Long Non-Coding RNA H19 Promotes Porcine Satellite Cell Differentiation by Interacting with TDP43

Li, Jingxuan; Zhao, Wenjuan; Li, Qianqian; Huang, Ziying; Shi, Gaoli; Li, Changchun

doi:10.3390/genes11030259

Cited by 18 publications

(13 citation statements)

References 45 publications

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“…There is increasing evidence that lncRNAs are functionally conserved among species. 15 , 23 , 24 The functional conservation of lncRNAs among species can be explained as follows: lncRNAs have conserved binding domains and secondary or higher structures. For example, the 2D structure of the A region of Xist can recruit components of PRC2 that are needed for X‐chromosome inactivation.…”

Section: Discussionmentioning

confidence: 99%

Conservative analysis of Synaptopodin‐2 intron sense‐overlapping lncRNA reveals its novel function in promoting muscle atrophy

Jin

Wang

et al. 2022

J cachexia sarcopenia muscle

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Background Dissection of the regulatory pathways that control skeletal muscle development and atrophy is important for the treatment of muscle wasting. Long noncoding RNA (lncRNA) play important roles in various stages of muscle development. We previously reported that Synaptopodin‐2 (SYNPO2) intron sense‐overlapping lncRNA (SYISL) regulates myogenesis through an interaction with enhancer of zeste homologue 2 (EZH2). However, it remains unclear whether SYISL homologues exist in humans and pigs, and whether the functions and mechanisms of these homologues are conserved among species. Methods Bioinformatics, cell fractionation, and quantitative real‐time polymerase chain reaction (qRT‐PCR) analyses were used for the identification and molecular characterization of SYISL homologues in humans and pigs. Effects on myogenesis and muscle atrophy were determined via loss‐of‐function or gain‐of‐function experiments using C2C12 myoblasts, myogenic progenitor cells, dexamethasone (DEX), and aging‐induced muscle atrophy models. RNA pulldown, RNA immunoprecipitation, dual luciferase reporting, and co‐transfection experiments were used to explore the mechanisms of SYISL interactions with proteins and miRNAs. Results We identified SYISL homologues in humans (designated hSYISL) and pigs (designated pSYISL). Functional experiments demonstrated that hSYISL and pSYISL regulate myogenesis through interactions with EZH2. Interestingly, we showed that SYISL functions to regulate muscle atrophy and sarcopenia through comparative analysis. SYISL is significantly up‐regulated after muscle atrophy (P < 0.01); it significantly promotes muscle atrophy in DEX‐induced muscle atrophy models (P < 0.01). SYISL knockdown or knockout alleviates muscle atrophy and sarcopenia in DEX‐induced and aged mice. The tibialis anterior (TA) muscle weight of 3‐month‐old wild‐type (WT) mice decreased by 33.24% after DEX treatment (P < 0.001), while the muscle weight loss of 3‐month‐old SYISL knockout mice was only 18.20% after DEX treatment (P < 0.001). SYISL knockout in 18‐month‐old WT mice significantly increased the weights of quadriceps (Qu), gastrocnemius (Gas), and TA muscles by 10.45% (P < 0.05), 13.95% (P < 0.01), and 24.82% (P < 0.05), respectively. Mechanistically, SYISL increases the expression levels of the muscle atrophy genes forkhead box protein O3a (FoxO3a), muscle ring finger 1 (MuRF1), and muscle atrophy‐related F‐box (Atrogin‐1) via sponging of miR‐23a‐3p/miR‐103‐3p/miR‐205‐5p and thus promotes muscle atrophy. Additionally, we verified that human SYISL overexpression in muscles of 18‐month‐old WT mice significantly decreased the weights of Gas, Qu, and TA muscles by 7.76% (P < 0.01), 12.26% (P < 0.05), and 13.44% (P < 0.01), respectively, and accelerates muscle atrophy through conserved mechanisms. Conclusions Our results identify SYISL as a conserved lncRNA that modulates myogenesis in mice, pigs, and humans. We also demonstrated its previously unknown ability to promote muscle atrophy.

