Dataset Information

Myocardial proteome from obese rats with cardiac dysfunction C4PR_LIV

ABSTRACT: Obesity is a complex metabolic disease considered a global pandemic and associated with high incidence of cardiovascular disease. The excess of adipose tissue may promotes maladaptation that result in alterations in structure and function of the heart; however, the mechanisms are not fully elucidated. Proteomics may provide a deeper understanding into the pathophysiological process and contribute to the identification of new potential therapeutic targets. Thus, the aim of this was evaluate the myocardial protein expression in healthy and obese rats induced by Western diet to better comprehend the network of mechanisms inherent to cardiac dysfunction in obesity. For this purpose, we performed proteomic approaches based on nano-liquid chromatography-tandem mass spectrometry (nLC-MS/MS) followed by label-free quantification.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Heart, Cardiac Muscle Myoblast

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Danielle Vileigas

LAB HEAD: Antonio Carlos Cicogna

PROVIDER: PXD013543 | Pride | 2019-12-04

REPOSITORIES: Pride

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Publications

Landscape of heart proteome changes in a diet-induced obesity model.

Vileigas Danielle F DF Harman Victoria M VM Freire Paula P PP Marciano Cecília L C CLC Sant'Ana Paula G PG de Souza Sérgio L B SLB Mota Gustavo A F GAF da Silva Vitor L VL Campos Dijon H S DHS Padovani Carlos R CR Okoshi Katashi K Beynon Robert J RJ Santos Lucilene D LD Cicogna Antonio C AC

Scientific reports 20191202 1

Obesity is a pandemic associated with a high incidence of cardiovascular disease; however, the mechanisms are not fully elucidated. Proteomics may provide a more in-depth understanding of the pathophysiological mechanisms and contribute to the identification of potential therapeutic targets. Thus, our study evaluated myocardial protein expression in healthy and obese rats, employing two proteomic approaches. Male Wistar rats were established in two groups (n = 13/group): control diet and Western ...[more]

PMID: 31792287

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related mortality among adults in developed countries. The discovery of the most common genetic alterations as well as the development of organoids models of pancreatic cancer have provided insight into the fundamental pathways driving the progression from normal cell, to non-invasive precursor lesion, to widely metastatic disease, offering new opportunities for the discovery of key activated pathways along cancer progression. Obesity is one of the most serious public health challenges of the 21st century. Several epidemiological studies have shown the positive association between obesity and cancer-related morbidity/mortality, as well as poor prognosis and poorer treatment outcome. Despite strong evidence indicates a link between obesity and cancer incidence, the molecular basis of the initiating events remains largely elusive. This is mainly due to the lack of an accurate and reliable model of pancreatic carcinogenesis that mimics human obesity-associated PDAC, making data interpretation difficult and often confusing. Here we propose, to our knowledge, the best suitable and manageable preclinical tool, based on next-generation cell culture models, to study the effects of obesity on pancreatic carcinogenesis. Therefore we tracked the effects of obesity on the natural evolution of PDAC in a genetically-defined transplantable model of syngeneic murine pancreatic preneoplastic lesion (mP) and tumor (mT) derived organoids that recapitulates the progression of human disease from early preinvasive lesions to metastatic disease. Our models indicated that both genetic- and diet-induced obesity promoted incidence engraftment rate and growth of both preneoplastic and neoplastic organoids, favoring pancreatic cancer progression and distant metastases dissemination. Our obesity models of carcinogenesis mimic the evolution of human pancreatic cancer pathology, promoting carcinogenesis and concomitant accumulation of a myeloid infiltrate. These changes in cancer immune infiltrate were also associated to a specific pattern of anti-inflammatory Th2 signature. Moreover, gene expression profile analysis revealed a change in gene expression programs that addresses cells to different pancreatic subtypes and stromal conditions. Our results suggest that organoid-derived transplants in obese mice represent a suitable system to study early step of carcinogenesis and support the hypothesis that inflammation induced by obesity stimulates tumor progression and metastatization during pancreatic carcinogenesis.

Dataset Information

Myocardial proteome from obese rats with cardiac dysfunction C4PR_LIV

Publications

Landscape of heart proteome changes in a diet-induced obesity model.

Similar Datasets

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