Dataset Information

Proteomics analysis of tibialis anterior muscle and descending thoracic aorta from Mustn1 whole-body knockout mice and wild-type littermates

ABSTRACT: Skeletal muscle is a highly adaptive tissue that changes with many physiological stimuli and is composed of many cell types. Upon muscle injury, the concerted action of these cells is required to proceed through the process of inflammation, extracellular matrix remodeling, and restoration of function. To uncover novel genes and molecular pathways important for skeletal muscle remodeling and regeneration, we used a mouse hindlimb unloading and reloading protocol, and performed transcriptomics analysis. This study focuses on the microprotein Mustn1 (Musculoskeletal embryonic nuclear protein 1, also known as Mustang), whose gene expression is increased in muscle at the onset of hindlimb reloading, exercise, and injury. We generated a whole-body Mustn1 knockout mouse model and performed proteomics analysis of muscle and aorta.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skeletal Muscle, Aorta

SUBMITTER: Marta Murgia

LAB HEAD: Jorge L. Ruas

PROVIDER: PXD046610 | Pride | 2024-05-24

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	AortarawPRIDE.7z	Other
	AortasearchPRIDE.7z	Other
	TAmuscletriplicates_rawPRIDE.7z	Other
	TAmuscletriplicates_searchPRIDE.7z	Other

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Publications

Mustn1 is a smooth muscle cell-secreted microprotein that modulates skeletal muscle extracellular matrix composition.

Ducommun Serge S Jannig Paulo R PR Cervenka Igor I Murgia Marta M Mittenbühler Melanie J MJ Chernogubova Ekaterina E Dias José M JM Jude Baptiste B Correia Jorge C JC Van Vranken Jonathan G JG Ocana-Santero Gabriel G Porsmyr-Palmertz Margareta M McCann Haworth Sarah S Martínez-Redondo Vicente V Liu Zhengye Z Carlström Mattias M Mann Matthias M Lanner Johanna T JT Teixeira Ana I AI Maegdefessel Lars L Spiegelman Bruce M BM Ruas Jorge L JL

Molecular metabolism 20240306

<h4>Objective</h4>Skeletal muscle plasticity and remodeling are critical for adapting tissue function to use, disuse, and regeneration. The aim of this study was to identify genes and molecular pathways that regulate the transition from atrophy to compensatory hypertrophy or recovery from injury. Here, we have used a mouse model of hindlimb unloading and reloading, which causes skeletal muscle atrophy, and compensatory regeneration and hypertrophy, respectively.<h4>Methods</h4>We analyzed mouse ...[more]

PMID: 38458566

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Project description:Mice were subjected to 50 eccentric contractions (EC) or 50 isometric contractions (IC) using a non-invasive model, and then sacrificed 48 hours later. RNA from the tibialis anterior of 4 animals were pooled and then split into two groups for hybridization onto two separate Affymetrix MGU74Av2 chips. Control samples were contralateral to the exercised legs, and were only subjected to enough contractions to measure isometric torque. Eccentric contractions (ECs), in which a muscle is forced to lengthen while activated, result in muscle injury and, eventually, muscle strengthening and prevention of further injury. Although the mechanical basis of eccentric contraction-induced injury has been studied in detail, muscle's biological response is less well characterized. This study presents the development of a minimally-invasive model of EC injury in the mouse, follows the time course of torque recovery after an injurious bout of ECs, and uses Affymetrix microarrays to compare the gene expression profile 48 hours after ECs to both isometrically stimulated muscles and contralateral muscles. Torque dropped by about 55% immediately after the exercise bout, and recovered to initial levels 7 days later. 36 known genes were upregulated after ECs compared to contralateral and isometrically stimulated muscles, including five muscle specific genes: muscle LIM protein (MLP), Muscle Ankyrin Repeat Proteins (MARP 1 and 2; also known as cardiac ankyrin repeat protein and Arpp/Ankrd2, respectively), Xin, and Myosin Binding Protein H. The time courses of MLP and MARP expression after the injury bout (determined by quantitative real-time polymerase chain reaction) indicate that these genes are rapidly induced, reaching a peak expression level of 6-11 times contralateral values 12-24 hours after the EC bout and returning to baseline within 72 hours. Very little gene induction was seen after either isometric activation or passive stretch, indicating that the MLP and MARP genes may play an important and specific role in the biological response of muscle to EC-induced injury. Keywords = mouse tibialis anterior eccentric contraction muscle