mmu-lncRNA 121686/hsa-lncRNA 520657 induced by METTL3 drive the progression of AKI by targeting miR-328-5p/HtrA3 signaling axis

Pan, Jian; Xie, Yuxin; Li, Huiling; Li, Xiaozhou; Chen, Junxiang; Liu, Xiangfeng; Zhou, Jun; Tang, Xianming; He, Zhijun; Peng, Zhenyu; Zhang, Hongliang; Li, Yijian; Xiang, Xudong; Yuan, Yunchang; Zhang, Dongshan

doi:10.1016/j.ymthe.2022.07.014

Cited by 25 publications

(13 citation statements)

References 48 publications

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“…The RNA m6A level in AKI renal tissues was higher than that in control tissues 66 , suggesting a vital role of m6A in AKI, and berberine may alleviate this process 67 . Meanwhile, genetic and pharmacological inhibition of METTL3, a typical m6A writer, attenuated renal injury and inflammation 68 , 69 . IGF2BP1 is one of the common m6A readers but has not been reported in septic AKI; however, studies confirmed that its level could be elevated when induced by LPS and regulate the inflammatory responses 24 , 70 .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

Mao

Jiang

et al. 2023

Int. J. Biol. Sci.

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Septic acute kidney injury (AKI) is characterized by inflammation. Pyroptosis often occurs during AKI and is associated with the development of septic AKI. This study found that induction of insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to a higher level can induce pyroptosis in renal tubular cells. Meanwhile, macrophage migration inhibitory factor (MIF), a subunit of NLRP3 inflammasomes, was essential for IGF2BP1-induced pyroptosis. A putative m6A recognition site was identified at the 3′-UTR region of E2F transcription factor 1 (E2F1) mRNA via bioinformatics analyses and validated using mutation and luciferase experiments. Further actinomycin D (Act D) chase experiments showed that IGF2BP1 stabilized E2F1 mRNA dependent on m6A. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) indicated that E2F1 acted as a transcription factor to promote MIF expression. Thus, IGF2BP1 upregulated MIF through directly upregulating E2F1 expression via m6A modification. Experiments on mice with cecum ligation puncture (CLP) surgery verified the relationships between IGF2BP1, E2F1, and MIF and demonstrated the significance of IGF2BP1 in MIF-associated pyroptosis in vivo. In conclusion, IGF2BP1 was a potent pyroptosis inducer in septic AKI through targeting the MIF component of NLRP3 inflammasomes. Inhibiting IGF2BP1 could be an alternate pyroptosis-based treatment for septic AKI.

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Section: Discussionmentioning

confidence: 99%

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

Mao

Jiang

et al. 2023

Int. J. Biol. Sci.

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“…Total RNA was extracted from BUMPT cells and mouse kidney cortex with Trizol, and 1 μg of it was reversed to single-stranded DNA by using Evo M-MLV. For the cytoplasmic and nuclear RNA separation, BUMPT cell fractionation and purification were conducted using the Cytoplasmic and Nuclear RNA Purification Kit (Norgen, #21000,37400) [ 22 ]. RT-qPCR was carried out using the LightCycler ® 480 II (Basel, Switzerland).…”

Section: Methodsmentioning

confidence: 99%

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

Wang

Zhang

2022

Cells

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Background: Numerous studies have suggested that long non-coding RNA (lncRNA) affects the progression of ischemic acute kidney injury (IAKI). However, little information is currently available concerning the mechanisms of lncRNA171502 involved in IAKI. Methods: We applied an RT-qPCR assay for the expression of lncRNA171502 and miRNA-130b-3p, immunoblotting for the detection of Mybl-1-myeloblastosis oncogene-like 1 (Mybl-1) and cleaved caspase-3 (CC3) expression, and flow cytometry (FCM) for the evaluation of apoptosis. Result: Initially, lncRNA171502 was induced by HIF-1α in the mouse proximal tubular (BUMPT) cell line and C57BL/6J mice during ischemic injury. Secondly, ischemic injury-induced BUMPT cell apoptosis was markedly relieved following the overexpression of lncRNA171502. However, this effect was enhanced by the knockdown of lncRNA171502. Mechanistically, lncRNA171502 could sponge miRNA-130b-3p and would subsequently upregulate the expression of Mybl-1 to drive the apoptotic process. Lastly, the overexpression of lncRNA171502 alleviated the development of IAKI by targeting miRNA-130b-3p/Mybl-1 pathways. Conclusions: In summary, the HIF-1α/lncRNA171502/miRNA-130b-3p/Mybl-1 axis prevented the progression of IAKI and might serve as a potential therapeutic target.

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“…A recent study found that METTL3 directly binds to the m 6 A sites of mmu-lncRNA 121686 and hsa-lncRNA 520657 to enhance their modification and expression, which facilitates lncRNA direct sponging of miR-328-5p to aggravate high-temperature requirement factor A 3 (Htra3)-mediated tubular epithelial cell apoptosis and ischaemia-reperfusion-, sepsisand vancomycin-induced AKI. This finding revalidated the target potential and intervention value of METTL3-mediated m 6 A modification in the progression of AKI(Pan et al, 2022). Additionally, METTL14 enhanced the methylation of yes-associated protein 1 (YAP1) mRNA through an m 6 Adependent mechanism and decreased its level by accelerating the decay rate of YAP1 mRNA, thereby inhibiting YAP1-TEAD signalling and promoting the progression of I/R-AKI(Xu et al, 2020).…”

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confidence: 88%

RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

et al. 2022

British J Pharmacology

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Epigenetic modifications have received increasing attention and have been shown to be extensively involved in kidney development and disease progression. Among them, the most common RNA modification, N6‐methyladenosine (m6A), has been shown to dynamically and reversibly exert its functions in multiple ways, including splicing, export, decay and translation initiation efficiency to regulate mRNA fate. Moreover, m6A has also been reported to exert biological effects by destabilizing base pairing to modulate various functions of RNAs. Most importantly, an increasing number of kidney diseases, such as renal cell carcinoma, acute kidney injury and chronic kidney disease, have been found to be associated with aberrant m6A patterns. In this review, we comprehensively review the critical roles of m6A in kidney diseases and discuss the possibilities and relevance of m6A‐targeted epigenetic therapy, with an integrated comprehensive description of the detailed alterations in specific loci that contribute to cellular processes that are associated with kidney diseases.

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mmu-lncRNA 121686/hsa-lncRNA 520657 induced by METTL3 drive the progression of AKI by targeting miR-328-5p/HtrA3 signaling axis

Cited by 25 publications

References 48 publications

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

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mmu-lncRNA 121686/hsa-lncRNA 520657 induced by METTL3 drive the progression of AKI by targeting miR-328-5p/HtrA3 signaling axis

Cited by 25 publications

References 48 publications

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

Inhibition of IGF2BP1 attenuates renal injury and inflammation by alleviating m6A modifications and E2F1/MIF pathway

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis

RNA N6‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

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RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease