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A mitochondrial proteome profile of type 2 diabetes mellitus in skeletal muscles

ABSTRACT: The goal of the project is to understand the mitochondrial proteome profiles related to T2DM. We performed comprehensive proteome profiling of mitochondria isolated from skeletal muscles in nine T2DM patients and nine control subjects with normal glucose tolerance (NGT).

INSTRUMENT(S): LTQ FT

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Sang-Won Lee

PROVIDER: MSV000083560 | MassIVE | Wed Mar 13 00:01:00 GMT 2019

SECONDARY ACCESSION(S): PXD004312

REPOSITORIES: MassIVE

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A mitochondrial proteome profile indicative of type 2 diabetes mellitus in skeletal muscles.

Chae Sehyun S Kim Su-Jin SJ Do Koo Young Y Lee Jung Hwa JH Kim Hokeun H Ahn Byung Yong BY Ha Yong-Chan YC Kim Yong-Hak YH Jang Mi Gyeong MG Koo Kyung-Hoi KH Choi Sung Hee SH Lim Soo S Park Young Joo YJ Jang Hak Chul HC Hwang Daehee D Lee Sang-Won SW Park Kyong Soo KS

Experimental & molecular medicine 20180928 9

The pathogenesis of type 2 diabetes mellitus (T2DM) is closely associated with mitochondrial functions in insulin-responsive tissues. The mitochondrial proteome, compared with the mitochondrial genome, which only contains 37 genes in humans, can provide more comprehensive information for thousands of mitochondrial proteins regarding T2DM-associated mitochondrial functions. However, T2DM-associated protein signatures in insulin-responsive tissues are still unclear. Here, we performed extensive pr ...[more]

PMID: 30266947

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A mitochondrial proteome profile of type 2 diabetes mellitus in skeletal muscles

Project description:The goal of the project is to understand the mitochondrial proteome profiles related to T2DM. We performed comprehensive proteome profiling of mitochondria isolated from skeletal muscles in nine T2DM patients and nine control subjects with normal glucose tolerance (NGT).

2018-10-02 | PXD004312 | Pride

A transcriptome atlas of human skeletal muscles

Project description:We generated a large transcriptome atlas of human skeletal muscles by collecting biopsies from 6 different muscles to determine molecular signatures that may be distinct between leg muscles. The biopsies were collected from gracilis (GR), semitendinosus (ST), vastus lateralis (VL), vastus medialis (VM), rectus femoris (RF), and gastrocnemius lateralis (GL) muscles. We also investigated molecular differences within the muscle by including two biopsies from the middle and distal sides of the semitendinosus muscle (STM and STD, respectively). In total, 128 samples from 20 individuals (aged 25 Ã‚Â± 3.6 yr) were analyzed.

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A mitochondrial proteome profile indicative of type 2 diabetes mellitus in skeletal muscles.

Project description:The pathogenesis of type 2 diabetes mellitus (T2DM) is closely associated with mitochondrial functions in insulin-responsive tissues. The mitochondrial proteome, compared with the mitochondrial genome, which only contains 37 genes in humans, can provide more comprehensive information for thousands of mitochondrial proteins regarding T2DM-associated mitochondrial functions. However, T2DM-associated protein signatures in insulin-responsive tissues are still unclear. Here, we performed extensive proteome profiling of mitochondria from skeletal muscles in nine T2DM patients and nine nondiabetic controls. A comparison of the mitochondrial proteomes identified 335 differentially expressed proteins (DEPs) between T2DM and nondiabetic samples. Functional and network analyses of the DEPs showed that mitochondrial metabolic processes were downregulated and mitochondria-associated ER membrane (MAM) processes were upregulated. Of the DEPs, we selected two (NDUFS3 and COX2) for downregulated oxidative phosphorylation and three (CALR, SORT, and RAB1A) for upregulated calcium and protein transport as representative mitochondrial and MAM processes, respectively, and then confirmed their differential expression in independent mouse and human samples. Therefore, we propose that these five proteins be used as a potential protein profile that is indicative of the dysregulation of mitochondrial functions in T2DM, representing downregulated oxidative phosphorylation and upregulated MAM functions.

