PMID- 35611986
OWN - NLM
STAT- MEDLINE
DCOM- 20220526
LR  - 20220716
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 5
DP  - 2022 May
TI  - Long non-coding RNA LINC00616 promotes ferroptosis of periodontal ligament stem 
      cells via the microRNA-370 / transferrin receptor axis.
PG  - 13070-13081
LID - 10.1080/21655979.2022.2076508 [doi]
AB  - This study was designed to explore the role of lncRNA LINC00616 in the regulation 
      of periodontitis. Cellular functions were measured using 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays. The 
      content of reactive oxygen species, Fe(2+), glutathione, and malondialdehyde were 
      measured to determine ferroptosis in Porphyromonas gingivalis lipopolysaccharide 
      (LPS-PG) treated periodontal ligament stem cells (PDLSCs), as well as expression 
      of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11, and 
      acyl-CoA synthetase long-chain family member 4 proteins mRNA and miRNA levels 
      were measured by quantitative reverse-transcription polymerase chain reaction 
      (qRT-PCR). Western blot analysis was performed to assess protein expression. 
      Targeting relationships were predicted using StarBase and TargetScan and verified 
      by a dual luciferase reporter assay. The lncRNA LINC00616 was upregulated in 
      periodontitis ligament tissues of patients with periodontitis and in PDLSCs 
      treated with LPS-PG. Inhibition of LINC00616 promoted cell viability and 
      suppressed ferroptosis of PDLSCs. miR-370 was verified to be a target of 
      LINC00616, and suppressed miR-370 reversed the effects of LINC00616 knockdown on 
      cell viability and ferroptosis in PDLSCs. Additionally, miR-370 targeting the 
      transferrin receptor protein and upregulated transferrin receptor (TFRC) 
      abolished the effects of overexpressed miR-370 on cell viability and ferroptosis 
      of PDLSCs. LINC00616 acted as a competitive endogenous RNA (ceRNA) to promote 
      ferroptosis of PDLSCs via the miR-370/TFRC axis. Therefore, LINC00616 knockdown 
      may be a promising therapeutic strategy for periodontitis.
FAU - Wang, Hongwei
AU  - Wang H
AD  - Department of Orthodontics, Eye Hospital of Hebei, Xingtai, Hebei, China.
FAU - Qiao, Xiaotong
AU  - Qiao X
AD  - Department of Oral Medicine, College of Stomatology, Hebei Medical University, 
      Shijiazhuang, Hebei, China.
FAU - Zhang, Chao
AU  - Zhang C
AD  - Department of Orthodontics, Eye Hospital of Hebei, Xingtai, Hebei, China.
FAU - Hou, Jingyi
AU  - Hou J
AD  - Department of Orthodontics, Beijing Stomatological Hospital, Capital Medical 
      University, Beijing, China.
FAU - Qi, Suqing
AU  - Qi S
AD  - Department of Orthodontics, Eye Hospital of Hebei, Xingtai, Hebei, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MIRN370 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Receptors, Transferrin)
SB  - IM
MH  - *Ferroptosis/genetics
MH  - Humans
MH  - Lipopolysaccharides/metabolism
MH  - *MicroRNAs/genetics/metabolism
MH  - Periodontal Ligament
MH  - *Periodontitis/genetics/metabolism
MH  - *RNA, Long Noncoding/genetics/metabolism
MH  - Receptors, Transferrin/metabolism
MH  - Stem Cells/metabolism
PMC - PMC9276003
OTO - NOTNLM
OT  - LINC00616
OT  - Periodontitis
OT  - TFRC
OT  - bone marrow mesenchymal stem cells
OT  - ferroptosis
OT  - miR-370
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/05/26 06:00
MHDA- 2022/05/27 06:00
PMCR- 2022/05/25
CRDT- 2022/05/25 08:24
PHST- 2022/05/25 08:24 [entrez]
PHST- 2022/05/26 06:00 [pubmed]
PHST- 2022/05/27 06:00 [medline]
PHST- 2022/05/25 00:00 [pmc-release]
AID - 2076508 [pii]
AID - 10.1080/21655979.2022.2076508 [doi]
PST - ppublish
SO  - Bioengineered. 2022 May;13(5):13070-13081. doi: 10.1080/21655979.2022.2076508.