Differentiation of Monocytic Cells Is Accompanied by a Change in the Expression of the Set of Oct-1 Isoforms

Степченко, А. Г.; Lyanova, B. M.; Крылова, И. Д.; Ilyin, Yu. V.; Георгиева, С. Г.; Pankratova, E. V.

doi:10.1134/s1607672918060066

Cited by 4 publications

(4 citation statements)

References 15 publications

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“…Pou2F1 (Pou Class 2 Homeobox 1, also known as Oct-1) isoforms were found to be the most upregulated DET (Pou2f1-208, ENS-MUST00000160260.9), as well as the most downregulated DET (Pou2f1-205, ENSMUST00000111427.9) by RGMa treatment in skeletal muscle cells. Although the specific functions of each of these isoforms have not been described thus far, it is known that Pou2F1 is an ubiquitously expressed member of the Pou transcription factor family and is associated with a plethora of processes, including the activation of some snRNA, histone H2B, immunoglobulins, and other housekeeping genes [41], the regulation of the circadian clock [42], and glycolytic metabolism [43]. In skeletal muscle cells, this transcription factor was associated with the activation of pro-inflammatory immune response in patients with myalgia [44] and with MyHC IIB expression, when associated with MEF2 and the serum response factor (SRF) [45][46][47].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy

et al. 2022

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Background The repulsive guidance molecule a (RGMa) is a GPI-anchor axon guidance molecule first found to play important roles during neuronal development. RGMa expression patterns and signaling pathways via Neogenin and/or as BMP coreceptors indicated that this axon guidance molecule could also be working in other processes and diseases, including during myogenesis. Previous works from our research group have consistently shown that RGMa is expressed in skeletal muscle cells and that its overexpression induces both nuclei accretion and hypertrophy in muscle cell lineages. However, the cellular components and molecular mechanisms induced by RGMa during the differentiation of skeletal muscle cells are poorly understood. In this work, the global transcription expression profile of RGMa-treated C2C12 myoblasts during the differentiation stage, obtained by RNA-seq, were reported. Results RGMa treatment could modulate the expression pattern of 2,195 transcripts in C2C12 skeletal muscle, with 943 upregulated and 1,252 downregulated. Among them, RGMa interfered with the expression of several RNA types, including categories related to the regulation of RNA splicing and degradation. The data also suggested that nuclei accretion induced by RGMa could be due to their capacity to induce the expression of transcripts related to ‘adherens junsctions’ and ‘extracellular-cell adhesion’, while RGMa effects on muscle hypertrophy might be due to (i) the activation of the mTOR-Akt independent axis and (ii) the regulation of the expression of transcripts related to atrophy. Finally, RGMa induced the expression of transcripts that encode skeletal muscle structural proteins, especially from sarcolemma and also those associated with striated muscle cell differentiation. Conclusions These results provide comprehensive knowledge of skeletal muscle transcript changes and pathways in response to RGMa.

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Section: Discussionmentioning

confidence: 99%

Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy

et al. 2022

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“…Pou2F1 (Pou Class 2 Homeobox 1, also known as Oct-1) isoforms were found to be the most upregulated DETs (Pou2f1-208, ENSMUST00000160260.9), as well as the most downregulated DETs (Pou2f1-205, ENSMUST00000111427.9) by RGMa treatment in skeletal muscle cells. Pou2F1 is a member of the Pou transcription factor family and is associated with a plethora of processes, including the activation of some snRNA, histone H2B, immunoglobulins, and other housekeeping genes [42], the regulation of the circadian clock [43], and glycolytic metabolism [44]. In skeletal muscle cells, this transcription factor was associated with the activation of pro-in ammatory immune response in patients with myalgia [45] and with MyHC IIB expression, when associated with MEF2 and the serum response factor (SRF) [46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Characterisation of the Molecular Mechanisms Induced by RGMa During Skeletal Muscle Hyperplasia and Hypertrophy

