PMID- 31243572
OWN - NLM
STAT- MEDLINE
DCOM- 20190827
LR  - 20190827
IS  - 1432-0584 (Electronic)
IS  - 0939-5555 (Linking)
VI  - 98
IP  - 9
DP  - 2019 Sep
TI  - miR-144 regulates oxidative stress tolerance of thalassemic erythroid cell via 
      targeting NRF2.
PG  - 2045-2052
LID - 10.1007/s00277-019-03737-4 [doi]
AB  - Thalassemia has a high prevalence in Thailand. Oxidative damage to erythroid 
      cells is known to be one of the major etiologies in thalassemia pathophysiology. 
      Oxidative stress status of thalassemia is potentiated by the heme, nonheme iron, 
      and free iron resulting from imbalanced globin synthesis. In addition, levels of 
      antioxidant proteins are reduced in alpha-thalassemia and beta-thalassemia erythrocytes. 
      However, the primary molecular mechanism for this phenotype remains unknown. Our 
      study showed a high expression of miR-144 in beta- and alpha-thalassemia. An increased 
      miR-144 expression leads to decreased expression of nuclear factor erythroid 
      2-related factor 2 (NRF2) target, especially in alpha-thalassemia. In alpha-thalassemia, 
      miR-144 and NRF2 target are associated with glutathione level and anemia 
      severity. To study the effect of miR-144 expression, the gain-loss of miR-144 
      expression was performed by miR inhibitor and mimic transfection in the 
      erythroblastic cell line. This study reveals that miR-144 expression was 
      upregulated, whereas NRF2 expression and glutathione levels were decreased in 
      comparison with the untreated condition after miR mimic transfection, while the 
      reduction of miR-144 expression contributed to the increased NRF2 expression and 
      glutathione level compared with the untreated condition after miR inhibitor 
      transfection. Moreover, miR-144 overexpression leads to significantly increased 
      sensitivity to oxidative stress at indicated concentrations of hydrogen peroxide 
      (H(2)O(2)) and rescued by miR-144 inhibitor. Taken together, our findings suggest 
      that dysregulation of miR-144 may play a role in the reduced ability of 
      erythrocyte to deal with oxidative stress and increased RBC hemolysis 
      susceptibility especially in thalassemia.
FAU - Srinoun, Kanitta
AU  - Srinoun K
AUID- ORCID: 0000-0003-1806-2544
AD  - Faculty of Medical Technology, Prince of Songkla University, 15, Kanjanavanit Rd. 
      Hat Yai, Songkhla, 90110, Thailand. kanitta.s@psu.ac.th.
FAU - Sathirapongsasuti, Nuankanya
AU  - Sathirapongsasuti N
AD  - Section for Translational Medicine, Faculty of Medicine Ramathibodi Hospital, 
      Mahidol University, 25/25, 270 Rama VI Rd., Ratchathewi, Bangkok, 10400, 
      Thailand.
FAU - Paiboonsukwong, Kittiphong
AU  - Paiboonsukwong K
AD  - Thalassemia Research Center, Institute of Molecular Biosciences, Mahidol 
      University, 25/25, Putthamonthon Sai 4 Rd. Salaya, Putthamonthon, Nakron Pratom, 
      73170, Thailand.
FAU - Sretrirutchai, Somporn
AU  - Sretrirutchai S
AD  - Department of Pathology, Faculty of Medicine, Prince of Songkla University, 15, 
      Kanjanavanit Rd. Hat Yai, Songkhla, 90110, Thailand.
FAU - Wongchanchailert, Malai
AU  - Wongchanchailert M
AD  - Department of Pediatrics, Faculty of Medicine, Prince of Songkla University, 15, 
      Kanjanavanit Rd. Hat Yai, Songkhla, 90110, Thailand.
FAU - Fucharoen, Suthat
AU  - Fucharoen S
AD  - Thalassemia Research Center, Institute of Molecular Biosciences, Mahidol 
      University, 25/25, Putthamonthon Sai 4 Rd. Salaya, Putthamonthon, Nakron Pratom, 
      73170, Thailand.
LA  - eng
GR  - TRG5780103/Thailand Research Fund (TH)/
GR  - MET6201015S/the government budget of Prince of Songkla University/
PT  - Journal Article
DEP - 20190626
PL  - Germany
TA  - Ann Hematol
JT  - Annals of hematology
JID - 9107334
RN  - 0 (MIRN144 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Erythrocytes/*metabolism/pathology
MH  - Female
MH  - Glutathione/biosynthesis/genetics
MH  - Hemolysis
MH  - Humans
MH  - Hydrogen Peroxide/metabolism
MH  - K562 Cells
MH  - Male
MH  - MicroRNAs/*biosynthesis/genetics
MH  - NF-E2-Related Factor 2/*biosynthesis/genetics
MH  - *Oxidative Stress
MH  - *Up-Regulation
MH  - alpha-Thalassemia/genetics/*metabolism/pathology
MH  - beta-Thalassemia/genetics/*metabolism/pathology
OTO - NOTNLM
OT  - Hemolysis
OT  - Oxidative stress
OT  - Thalassemia
OT  - miR-144
EDAT- 2019/06/28 06:00
MHDA- 2019/08/28 06:00
CRDT- 2019/06/28 06:00
PHST- 2018/10/07 00:00 [received]
PHST- 2019/06/10 00:00 [accepted]
PHST- 2019/06/28 06:00 [pubmed]
PHST- 2019/08/28 06:00 [medline]
PHST- 2019/06/28 06:00 [entrez]
AID - 10.1007/s00277-019-03737-4 [pii]
AID - 10.1007/s00277-019-03737-4 [doi]
PST - ppublish
SO  - Ann Hematol. 2019 Sep;98(9):2045-2052. doi: 10.1007/s00277-019-03737-4. Epub 2019 
      Jun 26.