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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 (human)

TISSUE(S): Skeletal Muscle

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: Dong-Gi Mun

LAB HEAD: Sang-Won Lee

PROVIDER: PXD004312 | Pride | 2018-10-02

REPOSITORIES: Pride

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	Mito_OG0_4ug_1_091109.RAW	Raw
	Mito_OG0_4ug_2_091109.RAW	Raw
	Mito_OG0_4ug_3_091109.RAW	Raw
	Mito_OG0_4ug_4_091109.RAW	Raw
	Mito_OG0_4ug_5_091109.RAW	Raw

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Publications

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).

2019-03-13 | MSV000083560 | MassIVE

Online non-contiguous fractionating and concatenating device coupled to two dimensional reverse phase/reverse phase liquid chromatography system for efficient and comprehensive proteomic analyses

Project description:The goal of the project is development of an online two dimensional reverse phase/reverse phase liquid chromatography (2D-RP/RPLC) separation platform, employing an online non-contiguous fractionating and concatenating device (NCFC fractionator) in order to provide highly improve separation orthogonality of the two RPs, resulting in significant increase in peptide identification sensitivity compared with those of the conventional contiguous 2D-RP/RPLC method.

2016-12-22 | PXD004710 | Pride

Mouse retinal tissue study in VEGF-induced hyperpermeability.

Project description:The goal of the project is to identify novel therapeutic targets for retinal vascular hyperpermeability. Three condition (Control, VEGF, and Anti-VEGF) sample of mouse retinal tissues were extensively characterized by global proteome profiling.

2016-03-22 | PXD003656 | Pride

PGRC Cancer Proteome Study of Gastric Tissue

Project description:The goal of the project is to analyze different layers of proteome information including protein abundance and post-translational modifications of PGRC gastric tissue samples. Three pairs of human gastric cancer and adjacent normal tissues were extensively characterized by serial enrichments of phosphorylation and N-glycosylation (SEPG) coupled to LC-MS/MS method.

2016-03-18 | PXD003115 | Pride

Disruption of nucleocytoplasmic trafficking as a cellular senescence driver

Project description:Senescent cells exhibit a reduced response to intrinsic and extrinsic stimuli. This reduction could be explained by disrupted nuclear transmission of signals. However, this hypothesis required more evidence to complete as a new modality of cellular senescence. Proteomic analysis of the cytoplasmic and nuclear fractions from young and senescent cells revealed disruption of nucleocytoplasmic trafficking (NCT) as an essential feature of replicative senescence (RS) at the global level. Blocking NCT either chemically or genetically induced RS-like senescence phenotypes, named as nuclear barrier-induced senescence (NBIS). Transcriptomic analysis revealed that NBIS had the most similar gene expression pattern to RS, compared with other stress-induced types of cellular senescence. Core proteomic and transcriptomic shared patterns between RS and NBIS included upregulation of endocytosis-lysosome network and downregulation of NCT in senescent cells, which were also conserved in yeast aging model. These results implicate an aging-dependent coordinated reduction in the transmission of extrinsic signals to the nucleus and in the nucleus-to-cytoplasm supply of proteins/RNAs. We further showed that the aging-associated decrease in Sp1 transcription factor expression was responsible for downregulation of NCT. Our results suggest that NBIS is a modality of cellular senescence that can represent the nature of physiological aging in eukaryotes.

2021-06-18 | PXD025618 | Pride

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

Project description:Glucagon and insulin are counter-regulatory pancreatic hormones that precisely control blood glucose homeostasis1. Type 2 diabetes mellitus (T2DM) is characterized by inappropriately elevated blood glucagon2-5 levels as well as insufficient glucose stimulated insulin secretion (GSIS) by pancreatic ß-cells6. Early in the pathogenesis of T2DM, hyperglucagonemia is observable antecedent to ß-cell dysfunction7-9; and in mice, liver-specific activation of glucagon receptor-dependent signaling results in impaired GSIS10. However, the mechanistic relationship between hyperglucagonemia, hepatic glucagon action, and ß-cell dysfunction remains poorly understood. Here we show that glucagon action stimulates hepatic production of the neuropeptide kisspeptin1, which acts in an endocrine manner on ß-cells to suppress GSIS. In vivo glucagon administration acutely stimulates hepatic kisspeptin1 production, and kisspeptin1 is increased in livers from humans with T2DM and from mouse models of diabetes mellitus. Synthetic kisspeptin1 potently suppresses GSIS in vivo and in vitro from normal isolated islets, which express the kisspeptin1 receptor Kiss1R. Administration of a Kiss1R antagonist in diabetic Leprdb/db mice potently augments GSIS and reduces glycemia. Our observations indicate in the pathogenesis of T2DM an endocrine mechanism sequentially linking hyperglucagonemia via hepatic kisspeptin1 production to impaired insulin secretion. In addition, our findings suggest Kiss1R antagonism as a therapeutic avenue to improve ß-cell function in T2DM. Total RNA from L-Δprkar1a KO mice compared to control D-glucose mice

2014-04-01 | E-GEOD-48815 | biostudies-arrayexpress

Comprehensive proteome profiling of platelet identified a protein profile predictive of responses to an antiplatelet agent sarpogrelate.