Copola¹,

Santos²,

Coutinho³

et al. 2021

Preprint

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Background: The repulsive guidance molecule a (RGMa) is a GPI-anchor axon guidance molecule first found to play important roles during neuronal development. RGMa expression patterns and signalling pathways via Neogenin and/or as BMP coreceptors indicated that this axon guidance molecule could also be working in other processes and diseases, including during myogenesis. Previous works have consistently shown that RGMa is expressed in skeletal muscle cells and that its overexpression induces both nuclei accretion and hypertrophy in muscle cell lineages. However, the cellular components and molecular mechanisms induced by RGMa during the differentiation of skeletal muscle cells are poorly understood. In this work, the global transcription expression profile of RGMa-treated C2C12 myoblasts during the differentiation stage, obtained by RNA-seq, were reported. Results: RGMa treatment could modulate the expression pattern of 2,195 transcripts in C2C12 skeletal muscle, with 943 upregulated and 1,252 downregulated. Among them, RGMa interfered with the expression of several RNA types, including categories related to the regulation of RNA splicing and degradation. The data also suggested that RGMa hyperplasia effects could be due to their capacity to induce the expression of transcripts related to cell-cell adhesion, while RGMa effects on muscle hypertrophy might be due to (i) the activation of the mTOR-Akt independent axis and (ii) the regulation of the expression of transcripts related to atrophy. Finally, RGMa induced the expression of transcripts that encode skeletal muscle structural proteins and members of the signalling pathways associated with GEF and Rho/Rac, common secondary signals of skeletal muscle hypertrophy, and the canonical pathway of the RGMa/Neogenin signalling. Conclusions: These results provide comprehensive knowledge of skeletal muscle transcript changes and pathways in response to RGMa.

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“…The expression of Oct-1 isoforms changes during hematopoietic cell differentiation: in pluripotent CD34+ hematopoietic cells (PHC), Oct-1L is expressed at a high level; its expression level drastically decreases during the differentiation of T cells (CD3+) and monocytic cells (CD14+) but almost does not change during the differentiation of B cells (CD19+) [ 13 , 14 ]. The human Oct-1R isoform is expressed only in B cells and was not found in PHCs [ 13 ].…”

mentioning

confidence: 99%

“…Previously, it was shown that overexpression of Oct-1R and Oct-1L in Namalwa cells leads to repression of many genes involved in the differentiation of B and T cells, as well as monocytic cells (CD14+) [ 13 , 14 ]. The high level of the Oct-1L isoform observed in lymphoblastic tumor cell lines indicates that an excess of Oct-1L, apparently, significantly reduces their ability to differentiate.…”

mentioning

confidence: 99%

5-Azacytidine Suppresses the Expression of Tissue-Specific Oct-1 Isoform in Namalwa Burkitt’s Lymphoma Cell Culture

Котнова

Степченко

Ilyin

et al. 2022

Dokl Biochem Biophys

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Overexpression of the transcription factor POU2F1 (Oct-1) increases the malignant potential of the tumor and determines the unfavorable prognosis for both solid and hematological cases of the disease in human carcinogenesis. The Oct-1 level determines the rate of development of the disease in acute myelodysplastic leukemia (AML), and a decrease in its expression significantly delays the development of leukemia in mice; however, a complete knockout of Oct-1 leads to the death of the animals. POU2F1 (Oct-1) is expressed as several isoforms transcribed from alternative promoters. They include both ubiquitous and tissue-specific isoforms. It was shown that in Burkitt’s lymphoma Namalwa cells 5-azacytidine specifically suppresses the expression of the tissue-specific isoform Oct-1L mRNA (level of Oct-1L is abnormally increased in these cells), while not causing changes in the amount of the ubiquitous isoform Oct-1A mRNA. These results show that it is possible to selectively reduce the transcription level of the Oct-1L isoform aberrantly expressed in human tumor cells.

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Differentiation of Monocytic Cells Is Accompanied by a Change in the Expression of the Set of Oct-1 Isoforms

Cited by 4 publications

References 15 publications

Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy

Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy

Transcriptomic Characterisation of the Molecular Mechanisms Induced by RGMa During Skeletal Muscle Hyperplasia and Hypertrophy

5-Azacytidine Suppresses the Expression of Tissue-Specific Oct-1 Isoform in Namalwa Burkitt’s Lymphoma Cell Culture

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