PMID- 32733280
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200928
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 11
DP  - 2020
TI  - Selenium-Containing Protein From Selenium-Enriched Spirulina platensis Attenuates 
      High Glucose-Induced Calcification of MOVAS Cells by Inhibiting ROS-Mediated DNA 
      Damage and Regulating MAPK and PI3K/AKT Pathways.
PG  - 791
LID - 10.3389/fphys.2020.00791 [doi]
LID - 791
AB  - Hyperglycemia is the main feature of diabetes and may increase the risk of 
      vascular calcification (VC), which is an independent predictor for cardiovascular 
      and cerebrovascular diseases (CCD). Selenium (Se) may decrease the risk of CCD, 
      and previous studies confirmed that Se-containing protein from Se-enriched 
      Spirulina platensis (Se-SP) exhibited novel antioxidant potential. However, the 
      effect of Se-SP against VC has been not investigated. Herein, the protective 
      effect and underlying mechanism of Se-SP against high glucose-induced 
      calcification in mouse aortic vascular smooth muscle cells (MOVAS) were explored. 
      Inductively coupled plasma atomic emission spectroscopy (ICP-AES) results showed 
      time-dependent uptake of Se-SP in MOVAS cells, which significantly inhibited high 
      glucose-induced abnormal proliferation. Se-SP co-treatment also effectively 
      attenuated high glucose-induced calcification of MOVAS cells, followed by 
      decreased activity and expression of alkaline phosphatase (ALP). Further 
      investigation revealed that Se-SP markedly prevented reactive oxygen species 
      (ROS)-mediated DNA damage in glucose-treated MOVAS cells. ROS inhibition by 
      glutathione (GSH) effectively inhibited high glucose-induced calcification, 
      indicating that Se-SP could act as ROS inhibitor to inhibit high glucose-induced 
      DNA damage and calcification. Moreover, Se-SP dramatically attenuated high 
      glucose-induced dysfunction of mitogen-activated protein kinases (MAPKs) and 
      phosphatidylinositol-3-kinase/AKT (PI3K/AKT) pathways. Se-SP after Se addition 
      achieved enhanced potential in inhibiting high glucose-induced calcification, 
      which validated that Se-SP as a new Se species could be a highly effective 
      treatment for human CCD.
CI  - Copyright (c) 2020 Lin, Zhang, Li, Zhang, Shen, Kong, Wang, Cui, Dai, Cao and 
      Zhang.
FAU - Lin, Cong
AU  - Lin C
AD  - Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou, China.
FAU - Zhang, Li-Jun
AU  - Zhang LJ
AD  - Department of Neurology, People's Hospital of Linyi Affiliated to Qingdao 
      University, Linyi, China.
FAU - Li, Bo
AU  - Li B
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Zhang, Feng
AU  - Zhang F
AD  - Physical Examination Center, Taian City Central Hospital, Taian, China.
FAU - Shen, Qing-Rong
AU  - Shen QR
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Kong, Guo-Qing
AU  - Kong GQ
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Wang, Xiao-Fan
AU  - Wang XF
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Cui, Shou-Hong
AU  - Cui SH
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Dai, Rong
AU  - Dai R
AD  - Department of Emergency, Taian City Central Hospital, Taian, China.
FAU - Cao, Wen-Qiang
AU  - Cao WQ
AD  - Department of Biotechnology, Zhuhai Hopegenes Medical and Phamaceutical 
      Institute, Zhuhai, China.
FAU - Zhang, Pu
AU  - Zhang P
AD  - Department of Cardiovascular Medicine, Taian City Central Hospital, Taian, China.
LA  - eng
PT  - Journal Article
DEP - 20200709
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC7363841
OTO - NOTNLM
OT  - ROS
OT  - Se-containing protein
OT  - Spirulina platensis
OT  - cardiovascular and cerebrovascular diseases
OT  - hyperglycemia
OT  - vascular calcification
EDAT- 2020/08/01 06:00
MHDA- 2020/08/01 06:01
PMCR- 2020/07/09
CRDT- 2020/08/01 06:00
PHST- 2020/03/30 00:00 [received]
PHST- 2020/06/15 00:00 [accepted]
PHST- 2020/08/01 06:00 [entrez]
PHST- 2020/08/01 06:00 [pubmed]
PHST- 2020/08/01 06:01 [medline]
PHST- 2020/07/09 00:00 [pmc-release]
AID - 10.3389/fphys.2020.00791 [doi]
PST - epublish
SO  - Front Physiol. 2020 Jul 9;11:791. doi: 10.3389/fphys.2020.00791. eCollection 
      2020.