PMID- 29724989
OWN - NLM
STAT- MEDLINE
DCOM- 20180928
LR  - 20210617
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 24
DP  - 2018 May 4
TI  - Role of Hypoxia-Inducible Factors 1alpha (HIF1alpha) in SH-SY5Y Cell Autophagy Induced by 
      Oxygen-Glucose Deprivation.
PG  - 2758-2766
LID - 10.12659/MSM.905140 [doi]
AB  - BACKGROUND HIF-1alpha plays an important role in hypoxia-ischemia brain damage. 
      Accumulating evidences demonstrates that HIF-1alpha can contribute to cell autophagy. 
      Oxygen-glucose deprivation (OGD) is a commonly used ischemic model in vitro. Our 
      study was performed to investigate the influences of HIF-1alpha on autophagy in 
      SH-SY5Y cells under OGD treatment. MATERIAL AND METHODS An OGD model was 
      constructed in SH-SY5Y cells. PI method and MTT assay were used to test cell 
      death and viability, respectively. Western blot assay was used to estimate the 
      protein levels of HIF-1alpha and LC3. Quantitative GFP-LC3 light microscopy autophagy 
      assay was performed for SH-SY5Y cells. 2ME2 and siRNA-HIF-1alpha were applied to 
      investigate the effects of HIF-1alpha-knockdown on LC3 expression. Additionally, 3-MA 
      (autophagy inhibitor) and autophagy inducer rapamycin (Rapa) were used to 
      investigate the effects of autophagy on cell survival under OGD condition. 
      RESULTS Under OGD, the apoptosis of SH-SY5Ycells was increased while cell 
      viability rate was decreased. The expression of HIF-1alpha was increased along with 
      the advancement of OGD treatment and achieved the highest level at 24 h. However, 
      inhibiting HIF-1alpha expression decreased the cell apoptosis and increased cell 
      viability. LC3-II expression was gradually increased with the duration of OGD 
      condition and knockdown of HIF-1alpha resulted in decreased expression of LC3. 
      Inhibiting autophagy significantly enhanced the viability and reduced the 
      apoptosis of SH-SY5Y cells, while enhancing autophagy showed the opposite 
      effects. CONCLUSIONS Enhanced expression of HIF-1alpha may be related to autophagy 
      activation in SH-SY5Y cells, thus contributing to ischemic/hypoxic brain damage.
FAU - Niu, Guohui
AU  - Niu G
AD  - Department of Pediatric Rehabilitation, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
FAU - Zhu, Dengna
AU  - Zhu D
AD  - Department of Pediatric Rehabilitation, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
FAU - Zhang, Xiaoli
AU  - Zhang X
AD  - Department of Pediatric Internal Medicine, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
FAU - Wang, Jun
AU  - Wang J
AD  - Department of Pediatric Rehabilitation, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
FAU - Zhao, Yunxia
AU  - Zhao Y
AD  - Department of Pediatric Rehabilitation, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
FAU - Wang, Xin
AU  - Wang X
AD  - Department of Pediatric Rehabilitation, Third Affiliated Hospital of Zhengzhou 
      University, Zhengzhou, Henan, China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20180504
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (MAP1LC3A protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - 147336-22-9 (Green Fluorescent Proteins)
RN  - 5142-23-4 (3-methyladenine)
RN  - IY9XDZ35W2 (Glucose)
RN  - JAC85A2161 (Adenine)
RN  - S88TT14065 (Oxygen)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Adenine/analogs & derivatives/pharmacology
MH  - Apoptosis/drug effects
MH  - *Autophagy/drug effects
MH  - Cell Hypoxia/drug effects
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Gene Knockdown Techniques
MH  - Glucose/*deficiency
MH  - Green Fluorescent Proteins/metabolism
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism
MH  - Microtubule-Associated Proteins/metabolism
MH  - Models, Biological
MH  - Oxygen/*metabolism
MH  - RNA, Small Interfering/metabolism
MH  - Sirolimus/pharmacology
PMC - PMC5954843
EDAT- 2018/05/05 06:00
MHDA- 2018/10/03 06:00
PMCR- 2018/05/04
CRDT- 2018/05/05 06:00
PHST- 2018/05/05 06:00 [entrez]
PHST- 2018/05/05 06:00 [pubmed]
PHST- 2018/10/03 06:00 [medline]
PHST- 2018/05/04 00:00 [pmc-release]
AID - 905140 [pii]
AID - 10.12659/MSM.905140 [doi]
PST - epublish
SO  - Med Sci Monit. 2018 May 4;24:2758-2766. doi: 10.12659/MSM.905140.