General Information of the Ferroptosis Regulator (ID: REG20105)
Regulator Name rno-miR-335 (miRNA)
Synonyms
rno-miR-335
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Gene Name rno-miR-335
Regulator Type miRNA
MiRBase ID MIMAT0000575
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
rno-miR-335 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
Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Marker/Suppressor
Responsed Disease Parkinson disease ICD-11: 8A00
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
In Vivo Model
A total of 48 male Sprague-Dawley rats (weighing, 180-220 g; 6-8 weeks of age) were purchased from the Animal Center of Guangzhou University of Chinese Medicine (Guangzhou, China). The rats were anesthetized (100 mg/kg ketamine and 10 mg/kg xylazine, intraperitoneal injection) and placed in a stereotaxic apparatus with the skull flat. An intracerebral injection of 6-OHDA was performed at 2 sites in the right SN pars compacta (SNpc) and ventral tegmental area (VTA): Anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.9 mm; dorsoventral (D/V)=-7.5 mm; and anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.1 mm; dorsoventral (D/V)=8.0 mm. During the surgery, body temperature was maintained at ~36.5 using a heating pad. All rats received meticulous post-operative care.

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Response regulation MiR335 promotes ferroptosis by targeting FTH1 inin vitroandin vivomodels of Parkinson's disease, providing a potential therapeutic target for the treatment of PD. Mechanistically, miR335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP).
Parkinson disease [ICD-11: 8A00]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator rno-miR-335 (miRNA) miRNA
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
PC12 cells Adrenal gland pheochromocytoma Rattus norvegicus CVCL_0481
In Vivo Model
A total of 48 male Sprague-Dawley rats (weighing, 180-220 g; 6-8 weeks of age) were purchased from the Animal Center of Guangzhou University of Chinese Medicine (Guangzhou, China). The rats were anesthetized (100 mg/kg ketamine and 10 mg/kg xylazine, intraperitoneal injection) and placed in a stereotaxic apparatus with the skull flat. An intracerebral injection of 6-OHDA was performed at 2 sites in the right SN pars compacta (SNpc) and ventral tegmental area (VTA): Anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.9 mm; dorsoventral (D/V)=-7.5 mm; and anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.1 mm; dorsoventral (D/V)=8.0 mm. During the surgery, body temperature was maintained at ~36.5 using a heating pad. All rats received meticulous post-operative care.

    Click to Show/Hide
Response regulation MiR335 promotes ferroptosis by targeting FTH1 inin vitroandin vivomodels of Parkinson's disease, providing a potential therapeutic target for the treatment of PD. Mechanistically, miR335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP).
References
Ref 1 miR335 promotes ferroptosis by targeting ferritin heavy chain 1 in invivo and invitro models of Parkinson's disease. Int J Mol Med. 2021 Apr;47(4):61. doi: 10.3892/ijmm.2021.4894. Epub 2021 Mar 2.