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Section: Discussionmentioning

confidence: 99%

Conservative analysis of Synaptopodin‐2 intron sense‐overlapping lncRNA reveals its novel function in promoting muscle atrophy

Jin

Wang

et al. 2022

J cachexia sarcopenia muscle

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“…Recently, Li et al found that the lncRNA MSTRG.42019 was associated with skeletal muscle fiber-type switching in pigs [ 53 ]. Several lncRNAs, such as LncMyoD , SAM , H19 , and CTTN-IT1 , affect the activity of satellite cells in mice, pigs, and sheep [ 54 , 55 , 56 , 57 ]. The in vivo silencing of Pvt1 results in increases in the size and number of mitochondria [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

Hitachi

Nakatani

Kiyofuji

et al. 2021

IJMS

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The loss of skeletal muscle mass (muscle atrophy or wasting) caused by aging, diseases, and injury decreases quality of life, survival rates, and healthy life expectancy in humans. Although long non-coding RNAs (lncRNAs) have been implicated in skeletal muscle formation and differentiation, their precise roles in muscle atrophy remain unclear. In this study, we used RNA-sequencing (RNA-Seq) to examine changes in the expression of lncRNAs in four muscle atrophy conditions (denervation, casting, fasting, and cancer cachexia) in mice. We successfully identified 33 annotated lncRNAs and 18 novel lncRNAs with common expression changes in all four muscle atrophy conditions. Furthermore, an analysis of lncRNA–mRNA correlations revealed that several lncRNAs affected small molecule biosynthetic processes during muscle atrophy. These results provide novel insights into the lncRNA-mediated regulatory mechanism underlying muscle atrophy and may be useful for the identification of promising therapeutic targets.

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“…Recently, Li reported that 2310043L19Rik (lnc-231) inhibited differentiation and promoted proliferation of myoblasts as ceRNA to target miR-125a-5p, thereby inhibiting the function of E2F3 mRNA (Li et al, 2020b ). Conversely, H19 can act as a molecular scaffold to recruit TDP43 to promoters of MyoD and activate transcription, thereby promoting porcine SC differentiation (Li et al, 2020a ). Furthermore, some lncRNAs can give rise to functional micropeptides.…”

Section: Lncrnas In Myogenesismentioning

confidence: 99%

Functional Non-coding RNA During Embryonic Myogenesis and Postnatal Muscle Development and Disease

Luo

Tong

et al. 2021

Front. Cell Dev. Biol.

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Skeletal muscle is a highly heterogeneous tissue that plays a crucial role in mammalian metabolism and motion maintenance. Myogenesis is a complex biological process that includes embryonic and postnatal development, which is regulated by specific signaling pathways and transcription factors. Various non-coding RNAs (ncRNAs) account for the majority of total RNA in cells and have an important regulatory role in myogenesis. In this review, we introduced the research progress in miRNAs, circRNAs, and lncRNAs related to embryonic and postnatal muscle development. We mainly focused on ncRNAs that regulate myoblast proliferation, differentiation, and postnatal muscle development through multiple mechanisms. Finally, challenges and future perspectives related to the identification and verification of functional ncRNAs are discussed. The identification and elucidation of ncRNAs related to myogenesis will enrich the myogenic regulatory network, and the effective application of ncRNAs will enhance the function of skeletal muscle.

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Long Non-Coding RNA H19 Promotes Porcine Satellite Cell Differentiation by Interacting with TDP43

Cited by 18 publications

References 45 publications

Conservative analysis of Synaptopodin‐2 intron sense‐overlapping lncRNA reveals its novel function in promoting muscle atrophy

Conservative analysis of Synaptopodin‐2 intron sense‐overlapping lncRNA reveals its novel function in promoting muscle atrophy

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

Functional Non-coding RNA During Embryonic Myogenesis and Postnatal Muscle Development and Disease

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