PMID- 31186419
OWN - NLM
STAT- MEDLINE
DCOM- 20200717
LR  - 20210109
IS  - 2041-4889 (Electronic)
VI  - 10
IP  - 6
DP  - 2019 Jun 11
TI  - Sonodynamic therapy inhibits palmitate-induced beta cell dysfunction via 
      PINK1/Parkin-dependent mitophagy.
PG  - 457
LID - 10.1038/s41419-019-1695-x [doi]
LID - 457
AB  - In type 2 diabetes mellitus (T2DM), the overload of glucose and lipids can 
      promote oxidative stress and inflammatory responses and contribute to the failure 
      of beta cells. However, therapies that can modulate the function of beta cells 
      and thus prevent their failure have not been well explored. In this study, beta 
      cell injury model was established with palmitic acid (PA) to simulate the 
      lipotoxicity (high-fat diet) found in T2DM. Sonodynamic therapy (SDT), a novel 
      physicochemical treatment, was applied to treat injured beta cells. We found that 
      SDT had specific effects on mitochondria and induced transient large amount of 
      mitochondrial reactive oxygen species (ROS) production in beta cells. SDT also 
      improved the morphology and function of abnormal mitochondria, inhibited 
      inflammatory response and reduced beta cell dysfunction. The improvement of 
      mitochondria was mediated by PINK1/Parkin-dependent mitophagy. Additionally, SDT 
      rescued the transcription of PINK1 mRNA which was blocked by PA treatment, thus 
      providing abundant PINK1 for mitophagy. Moreover, SDT also increased insulin 
      secretion from beta cells. The protective effects of SDT were abrogated when 
      mitophagy was inhibited by cyclosporin A (CsA). In summary, SDT potently inhibits 
      lipotoxicity-induced beta cell failure via PINK1/Parkin-dependent mitophagy, 
      providing theoretical guidance for T2DM treatment in aspects of islet protection.
FAU - Guo, Tian
AU  - Guo T
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Liu, Tianyang
AU  - Liu T
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Sun, Yun
AU  - Sun Y
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Liu, Xianna
AU  - Liu X
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Xiong, Rongguo
AU  - Xiong R
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Li, He
AU  - Li H
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Li, Zhitao
AU  - Li Z
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.
FAU - Zhang, Zhiguo
AU  - Zhang Z
AD  - Laboratory of Photo- and Sono-theranostic Technologies and Condensed Matter 
      Science and Technology Institute, Harbin Institute of Technology, Harbin, 150001, 
      China.
FAU - Tian, Zhen
AU  - Tian Z
AUID- ORCID: 0000-0001-9044-637X
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China. 
      tianzhen@hrbmu.edu.cn.
AD  - Key Laboratory of Acoustic Photoelectric Magnetic Diagnosis and Treatment of 
      Cardiovascular Diseases in Heilongjiang Province, Harbin, 150081, China. 
      tianzhen@hrbmu.edu.cn.
FAU - Tian, Ye
AU  - Tian Y
AD  - Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China. 
      yetian@ems.hrbmu.edu.cn.
AD  - Key Laboratory of Acoustic Photoelectric Magnetic Diagnosis and Treatment of 
      Cardiovascular Diseases in Heilongjiang Province, Harbin, 150081, China. 
      yetian@ems.hrbmu.edu.cn.
AD  - Department of Cardiology, The First Affiliated Hospital, Cardiovascular 
      Institute, Harbin Medical University, Harbin, 150001, China. 
      yetian@ems.hrbmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190611
PL  - England
TA  - Cell Death Dis
JT  - Cell death & disease
JID - 101524092
RN  - 0 (Carrier Proteins)
RN  - 0 (Protoporphyrins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, GABA-A)
RN  - 141440-82-6 (Tspo protein, rat)
RN  - 2V16EO95H1 (Palmitic Acid)
RN  - C2K325S808 (protoporphyrin IX)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.3.2.27 (parkin protein)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.11.1 (PTEN-induced putative kinase)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/metabolism
MH  - Cell Line
MH  - Cell Survival/drug effects/genetics/radiation effects
MH  - Diabetes Mellitus, Type 2/metabolism/*therapy
MH  - Inflammation/metabolism/radiotherapy
MH  - Insulin-Secreting Cells/drug effects/*metabolism/radiation effects
MH  - Mitochondria/genetics/metabolism/*radiation effects/ultrastructure
MH  - Mitophagy/drug effects/genetics/*radiation effects
MH  - Palmitic Acid/pharmacology/toxicity
MH  - Protein Kinases/genetics/*metabolism
MH  - Protoporphyrins/metabolism
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, GABA-A/metabolism
MH  - Ubiquitin-Protein Ligases/genetics/*metabolism
MH  - *Ultrasonic Waves
PMC - PMC6560035
COIS- The authors declare that they have no conflict of interest.
EDAT- 2019/06/13 06:00
MHDA- 2020/07/18 06:00
PMCR- 2019/06/11
CRDT- 2019/06/13 06:00
PHST- 2019/01/08 00:00 [received]
PHST- 2019/05/28 00:00 [accepted]
PHST- 2019/05/27 00:00 [revised]
PHST- 2019/06/13 06:00 [entrez]
PHST- 2019/06/13 06:00 [pubmed]
PHST- 2020/07/18 06:00 [medline]
PHST- 2019/06/11 00:00 [pmc-release]
AID - 10.1038/s41419-019-1695-x [pii]
AID - 1695 [pii]
AID - 10.1038/s41419-019-1695-x [doi]
PST - epublish
SO  - Cell Death Dis. 2019 Jun 11;10(6):457. doi: 10.1038/s41419-019-1695-x.