physiological events such as hypothermia adaptation and 
      pathophysiological disorders such as obesity and cancer-related cachexia.
CI  - Copyright (c) 2019 Elsevier B.V. All rights reserved.
FAU - Cheng, Hao
AU  - Cheng H
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Qi, Tao
AU  - Qi T
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Zhang, Xiaojin
AU  - Zhang X
AD  - Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, First 
      Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China.
FAU - Kong, Qiuyue
AU  - Kong Q
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Min, Xinxu
AU  - Min X
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Mao, Qian
AU  - Mao Q
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Cao, Xiaofei
AU  - Cao X
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China.
FAU - Liu, Li
AU  - Liu L
AD  - Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, First 
      Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China; Key 
      Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative 
      Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing 
      Medical University, Nanjing 210029, China.
FAU - Ding, Zhengnian
AU  - Ding Z
AD  - Department of Anaesthesiology, First Affiliated Hospital with Nanjing Medical 
      University, Nanjing 210029, China. Electronic address: zhengnianding@njmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190222
PL  - Netherlands
TA  - Biochim Biophys Acta Mol Basis Dis
JT  - Biochimica et biophysica acta. Molecular basis of disease
JID - 101731730
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (HSP70 Heat-Shock Proteins)
RN  - 0 (Hspa12a protein, mouse)
SB  - IM
MH  - Adaptation, Physiological/*genetics
MH  - Adipocytes, White/cytology/drug effects/metabolism
MH  - Adipose Tissue, Brown/cytology/*metabolism
MH  - Adipose Tissue, White/cytology/*metabolism
MH  - Animals
MH  - Body Temperature
MH  - Cell Nucleus/drug effects/metabolism
MH  - Cold Temperature
MH  - Culture Media, Conditioned/pharmacology
MH  - Energy Metabolism/*genetics
MH  - Gene Expression
MH  - HSP70 Heat-Shock Proteins/*genetics/metabolism
MH  - Macrophages/cytology/drug effects/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Paracrine Communication/genetics
MH  - Primary Cell Culture
MH  - RAW 264.7 Cells
OTO - NOTNLM
OT  - Adipocyte
OT  - Adipose tissue
OT  - Browning
OT  - Heat shock protein A12A (HSPA12A)
OT  - Macrophage
EDAT- 2019/02/25 06:00
MHDA- 2020/02/06 06:00
CRDT- 2019/02/25 06:00
PHST- 2018/10/12 00:00 [received]
PHST- 2019/01/30 00:00 [revised]
PHST- 2019/02/19 00:00 [accepted]
PHST- 2019/02/25 06:00 [pubmed]
PHST- 2020/02/06 06:00 [medline]
PHST- 2019/02/25 06:00 [entrez]
AID - S0925-4439(19)30069-9 [pii]
AID - 10.1016/j.bbadis.2019.02.017 [doi]
PST - ppublish
SO  - Biochim Biophys Acta Mol Basis Dis. 2019 Jun 1;1865(6):1451-1459. doi: 
      10.1016/j.bbadis.2019.02.017. Epub 2019 Feb 22.