Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG30036)
Regulator Name MIR9-3HG (IncRNA)
Synonyms
MIR9-3HG
    Click to Show/Hide
Gene Name MIR9-3HG
Gene ID 254559
Regulator Type lncRNA
Ensembl ID ENSG00000255571
HGNC ID
HGNC:27388
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
MIR9-3HG can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
hBMSCs (Bone marrow stromal cells)
In Vivo Model
A total of 96 C57BL/6 male mice (20-25 g) aged 11-12 weeks were purchased from experimental animal center of experimental animal center of Guangdong Medical University. 96 mice were randomly divided into four groups (24 mice per group): Sham group (200 ul of PBS), Sham + BMSCs-Exo group (200 ul of BMSCs-Exo), I/R group (200 ul of PBS) and I/R + BMSCs-Exo group (200 ul of BMSCs-Exo). After 10 days of adaptive feeding, all mice were injected intraperitoneally with 0.4-0.5 mL/100 g 1%Pentobarbital Sodium. I/R and I/R + BMSCs-Exo group mice were subjected to cardiac I/R injury induced by ligation of the left anterior descending artery (LAD) for 30 min followed by 24 h reperfusion. Sham and Sham + BMSCs-Exo mice were sham treated and subjected to the same surgical procedures as I/R mice except that they did not receive ligation of the left anterior descending coronary artery.

    Click to Show/Hide
Response regulation Cellular ferroptosis is involved in the pathogenesis of Ischemia-Reperfusion Injury. BMSCs-Exo lncRNA Mir9-3hg can inhibit ferroptosis by modulating the Pum2/PRDX6 axis to exhibit cardioprotective effectsinvivoandinvitro. Silence of PRDX6 markedly decreased cell proliferation, GSH content and Gpx4 protein level, as well as prominently increased iron ion concentration and levels of ROS content and ACSL4 protein in H/R-treated HL-1 cells.
Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [Driver]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
hBMSCs (Bone marrow stromal cells)
In Vivo Model
A total of 96 C57BL/6 male mice (20-25 g) aged 11-12 weeks were purchased from experimental animal center of experimental animal center of Guangdong Medical University. 96 mice were randomly divided into four groups (24 mice per group): Sham group (200 ul of PBS), Sham + BMSCs-Exo group (200 ul of BMSCs-Exo), I/R group (200 ul of PBS) and I/R + BMSCs-Exo group (200 ul of BMSCs-Exo). After 10 days of adaptive feeding, all mice were injected intraperitoneally with 0.4-0.5 mL/100 g 1%Pentobarbital Sodium. I/R and I/R + BMSCs-Exo group mice were subjected to cardiac I/R injury induced by ligation of the left anterior descending artery (LAD) for 30 min followed by 24 h reperfusion. Sham and Sham + BMSCs-Exo mice were sham treated and subjected to the same surgical procedures as I/R mice except that they did not receive ligation of the left anterior descending coronary artery.

    Click to Show/Hide
Response regulation Cellular ferroptosis is involved in the pathogenesis of Ischemia-Reperfusion Injury. BMSCs-Exo lncRNA Mir9-3hg can inhibit ferroptosis by modulating the Pum2/PRDX6 axis to exhibit cardioprotective effectsinvivoandinvitro. Silence of PRDX6 markedly decreased cell proliferation, GSH content and Gpx4 protein level, as well as prominently increased iron ion concentration and levels of ROS content and ACSL4 protein in H/R-treated HL-1 cells.
Ischemia/reperfusion injury [ICD-11: DB98]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator MIR9-3HG (IncRNA) lncRNA
 Regulator Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
hBMSCs (Bone marrow stromal cells)
In Vivo Model
A total of 96 C57BL/6 male mice (20-25 g) aged 11-12 weeks were purchased from experimental animal center of experimental animal center of Guangdong Medical University. 96 mice were randomly divided into four groups (24 mice per group): Sham group (200 ul of PBS), Sham + BMSCs-Exo group (200 ul of BMSCs-Exo), I/R group (200 ul of PBS) and I/R + BMSCs-Exo group (200 ul of BMSCs-Exo). After 10 days of adaptive feeding, all mice were injected intraperitoneally with 0.4-0.5 mL/100 g 1%Pentobarbital Sodium. I/R and I/R + BMSCs-Exo group mice were subjected to cardiac I/R injury induced by ligation of the left anterior descending artery (LAD) for 30 min followed by 24 h reperfusion. Sham and Sham + BMSCs-Exo mice were sham treated and subjected to the same surgical procedures as I/R mice except that they did not receive ligation of the left anterior descending coronary artery.

    Click to Show/Hide
Response regulation Cellular ferroptosis is involved in the pathogenesis of Ischemia-Reperfusion Injury. BMSCs-Exo lncRNA Mir9-3hg can inhibit ferroptosis by modulating the Pum2/PRDX6 axis to exhibit cardioprotective effectsinvivoandinvitro. Silence of PRDX6 markedly decreased cell proliferation, GSH content and Gpx4 protein level, as well as prominently increased iron ion concentration and levels of ROS content and ACSL4 protein in H/R-treated HL-1 cells.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator MIR9-3HG (IncRNA) lncRNA
 Regulator Info 
Pathway Response Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 HL-1 cells Normal Mus musculus CVCL_0303
hBMSCs (Bone marrow stromal cells)
In Vivo Model
A total of 96 C57BL/6 male mice (20-25 g) aged 11-12 weeks were purchased from experimental animal center of experimental animal center of Guangdong Medical University. 96 mice were randomly divided into four groups (24 mice per group): Sham group (200 ul of PBS), Sham + BMSCs-Exo group (200 ul of BMSCs-Exo), I/R group (200 ul of PBS) and I/R + BMSCs-Exo group (200 ul of BMSCs-Exo). After 10 days of adaptive feeding, all mice were injected intraperitoneally with 0.4-0.5 mL/100 g 1%Pentobarbital Sodium. I/R and I/R + BMSCs-Exo group mice were subjected to cardiac I/R injury induced by ligation of the left anterior descending artery (LAD) for 30 min followed by 24 h reperfusion. Sham and Sham + BMSCs-Exo mice were sham treated and subjected to the same surgical procedures as I/R mice except that they did not receive ligation of the left anterior descending coronary artery.

    Click to Show/Hide
Response regulation Cellular ferroptosis is involved in the pathogenesis of Ischemia-Reperfusion Injury. BMSCs-Exo lncRNA Mir9-3hg can inhibit ferroptosis by modulating the Pum2/PRDX6 axis to exhibit cardioprotective effectsinvivoandinvitro. Silence of PRDX6 markedly decreased cell proliferation, GSH content and Gpx4 protein level, as well as prominently increased iron ion concentration and levels of ROS content and ACSL4 protein in H/R-treated HL-1 cells.
References
Ref 1 The BMSC-derived exosomal lncRNA Mir9-3hg suppresses cardiomyocyte ferroptosis in ischemia-reperfusion mice via the Pum2/PRDX6 axis. Nutr Metab Cardiovasc Dis. 2022 Feb;32(2):515-527. doi: 10.1016/j.numecd.2021.10.017. Epub 2021 Nov 3.