Project description:Here, we performed a comprehensive proteome profiling of platelets collected from 18 healthy subjects before and after administration of sarpogrelate. For each subject, platelets were isolated before and then again after drug administration to investigate the alteration in the platelet proteome by sarpogrelate. A sample preparation method involving filter-aided sample preparation (FASP) was used to improve extraction of proteins including both soluble and membraneous proteins. Moreover, an ultra-high pressure liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) coupled with extensive fractionation was used to generate a comprehensive proteome of platelets.

2016-09-29 | PXD003613 | Pride

Glucagon regulates Hepatic Kisspeptin1 to Impair Insulin Secretion in Diabetes Mellitus

2014-04-01 | GSE48815 | GEO

Molecular Mechanism of type 2 diabetes mellitus-mediated heart failure with preserved ejection fraction

Project description:Type 2 diabetes mellitus (T2DM) is a metabolic disease associated with several comorbidities, including cardiac dysfunction leading to heart failure with preserved ejection fraction (HFpEF), in turn resulting in T2DM-induced cardiomyopathy (T2DM-CM). However, the molecular mechanisms underlying the development of T2DM-CM are poorly understood. It is hypothesized that molecular alterations in myopathic genes induced by diabetes promote the development of HFpEF, whereas cardiac myosin inhibitors can rescue the resultant T2DM-induced cardiomyopathy. To test this hypothesis, a Leptin receptor-deficient db/db homozygous (Lepr db/db) mouse model was used to define the pathogenesis of T2DM-CM. Echocardiographic studies at 4 and 6 months revealed that Lepr db/db hearts started developing cardiac dysfunction by four months, and left ventricular hypertrophy with diastolic dysfunction was evident at 6 months. Strikingly, the level of cardiac myosin binding protein-C phosphorylation was significantly increased in Lepr db/db mouse hearts. RNA-seq data analysis, followed by functional enrichment, revealed the differential regulation of genes related to cardiac dysfunction in Lepr db/db heart tissues. Finally, using isolated skinned papillary muscles and freshly isolated cardiomyocytes, CAMZYOS (mavacamten, which is a prescription heart medicine used for symptomatic obstructive hypertrophic cardiomyopathy treatment (herein after denotes as MYK-461), was tested for its ability to rescue T2DM-CM. Compared with controls, MYK-461 significantly reduced force generation in papillary muscle fibers and cardiomyocyte contractility in the db/db group. This line of evidence shows that 1) T2DM-CM is associated with hyperphosphorylation of cardiac myosin binding protein-C and 2) MYK-461 significantly lessened disease progression, suggesting its promise as a therapeutic treatment for HFpEF.

2024-08-01 | GSE235934 | GEO

Streptozotocin-induced Type 1 and 2 Diabetes Mellitus Mouse Models Show Different Functional, Cellular and Molecular Patterns of Diabetic Cardiomyopathy

Project description:The main cause of morbidity and mortality in diabetes mellitus (DM) are cardiovascular complications. Diabetic cardiomyopathy (DCM) remains incompletely understood. Animal models have been crucial in exploring DCM pathophysiology while identifying potential therapeutic targets. Streptozotocin (STZ) has been widely used to produce experimental models of both type 1 and type 2 DM (T1DM and T2DM). Here we compared these two models for their effects on cardiac structure, function, and transcriptome. Different doses of STZ and different diet chows were used to generate T1DM and T2DM in C57BL/6J mice. Normal euglycemic and non-obese sex and age-matched mice served as controls (CTRL). Immunohistochemistry, RT-PCR, and RNA-Seq were employed to compare hearts from the three animal groups. STZ-induced T1DM and T2DM differently affect left ventricular function and myocardial performance. T1DM displays an exaggerated apoptotic cardiomyocyte (CM) death and reactive hypertrophy and fibrosis along with increased cardiac oxidative stress, CM DNA damage and senescence when compared to T2DM mice. T1DM and T2DM differently affect whole cardiac transcriptome. In conclusion, STZ-induced T1DM and T2DM mouse models show significant differences in cardiac remodeling, function and whole transcriptome. These differences could be of key relevance when choosing an animal model to study specific features of DCM.

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