General Information of the Ferroptosis Regulator (ID: REG20028)
Regulator Name hsa-miR-9-5p (miRNA)
Synonyms
hsa-miR-9-5p
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Gene Name hsa-miR-9-5p
Regulator Type miRNA
MiRBase ID MIMAT0000441
Sequence
UCUUUGGUUAUCUAGCUGUAUGA

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Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-9-5p 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
Transferrin receptor protein 1 (TFRC) [Driver; Suppressor; Marker]
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Marker/Suppressor/Driver
Responsed Disease Sepsis ICD-11: 1G40
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell apoptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). The rats were housed under room temperatures (25 ± 2 and 12-h light/dark cycle) and given water and food ad libitum before the trial. Then, they were randomly assigned into the control group (n = 10), model group (n = 10), and model + miR-9-5p angomir group (n = 10). All animal procedures were performed under the Care and Use of Laboratory Animals guidelines and approved by the Guangdong Academy of Medical Sciences. According to a previous study, sepsis was induced by the cecal ligation and puncture (CLP) method. Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

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Response regulation NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro.
Experiment 2 Reporting the Ferroptosis Target of This Regulator [2]
Target for Ferroptosis Marker/Suppressor/Driver
Responsed Disease Sepsis ICD-11: 1G40
Pathway Response Glutathione metabolism hsa00480
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

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Response regulation Sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate sepsis-associated encephalopathy (SAE) by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis. And NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression.
Aspartate aminotransferase, cytoplasmic (GOT1) [Driver; Suppressor]
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver/Suppressor
Responsed Disease Sepsis ICD-11: 1G40
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell apoptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). The rats were housed under room temperatures (25 ± 2 and 12-h light/dark cycle) and given water and food ad libitum before the trial. Then, they were randomly assigned into the control group (n = 10), model group (n = 10), and model + miR-9-5p angomir group (n = 10). All animal procedures were performed under the Care and Use of Laboratory Animals guidelines and approved by the Guangdong Academy of Medical Sciences. According to a previous study, sepsis was induced by the cecal ligation and puncture (CLP) method. Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

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Response regulation NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro.
Experiment 2 Reporting the Ferroptosis Target of This Regulator [2]
Target for Ferroptosis Driver/Suppressor
Responsed Disease Sepsis ICD-11: 1G40
Pathway Response Glutathione metabolism hsa00480
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

    Click to Show/Hide
Response regulation Sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate sepsis-associated encephalopathy (SAE) by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis. And NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression.
Sepsis [ICD-11: 1G40]
In total 4 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator hsa-miR-9-5p (miRNA) miRNA
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell apoptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). The rats were housed under room temperatures (25 ± 2 and 12-h light/dark cycle) and given water and food ad libitum before the trial. Then, they were randomly assigned into the control group (n = 10), model group (n = 10), and model + miR-9-5p angomir group (n = 10). All animal procedures were performed under the Care and Use of Laboratory Animals guidelines and approved by the Guangdong Academy of Medical Sciences. According to a previous study, sepsis was induced by the cecal ligation and puncture (CLP) method. Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

    Click to Show/Hide
Response regulation NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro.
Experiment 2 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator hsa-miR-9-5p (miRNA) miRNA
Pathway Response Glutathione metabolism hsa00480
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

    Click to Show/Hide
Response regulation Sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate sepsis-associated encephalopathy (SAE) by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis. And NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression.
Experiment 3 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator hsa-miR-9-5p (miRNA) miRNA
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
Cell apoptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). The rats were housed under room temperatures (25 ± 2 and 12-h light/dark cycle) and given water and food ad libitum before the trial. Then, they were randomly assigned into the control group (n = 10), model group (n = 10), and model + miR-9-5p angomir group (n = 10). All animal procedures were performed under the Care and Use of Laboratory Animals guidelines and approved by the Guangdong Academy of Medical Sciences. According to a previous study, sepsis was induced by the cecal ligation and puncture (CLP) method. Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

    Click to Show/Hide
Response regulation NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression. Overexpression of NEAT1 enhanced ferroptosis stress in bEnd.3 cells. Increased miR-9-5p alleviated sepsis-induced ferroptosis by suppressing the expression of TFRC and GOT1 both in vivo and in vitro.
Experiment 4 Reporting the Ferroptosis-centered Disease Response [2]
Target Regulator hsa-miR-9-5p (miRNA) miRNA
Pathway Response Glutathione metabolism hsa00480
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
bEnd.3 cells Normal Mus musculus CVCL_0170
In Vivo Model
Thirty specific-pathogen-free (SPF) male C57BL/6 rats at 8 weeks weighing 200-250 g were obtained from the Experimental Animal Center of Sun Yat-sen University (Guangzhou, China). Briefly, we anesthetized the rats with 5% chloral hydrate (0.6 ml/100 g body weight) and made a 1.5 cm midline incision on the anterior abdomen to expose the cecum. Then, the cecum was ligated at 30%, punctured twice with a No.4 surgical needle to extrude the fecal content. Finally, 1 ml of normal saline was used for resuscitation. The rats in miR-9-5p angomir group were injected with 100 ng/ul miR-9-5p angomir (RiboBio, Guangzhou, China) into caudal vein (model + miR-9-5p angomir). The rats in the control group experienced the same procedure without ligation and puncture.

    Click to Show/Hide
Response regulation Sepsis induced high expression of serous exosome-derived NEAT1, and it might exacerbate sepsis-associated encephalopathy (SAE) by promoting ferroptosis through regulating miR-9-5p/TFRC and GOT1 axis. And NEAT1 functions as a ceRNA for miR-9-5p to facilitate TFRC and GOT1 expression.
References
Ref 1 Exosome-Derived lncRNA NEAT1 Exacerbates Sepsis-Associated Encephalopathy by Promoting Ferroptosis Through Regulating miR-9-5p/TFRC and GOT1 Axis. Mol Neurobiol. 2022 Mar;59(3):1954-1969. doi: 10.1007/s12035-022-02738-1. Epub 2022 Jan 17.
Ref 2 Correction to: Exosome-Derived lncRNA NEAT1 Exacerbates Sepsis-Associated Encephalopathy by Promoting Ferroptosis Through Regulating miR-9-5p/ TFRC and GOT1 Axis. Mol Neurobiol. 2022 Aug;59(8):5252. doi: 10.1007/s12035-022-02931-2.