Noncoding RNA in Liver Regeneration—From Molecular Mechanisms to Clinical Implications

Sergeeva, Olga V.; Sviridov, Evgeny; Zatsepin, Timofei S.

doi:10.1055/s-0039-1693513

Cited by 10 publications

(4 citation statements)

References 214 publications

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“…As a lot of lncRNA change expression during liver regeneration [ 42 ], we measured LL35 RNA levels after partial hepatectomy [ 26 ] and found its downregulation 2 h after surgery followed by an increase in the RNA level during the liver’s regeneration ( Figure 1 C). In addition, in our previous study we demonstrated ~70% decrease in the LL35 lncRNA level in mouse liver two weeks after the induction of fibrosis with carbon tetrachloride [ 22 ].…”

Section: Resultsmentioning

confidence: 99%

Murine Falcor/LL35 lncRNA Contributes to Glucose and Lipid Metabolism In Vitro and In Vivo

et al. 2022

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Glucose and lipid metabolism are crucial functional systems in eukaryotes. A large number of experimental studies both in animal models and humans have shown that long non-coding RNAs (lncRNAs) play an important role in glucose and lipid metabolism. Previously, human lncRNA DEANR1/linc00261 was described as a tumor suppressor that regulates a variety of biological processes such as cell proliferation, apoptosis, glucose metabolism and tumorigenesis. Here we report that murine lncRNA Falcor/LL35, a proposed functional analog of human DEANR1/linc00261, is predominantly expressed in murine normal hepatocytes and downregulated in HCC and after partial hepatectomy. The application of high-throughput approaches such as RNA-seq, LC-MS proteomics, lipidomics and metabolomics analysis allowed changes to be found in the transcriptome, proteome, lipidome and metabolome of hepatocytes after LL35 depletion. We revealed that LL35 is involved in the regulation of glycolysis and lipid biosynthesis in vitro and in vivo. Moreover, LL35 affects Notch and NF-κB signaling pathways in normal hepatocytes. All observed changes result in the decrease in the proliferation and migration of hepatocytes. We demonstrated similar phenotype changes between murine LL35 and human linc00261 depletion in vitro and in vivo that opens the opportunity to translate results for LL35 from a liver murine model to possible functions of human lncRNA linc00261.

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Section: Resultsmentioning

confidence: 99%

Murine Falcor/LL35 lncRNA Contributes to Glucose and Lipid Metabolism In Vitro and In Vivo

et al. 2022

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“…Liver regeneration may occur after partial hepatectomy, liver transplantation, viral infection, IRI or toxic injury. The regeneration process is complex and well-orchestrated (41,42), and it has been widely studied in order to understand the mechanisms that regulate hepatocyte proliferation and survival (43,44). In normal adult mouse liver, mature differentiated hepatocytes are not vegetative and are quiescent.…”

Section: Complement Cascades Are Essential In Liver Recovery and Regementioning

confidence: 99%

Emerging recognition of the complement system in hepatic ischemia/reperfusion injury, liver regeneration and recovery (Review)

Zhou

Lin

et al. 2021

Exp Ther Med

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Hepatic ischemia/reperfusion injury (IRI) is a result of the ischemic cascade and may occur in the settings of liver trauma, resection and transplantation. Components of the complement system have been indicated to be mediators of hepatic IRI and regulators of liver regeneration. As such, their potential to mediate both beneficial and harmful effects render them key targets for therapy. In the present study, the mechanisms of complement mediating hepatic IRI were discussed with a focus on the different functions of complement in hepatic injury and liver recovery, and an explanation for this apparent paradox is provided, i.e. that the complement products C3a and C5a have an important role in liver damage; however, C3a and C5a are also necessary for liver regeneration. Furthermore, situated at the end of the complement activation cascade, the membrane attack complex is crucial in hepatic IRI and inhibiting the complex with a site-targeted murine complement inhibitor, complement receptor 2-CD59, may improve liver regeneration after partial hepatectomy, even when hepatectomy is combined with ischemia and reperfusion. Contents 1. Introduction 2. Complement-mediated injury cascades in hepatic IRI 3. Complement cascades are essential in liver recovery and regeneration 4. Complement regulation between hepatic IRI and liver regeneration 5. Future perspective

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“…It is known that the liver has a high-level ability to regenerate damaged tissues compared with other organs [7]. In addition, regenerative medicine, as one of the interdisciplinary areas of the translational science that attracts the attention of the global research community, uses tissue engineering and stem cell therapy to replace a damaged organ with an artificial organ that is in direct connection with the immune system [8]. In various original reports or review articles, molecular and functional mechanisms have been investigated in detail in experimental models (e.g., in rats and mice) and in clinical studies to identify important genes and signaling pathways involved in the liver regeneration [7].…”

Section: Introductionmentioning

confidence: 99%

Mitochondria stimulate liver regeneration in rats

Kit¹,

Frantsiyants²,

Neskubina³

et al. 2022

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Regenerative medicine is a vital area that advances methods addressing the process of liver regeneration. The liver has the unique ability to return to standard size within a short period of time after its injury or partial hepatectomy. Hepatocytes are highly active metabolic cells, which have a large number of mitochondria, suggesting a biologically significant role for the mitochondrial dynamics in hepatocyte damage and repair. The aim hereof is to develop a method for accelerating the process of liver regeneration in rats based on the transplantation of mitochondria isolated from the liver of intact rats. Materials and methods. Experimental animals (n = 30) used by us were white outbred rats divided into groups as follows: 1) a comparison group to include intact animals (n = 10); 2) a reference group with liver resection + use of saline solution (n = 10); 3) the main group with liver resection + mitochondrial therapy (MCT) (n = 10). In the reference and the main groups, under xylazoletil anesthesia, median laparotomy was performed and the maximum allowable resection of the left lobe of the liver was executed. Mitochondria of the intact liver were diluted with a 0.9% NaCl solution to a protein concentration of 11.6 g/l and injected into the post-surgery rats of the main group (group No. 3). The above procedure was carried out for 14 days. Animals of the reference group were intraperitoneally injected with 0.5 ml of saline solution according to a similar scheme. Statistical analysis was performed with the Statistica 10.0 Software. Results. According to the weight indices of the liver after MCT, the mass of the organ increased by a factor of 1.7 р˂0.05) relative to the reference group without MCT. At the same time, compared with the indicators in animals of the comparison group (intact animals), the mass of the organ exceeded 1.6 times (p˂0.05), and the liver stump itself during MCT in its mass exceeded by 3.2 times the weight indicators of the liver stump in rats without the MCT. Conclusion. As a result of the experiment on the use of MCT of the liver, it can be concluded that the resection of the liver lobe and subsequent processes in the liver tissue against the background of MCT acquire pronounced features of accelerating the physiological regeneration, addressing the restoration of stromal and parenchymal components.

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Noncoding RNA in Liver Regeneration—From Molecular Mechanisms to Clinical Implications

Cited by 10 publications

References 214 publications

Murine Falcor/LL35 lncRNA Contributes to Glucose and Lipid Metabolism In Vitro and In Vivo

Murine Falcor/LL35 lncRNA Contributes to Glucose and Lipid Metabolism In Vitro and In Vivo

Emerging recognition of the complement system in hepatic ischemia/reperfusion injury, liver regeneration and recovery (Review)

Mitochondria stimulate liver regeneration in rats

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