YTHDF1 Regulates Pulmonary Hypertension through Translational Control of MAGED1

Hu, Li; Wang, Jie; Huang, Huijie; Yu, Yizhen; Ding, Jingjing; Yu, Youjia; Li, Kai; Dong, Wei; Ye, Qing; Wang, Fangzhu; Shen, Bin; Chen, Jingyu; Fulton, David; Chen, Feng

doi:10.1164/rccm.202009-3419oc

Cited by 88 publications

(92 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Discussionmentioning

confidence: 91%

“…Recent study confirmed that elevated m 6 A methylation and increased expression of YTHDF1 exist in pulmonary arterial hypertension, furthermore, YTHDF1 promotes pulmonary artery smooth muscle cells proliferation and PAH via enhancing MAGED1 translation [ 44 ]. However, there are only sporadic study concerned expression and function of methylation modifying enzymes in PAH [ 44 , 45 ]. In this study, expression of methylation modifying enzyme in lung tissues of PAH rats was detected, results showed decreased expressions of FTO and ALKBH5 accompanied with increased expressions of METTL3 and YTHDF1, while there was no significant difference in expressions of other methylation modifying enzyme between PAH and control rats.…”

Section: Discussionmentioning

confidence: 91%

See 1 more Smart Citation

Integrated analysis of m6A mRNA methylation in rats with monocrotaline-induced pulmonary arterial hypertension

Zeng

Huang

Zuo

et al. 2021

Aging

View full text Add to dashboard Cite

Background: N6-methyladenosine (m 6 A) modification is one of the most common chemical modifications of eukaryotic mRNAs, which play an important role in tumors and cardiovascular disease through regulating mRNA stability, splicing and translation. However, the changes of m 6 A mRNA and m 6 A-related enzymes in pulmonary arterial hypertension (PAH) remain largely unexplored. Methods: MeRIP-seq was used to identify m 6 A methylation in lung tissues from control and MCT-PAH rats. Western blot and immunofluorescence were used to evaluate expression of m 6 A-related enzymes. Results: Compared with control group, m 6 A methylation was mainly increased in lung tissues from MCT-PAH rats. The up-methylated coding genes in MCT-PAH rats were primarily enriched in processes associated with inflammation, glycolysis, ECM-receptor interaction and PDGF signal pathway, while genes with down-methylation were enriched in processes associated with TGF-β family receptor members. The expression of FTO and ALKBH5 downregulated, METTL3 and YTHDF1 increased and other methylation modification-related proteins was not significantly changed in MCT-PAH rats lung tissues. Immunofluorescence indicated that expression of FTO decreased and YTHDF1 increased in small pulmonary arteries of MCT-PAH rats. Conclusion: m 6 A levels and the expression of methylation-related enzymes were altered in PAH rats, in which FTO and YTHDF1 may play a crucial role in m 6 A modification.

show abstract

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 91%

Integrated analysis of m6A mRNA methylation in rats with monocrotaline-induced pulmonary arterial hypertension

Zeng

Huang

Zuo

et al. 2021

Aging

View full text Add to dashboard Cite

show abstract

“…YTHDF1 specifically binds to m6A-containing mRNAs and accelerates cap-dependent translation by recruiting eIF3, eIF4E, eIF4G, PABP and the 40S ribosomal subunit ( 108 ). As a ‘reader’ protein, YTHDF1 is also involved in several biological processes such as enhances protein synthesis and regulate Pulmonary Hypertension ( 42 , 109 ). A previous study demonstrated that YTHDF1 promotes the translation of mA-methylated neuronal mRNAs, which contributes to learning and memory ( 110 ).…”

Section: Enzymes and Proteins Involved In Modification By M6amentioning

confidence: 99%

Role of m6A in osteoporosis, arthritis and osteosarcoma (Review)

Zhao

2021

Exp Ther Med

View full text Add to dashboard Cite

RNA modification is a type of post-transcriptional modification that regulates important cellular pathways, such as the processing and metabolism of RNA. The most abundant form of methylation modification is RNA N6-methyladenine (m6A), which plays various post-transcriptional regulatory roles in cellular biological functions, including cell differentiation, embryonic development and disease occurrence. Bones play a pivotal role in the skeletal system as they support and protect muscles and other organs, facilitate movement and ensure haematopoiesis. The development and remodelling of bones require a delicate and accurate regulation of gene expression by epigenetic mechanisms that involve modifications of histone, DNA and RNA. The present review discusses the enzymes and proteins involved in mRNA m6A methylation modification and summarises current research progress and the mechanisms of mRNA m6A methylation in common orthopaedic diseases, including osteoporosis, arthritis and osteosarcoma.

show abstract

“…The functions of YTHDFs mainly depend on YTHDF1/2. YTHDF1 is linked to translation and metabolism 5 , 6 , while YTHDF2 is a well-studied m6A “reader” protein and influences mRNA stability and accelerates mRNA degradation 7 . Insulin-like growth factor-2 mRNA-binding proteins (IGF2BPs including IGF2BP1/2/3) are another category of “reader”, they could promote the stability and storage of their target mRNAs to affect gene expression 8 .…”

Section: Introductionmentioning

confidence: 99%

The interplay between m6A modification and non-coding RNA in cancer stemness modulation: mechanisms, signaling pathways, and clinical implications

Qin¹,

Mao²,

Wang³

et al. 2021

Int. J. Biol. Sci.

View full text Add to dashboard Cite

Cancer stemness, mainly consisting of chemo-resistance, radio-resistance, tumorigenesis, metastasis, tumor self-renewal, cancer metabolism reprogramming, and tumor immuno-microenvironment remodeling, play crucial roles in the cancer progression process and has become the hotspot of cancer research field in recent years. Nowadays, the exact molecular mechanisms of cancer stemness have not been fully understood. Extensive studies have recently implicated that non-coding RNA (ncRNA) plays vital roles in modulating cancer stemness. Notably, N6-methyladenosine (m6A) modification is of crucial importance for RNAs to exert their biological functions, including RNA splicing, stability, translation, degradation, and export. Emerging evidence has revealed that m6A modification can govern the expressions and functions of ncRNAs, consequently controlling cancer stemness properties. However, the interaction mechanisms between ncRNAs and m6A modification in cancer stemness modulation are rarely investigated. In this review, we elucidate the recent findings on the relationships of m6A modification, ncRNAs, and cancer stemness. We also focus on some key signaling pathways such as Wnt/β-catenin signaling, MAPK signaling, Hippo signaling, and JAK/STAT3 signaling to illustrate the underlying interplay mechanisms between m6A modification and ncRNAs in cancer stemness. In particular, we briefly highlight the clinical potential of ncRNAs and m6A modifiers as promising biomarkers and therapeutic targets for indicating cancer stemness properties and improving the diagnostic precision for a wide variety of cancers.

show abstract

YTHDF1 Regulates Pulmonary Hypertension through Translational Control of MAGED1

Cited by 88 publications

References 31 publications

Integrated analysis of m6A mRNA methylation in rats with monocrotaline-induced pulmonary arterial hypertension

Integrated analysis of m6A mRNA methylation in rats with monocrotaline-induced pulmonary arterial hypertension

Role of m6A in osteoporosis, arthritis and osteosarcoma (Review)

The interplay between m6A modification and non-coding RNA in cancer stemness modulation: mechanisms, signaling pathways, and clinical implications

Contact Info

Product

Resources

About