FAM49B, restrained by miR-22, relieved hepatic ischemia/reperfusion injury by inhibiting TRAF6/IKK signaling pathway in a Rac1-dependent manner

Huang, Zuotian; Pu, Jing; Luo, Yunhai; Fan, Jing; Li, Kaili; Peng, Dadi; Zong, Kezhen; Zhou, Baoyong; Guan, Xiangdong; Zhou, Fachun

doi:10.1016/j.molimm.2022.01.015

Cited by 9 publications

(2 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 120 FAM49B, constrained by miR-22, alleviates HIRI by inhibiting the TRAF6/IKK signal pathway in a Rac1-dependent manner. 121 …”

Section: Discussionmentioning

confidence: 99%

“…120 FAM49B, constrained by miR-22, alleviates HIRI by inhibiting the TRAF6/IKK signal pathway in a Rac1-dependent manner. 121 Taken together, we primarily concentrate on the related roles of p38, JNK and ERK1 / 2 in MAPK family in IR. It is worth noting that different researchers use different methods and time to create animal models, which may require more in-depth horizontal and vertical studies to compare these differences caused by different operation methods.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

MAPK Signaling Pathways in Hepatic Ischemia/Reperfusion Injury

Yu¹,

Zhang²,

Wang³

et al. 2023

JIR

View full text Add to dashboard Cite

The mitogen-activated protein kinase signaling pathway can be activated by a variety of growth factors, cytokines, and hormones, and mediates numerous intracellular signals related to cellular activities, including cell proliferation, motility, and differentiation. It has been widely studied in the occurrence and development of inflammation and tumor. Hepatic ischemia-reperfusion injury (HIRI) is a common pathophysiological phenomenon that occurs in surgical procedures such as lobectomy and liver transplantation, which is characterized by severe inflammatory reaction after ischemia and reperfusion. In this review, we mainly discuss the role of p38, ERK1/2, JNK in MAPK family and TAK1 and ASK1 in MAPKKK family in HIRI, and try to find an effective treatment for HIRI.

show abstract

“… 120 FAM49B, constrained by miR-22, alleviates HIRI by inhibiting the TRAF6/IKK signal pathway in a Rac1-dependent manner. 121 …”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MAPK Signaling Pathways in Hepatic Ischemia/Reperfusion Injury

Yu¹,

Zhang²,

Wang³

et al. 2023

JIR

View full text Add to dashboard Cite

show abstract

AEBP1 Silencing Protects Against Cerebral Ischemia/Reperfusion Injury by Regulating Neuron Ferroptosis and Microglia M2 Polarization Through PRKCA‐PI3K‐Akt Axis

Zhang,

Li,

Liu

2024

Drug Development Research

View full text Add to dashboard Cite

Cerebral ischemia/reperfusion injury is one of the main causes of neuronal damage. Neuron ferroptosis and microglia polarization are considered as critical processes during cerebral ischemia/reperfusion. Adipocyte enhancer‐binding protein 1 (AEBP1) usually acts as a transcriptional repressor which is involved in various diseases. However, it is still remains unknown whether AEBP1 could have important roles in regulating the neuron ferroptosis and microglia polarization in cerebral ischemia/reperfusion injury. The oxygen‐glucose deprivation and reperfusion (OGD/R)‐treated cells and middle cerebral artery occlusion (MCAO)‐treated mice were used as in vitro and in vivo models. The differentially expressed factors were analyzed according to GEO datasets. Relative mRNA and protein expression levels were detected by qRT‐PCR and western blot analysis. Cell viability was measured by CCK‐8 assay. ROS, GSH and iron contents were detected using specifical assay kits. CD26 and CD206 levels were measured by immunofluorescence assay. Inflammatory cytokines were detected by ELISA. The association between AEBP1 and PRKCA was assessed by luciferase reporter and ChIP analyses. The neuron damage in mice was analyzed by TTC staining and neurological deficit score. Transcription factor AEBP1 was increased in OGD/R‐treated HT22 and BV2 cells. AEBP1 silencing attenuated OGD/R‐induced HT22 cell ferroptosis through increasing cell viability, GSH and GPX4 levels, and decreasing ROS, iron and ACSL4 levels. AEBP1 knockdown promoted microglia M2 polarization by increasing CD206‐positive cells and Arg‐1 level, and reducing iNOS, TNF‐α, IL‐1β and IL‐6 levels in BV2 cells. AEBP1 transcriptionally repressed PRKCA expression, and further regulated PI3K/Akt signaling activation. Inhibition of PRKCA or PI3K/Akt reversed the effects of AEBP1 silencing on neuron ferroptosis and microglia M2 polarization. AEBP1 downregulation attenuated neuronal damage by decreasing infarct size and deficit scores in MCAO‐treated mice. AEBP1 silencing mitigated neuron ferroptosis and promoted microglia M2 polarization through increasing PRKCA and activating PI3K/Akt signaling, indicating the potentially protective action of AEBP1 knockdown in cerebral ischemia/reperfusion injury.

show abstract