PMID- 34156885
OWN - NLM
STAT- MEDLINE
DCOM- 20220228
LR  - 20220228
IS  - 1532-432X (Electronic)
IS  - 0363-0269 (Linking)
VI  - 45
IP  - 3
DP  - 2021 May
TI  - Upregulation of miR-214 Mediates Oxidative Stress in Hb H Disease via Targeting 
      of ATF4.
PG  - 197-202
LID - 10.1080/03630269.2021.1941081 [doi]
AB  - Thalassemia is a genetic disorder, occurring because of an imbalance in the 
      globin chain production. Oxidative stress in erythroid cells of thalassemia is 
      mainly generated from excess globin chains, by Fenton reaction, leading to 
      hemolysis and ineffective erythropoiesis. Previously, data has shown that 
      microRNAs (miRNAs) are involved in oxidative stress regulation in red blood cells 
      (RBCs). microR-214 has been reported to respond with an external oxidative stress 
      in erythroid cells by modulating activating transcription factor 4 (ATF4). In 
      this study, we illustrated the expressions of miR-214 and ATF4 in Hb H (beta4) 
      disease, and Hb E (HBB: c.79G>A)/beta-thalassemia (beta-thal) reticulocyte samples. Our 
      results showed miR-214 expression was increased in Hb H disease, but not 
      significantly different in Hb E/beta-thal reticulocytes. The ATF4 target was 
      decreased in both thalassemic groups. Moreover, miR-214 expression level 
      positively correlated with the reactive oxygen species (ROS) level, while it was 
      negatively correlated with mean corpuscular volume (MCV), mean corpuscular 
      hemoglobin (Hb) (MCH) and mean corpuscular Hb concentration (MCHC). We suggested 
      that the upregulation of miR-214 correlated with the oxidative stress as well as 
      anemia severity of Hb H disease patients, by suppression of ATF4. Understanding 
      the oxidative pathways in erythrocyte could be useful to manage and relieve the 
      clinical manifestation, such as anemia, in thalassemic patients.
FAU - Saensuwanna, Apisara
AU  - Saensuwanna A
AD  - Faculty of Medicine, Department of Biomedical Sciences, Prince of Songkla 
      University, Songkhla, Thailand.
FAU - Penglong, Tipparat
AU  - Penglong T
AD  - Faculty of Medicine, Department of Pathology, Prince of Songkla University, 
      Songkhla, Thailand.
FAU - Srinoun, Kanitta
AU  - Srinoun K
AUID- ORCID: 0000-0003-1806-2544
AD  - Faculty of Medical Technology, Prince of Songkla University, Songkhla, Thailand.
LA  - eng
PT  - Journal Article
DEP - 20210622
PL  - England
TA  - Hemoglobin
JT  - Hemoglobin
JID - 7705865
RN  - 0 (ATF4 protein, human)
RN  - 0 (MIRN214 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 145891-90-3 (Activating Transcription Factor 4)
RN  - 9004-22-2 (Globins)
SB  - IM
MH  - *Activating Transcription Factor 4/genetics
MH  - Globins
MH  - Humans
MH  - *MicroRNAs/genetics
MH  - *Oxidative Stress
MH  - Up-Regulation
MH  - *alpha-Thalassemia/genetics
MH  - *beta-Thalassemia/genetics
OTO - NOTNLM
OT  - Activating transcription factor 4 (ATF4)
OT  - anemia
OT  - microR-214 (miR-214)
OT  - oxidative stress
OT  - thalassemia
EDAT- 2021/06/23 06:00
MHDA- 2022/03/01 06:00
CRDT- 2021/06/22 17:13
PHST- 2021/06/23 06:00 [pubmed]
PHST- 2022/03/01 06:00 [medline]
PHST- 2021/06/22 17:13 [entrez]
AID - 10.1080/03630269.2021.1941081 [doi]
PST - ppublish
SO  - Hemoglobin. 2021 May;45(3):197-202. doi: 10.1080/03630269.2021.1941081. Epub 2021 
      Jun 22.