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Gene expression of Skeletal muscle in Tacrolimus-Induced Post-transplantation Diabetes Mellitus model

Project description:Post-transplantation diabetes mellitus (PTDM) is a known complication of transplantation which affected the prognosis. Tacrolimus (Tac, or FK506) is a widely used immunosuppressant, has been reported as a risk factor for PTDM and further develops complications in heart and skeletal muscle , while the mechanism is still largely unknown. The gene expression of rat muscles of control group and Tac induced PTDM group were analyzed.

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Deep proteome of aging skeletal muscles reveals Smoc2 as a modulator of satellite cell regenerative capacity

Project description:During aging, the number and functionality of muscle stem cells (MuSCs) decreases leading to impaired regeneration of aged skeletal muscle. In addition to intrinsic changes in aged MuSCs, extracellular matrix (ECM) proteins deriving from other cell types, e.g., fibrogenic-adipogenic progenitor cells (FAPs), contribute to the aging phenotype of MuSCs and impaired regeneration in the elderly. So far, no comprehensive analysis on how age-dependent changes in the whole skeletal muscle proteome affect MuSC function have been conducted. Here, we investigated age-dependent changes in the proteome of different skeletal muscle types by applying deep quantitative mass spectrometry. We identified 183 extracellular matrix proteins that show different abundances in skeletal muscles of old mice. By integrating single cell sequencing data, we reveal that transcripts of those ECM proteins are mainly expressed in FAPs, suggesting that FAPs are the main contributors to ECM remodelling during aging. We functionally investigated one of those ECM molecules, namely Smoc2, which is aberrantly expressed during aging. We show that Smoc2 levels are elevated during regeneration and that its accumulation in the aged MuSC niche causes impairment of MuSCs function through constant activation of integrin/MAPK signaling. In vivo, supplementation of exogenous Smoc2 hampers the regeneration of young muscles following serial injuries, leading to a phenotype reminiscent of regenerating aged skeletal muscle. Taken together, we provide a comprehensive resource of changes in the composition of the ECM of aged skeletal muscles, we pinpoint the cell types driving these changes, and we identify a new niche protein causing functional impairment of MuSCs thereby hampering the regeneration capacity of skeletal muscles.

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Deep proteome of aging skeletal muscles reveals Smoc2 as a modulator of satellite cell regenerative capacity

2021-11-25 | PXD015616 | Pride

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Project description:Skeletal muscle is a highly structured and differentiated tissue responsible for voluntary movement and metabolic regulation. Muscles however, are heterogeneous and depending on their location, speed of contraction, fatiguability and function, can be broadly subdivided into fast and slow twitch as well as subspecialized muscles, with each group expressing common as well as specific proteins. Congenital myopathies are a group of non-inflammatory non-dystrophic muscle diseases caused by mutations in a number of genes, leading to a weak muscle phenotype. In most cases specific muscles types are affected, with preferential involvement of fast twitch muscles as well as extraocular and facial muscles. The aim of this study is to compare the proteome of three groups of muscles from wild type and transgenic mice carrying compound heterozygous mutations in Ryr1 identified in a patient with a severe congenital myopathy. Qualitative proteomic analysis was performed by comparing the relative fold change of proteins in fast twitch and slow twitch muscles. Subsequently we compared the proteome of different muscles in wild type and Ryr1 mutant mice. Finally, we applied a quantitative analysis to determine the stoichiometry of the main protein components involved in excitation contraction coupling and calcium regulation. Our results show that recessive Ryr1 mutations do not only cause a change in RyR1 protein content in skeletal muscle, but they are accompanied by profound changes in protein expression in the different muscle types and that the latter effect may be responsible in part, for the weak muscle phenotype observed in patients.

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