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MiRNA transcriptome and myofiber characteristics of lamb skeletal muscle during hypertrophic growth

ABSTRACT: miRNA transcriptome and myofiber characteristics of lamb skeletal muscle during hypertrophic growth

PROVIDER: PRJNA853377 | ENA |

REPOSITORIES: ENA

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miRNA transcriptome and myofiber characteristics of lamb skeletal muscle during hypertrophic growth

Project description:Longissimus muscle samples were collected from lambs at 6 developmental time points (prenatal gestational d 85, 110, 133, and postnatal d 42, 65, and 243). Muscle samples were examined to determine the impact of myofiber hypertrophy on the miRNA profile.

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Antagonistic control of myofiber size and muscle protein quality control by the ubiquitin ligase UBR4 during aging

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Project description:Skeletal muscles are complex organs consisting of multiple tissues, including connective tissue, blood vessels, nerves and multinucleated myofibers. Single-nucleus transcriptomics analyses have revealed distinctive myonuclear populations related to myofiber type and to specialized regions, including neuromuscular and myotendinous junctions. However, the use of tissue dissociation methods prevented access to global spatial organization. Here we applied RNA tomography (TOMOseq), a spatial transcriptomics approach, to explore gene expression differences along murine tibialis anterior muscles.

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Spatial multi-omics in skeletal muscle unravel complex myofiber architecture

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The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy

Project description:Decline in skeletal muscle cell size (myofiber atrophy) is a key feature of cancer-induced wasting (cachexia). In particular, atrophy of the diaphragm, the major muscle responsible for breathing, is an important determinant of cancer-associated mortality. However, therapeutic options are limited. Here, we have used Drosophila transgenic screening to identify muscle-secreted factors (myokines) that act as paracrine regulators of myofiber growth. Subsequent testing in mouse myotubes revealed that mouse Fibcd1 is an evolutionary-conserved myokine that preserves myofiber size via ERK signaling. Local administration of recombinant Fibcd1 (rFibcd1) ameliorates cachexia-induced myofiber atrophy in the diaphragm of mice bearing patient-derived melanoma xenografts and LLC carcinomas. Moreover, rFibcd1 impedes cachexia-associated transcriptional changes in the diaphragm. Fibcd1-induced signaling appears to be muscle selective because rFibcd1 increases ERK activity in myotubes but not in several cancer cell lines tested. We propose that rFibcd1 may help reinstate myofiber size in the diaphragm of patients with cancer cachexia.

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The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy

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The myokine Fibcd1 is an endogenous determinant of myofiber size and mitigates cancer-induced myofiber atrophy

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