PMID- 32557691
OWN - NLM
STAT- MEDLINE
DCOM- 20210830
LR  - 20211204
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 236
IP  - 1
DP  - 2021 Jan
TI  - Asprosin promotes beta-cell apoptosis by inhibiting the autophagy of beta-cell via 
      AMPK-mTOR pathway.
PG  - 215-221
LID - 10.1002/jcp.29835 [doi]
AB  - Asprosin is a newly discovered adipokine. A recent study showed that asprosin 
      promoted the beta-cell apoptosis of MIN6 cells. This study aims to determine whether 
      asprosin induces the apoptosis in beta-cell via regulating autophagy. Mouse 
      insulinoma MIN6 cells were divided into the following four groups: control, 
      vehicle, high glucose, and asprosin groups. MIN6 cells in the asprosin group were 
      transfected with recombinant asprosin-T2A-GFP vector. MIN6 cells in the vehicle 
      group were transfected with vector only. Then the apoptosis of MIN6 cells was 
      detected using flow cytometry. Real-time polymerase chain reaction and western 
      blot were used to determine the expression of caspase 3, LC3-I, LC3-II, beclin 1, 
      P62, AMP activated protein kinase (AMPK), and mammalian target of rapamycin 
      (mTOR). AMPK pathway was enhanced using AMPK agonist AICAR. High glucose and 
      asprosin induced the apoptosis of MIN6 cells and elevated expression of caspase 
      3. In addition, high glucose and asprosin resulted in reduced expression of 
      LC3-II/LC3-I, beclin 1, and increased expression of P62. p-AMPK expression was 
      decreased and p-mTOR expression was increased after high glucose and asprosin 
      treatment. AMPK agonist AICAR was used to activate the AMPK pathway. Treatment 
      with AICAR significantly partly restored decreased autophagy and increased 
      apoptosis of beta-cell, which was induced by asprosin. Asprosin promotes the 
      apoptosis of beta-cell by inhibiting the autophagy of beta-cell via AMPK-mTOR pathway.
CI  - (c) 2020 Wiley Periodicals LLC.
FAU - Wang, Rui
AU  - Wang R
AD  - Department of Blood Transfusion, Qilu Hospital (Qingdao), Cheeloo College of 
      Medicine, Shandong University, Qingdao, China.
FAU - Hu, Wenchao
AU  - Hu W
AUID- ORCID: 0000-0003-0230-1264
AD  - Department of Endocrinology, Qilu Hospital (Qingdao), Cheeloo College of 
      Medicine, Shandong University, Qingdao, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200618
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Fibrillin-1)
RN  - 0 (Peptide Fragments)
RN  - 0 (Peptide Hormones)
RN  - 0 (asprosin protein, mouse)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Autophagy/drug effects
MH  - Cells, Cultured
MH  - Fibrillin-1/*metabolism
MH  - Insulin-Secreting Cells/*metabolism
MH  - Mice
MH  - Peptide Fragments/*metabolism
MH  - Peptide Hormones/*metabolism
MH  - Signal Transduction/*physiology
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - AMPK
OT  - apoptosis
OT  - asprosin
OT  - autophagy
OT  - beta-cell
EDAT- 2020/06/20 06:00
MHDA- 2021/08/31 06:00
CRDT- 2020/06/20 06:00
PHST- 2020/02/21 00:00 [received]
PHST- 2020/05/19 00:00 [revised]
PHST- 2020/05/20 00:00 [accepted]
PHST- 2020/06/20 06:00 [pubmed]
PHST- 2021/08/31 06:00 [medline]
PHST- 2020/06/20 06:00 [entrez]
AID - 10.1002/jcp.29835 [doi]
PST - ppublish
SO  - J Cell Physiol. 2021 Jan;236(1):215-221. doi: 10.1002/jcp.29835. Epub 2020 Jun 
      18.