PMID- 37528662
OWN - NLM
STAT- MEDLINE
DCOM- 20230919
LR  - 20240109
IS  - 1745-7270 (Electronic)
IS  - 1672-9145 (Print)
IS  - 1672-9145 (Linking)
VI  - 55
IP  - 9
DP  - 2023 Aug 1
TI  - Transaldolase inhibits CD36 expression by modulating glutathione-p38 signaling, 
      exerting protective effects against macrophage foam cell formation.
PG  - 1496-1505
LID - 10.3724/abbs.2023146 [doi]
AB  - In atherosclerosis, macrophage-derived foam cell formation is considered to be a 
      hallmark of the pathological process; this occurs via the uptake of modified 
      lipoproteins. In the present study, we aim to determine the role of transaldolase 
      in foam cell formation and atherogenesis and reveal the mechanisms underlying its 
      role. Bone marrow-derived macrophages (BMDMs) isolated from mice successfully 
      form foam cells after treatment with oxidized low-density lipoprotein (80 mug/mL). 
      Elevated transaldolase levels in the foam cell model are assessed by quantitative 
      polymerase chain reaction and western blot analysis. Transaldolase overexpression 
      and knockdown in BMDMs are achieved via plasmid transfection and small 
      interfering RNA technology, respectively. We find that transaldolase 
      overexpression effectively attenuates, whereas transaldolase knockdown 
      accelerates, macrophage-derived foam cell formation through the inhibition or 
      activation of cholesterol uptake mediated by the scavenger receptor cluster of 
      differentiation 36 (CD36) in a p38 mitogen-activated protein kinase (MAPK) 
      signaling-dependent manner. Transaldolase-mediated glutathione (GSH) homeostasis 
      is identified as the upstream regulator of p38 MAPK-mediated CD36-dependent 
      cholesterol uptake in BMDMs. Transaldolase upregulates GSH production, thereby 
      suppressing p38 activity and reducing the CD36 level, ultimately preventing foam 
      cell formation and atherosclerosis. Thus, our findings indicate that the 
      transaldolase-GSH-p38-CD36 axis may represent a promising therapeutic target for 
      atherosclerosis.
FAU - Li, Chengyi
AU  - Li C
AD  - Department of Immunology, School of Medicine, Yangtze University, Jingzhou 
      434023, China.
FAU - Song, Zihao
AU  - Song Z
AD  - Department of Immunology, School of Medicine, Yangtze University, Jingzhou 
      434023, China.
FAU - Gao, Pengyue
AU  - Gao P
AD  - Department of Immunology, School of Medicine, Yangtze University, Jingzhou 
      434023, China.
FAU - Duan, Wei
AU  - Duan W
AD  - Department of Oncology, Jingzhou Hospital Affiliated to Yangtze University, 
      Jingzhou 434023, China.
FAU - Liu, Xiu
AU  - Liu X
AD  - Department of Cardiovascular Surgery, Nanfang Hospital, Southern Medical 
      University, Guangzhou 510515, China.
FAU - Liang, Sijia
AU  - Liang S
AD  - Department of Pharmacology, and Cardiac & Cerebral Vascular Research Center, 
      Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China.
FAU - Gong, Quan
AU  - Gong Q
AD  - Department of Immunology, School of Medicine, Yangtze University, Jingzhou 
      434023, China.
FAU - Guo, Jiawei
AU  - Guo J
AD  - Department of Immunology, School of Medicine, Yangtze University, Jingzhou 
      434023, China.
LA  - eng
PT  - Journal Article
PL  - China
TA  - Acta Biochim Biophys Sin (Shanghai)
JT  - Acta biochimica et biophysica Sinica
JID - 101206716
RN  - EC 2.2.1.2 (Transaldolase)
RN  - 0 (CD36 Antigens)
RN  - 0 (Lipoproteins, LDL)
RN  - GAN16C9B8O (Glutathione)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Foam Cells
MH  - Transaldolase/metabolism/pharmacology
MH  - CD36 Antigens/genetics/metabolism
MH  - Macrophages/metabolism
MH  - Lipoproteins, LDL/metabolism
MH  - *Atherosclerosis/metabolism
MH  - Glutathione/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
MH  - Cholesterol/metabolism
PMC - PMC10520467
OTO - NOTNLM
OT  - CD36
OT  - GSH
OT  - foam cell formation
OT  - p38 MAPK
OT  - transaldolase
COIS- The authors declare that they have no conflict of interest.
EDAT- 2023/08/02 06:42
MHDA- 2023/09/19 06:42
PMCR- 2023/08/01
CRDT- 2023/08/02 02:33
PHST- 2023/09/19 06:42 [medline]
PHST- 2023/08/02 06:42 [pubmed]
PHST- 2023/08/02 02:33 [entrez]
PHST- 2023/08/01 00:00 [pmc-release]
AID - 10.3724/abbs.2023146 [doi]
PST - ppublish
SO  - Acta Biochim Biophys Sin (Shanghai). 2023 Aug 1;55(9):1496-1505. doi: 
      10.3724/abbs.2023146.