Dataset Information

Chronic intermittent hypoxia participates in the pathogenesis of atherosclerosis and perturbs the formation of intestinal microbiota

ABSTRACT: Chronic intermittent hypoxia participates in the pathogenesis of atherosclerosis and perturbs the formation of intestinal microbiota

PROVIDER: PRJEB42259 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	ERR5024330_1.fastq.gz	Fastqsanger.gz
	ERR5024330_2.fastq.gz	Fastqsanger.gz
	ERR5024340_1.fastq.gz	Fastqsanger.gz
	ERR5024340_2.fastq.gz	Fastqsanger.gz
	ERR5024331_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 46

Similar Datasets

Project description:Chronic intermittent hypoxia (CIH) is the prominent signature of highly prevalent obstructive sleep apnea (OSA) pathophysiology, which leads to increased risk and aggravation of atherosclerotic cardiovascular diseases. However, whether intestinal microbiota is implicated in the mechanisms linking CIH to arteriosclerosis (AS) pathogenesis remains unclear. The association of CIH with the development of altered gut microbiota (GM) may provide the opportunity to develop preventive strategies for atherosclerotic cardiovascular risk reduction. Animal models of apolipoprotein E-deficient (apoE-/-) mice treated with high-fat diet (HFD) and subjected to CIH conditions was applied to mimic the AS observed in patients with OSA. The physiological status and atherosclerotic lesion formation were confirmed by histological analysis. 16S rDNA sequencing of fecal samples was conducted to determine the changes in gut microbial composition. Morphometric analysis demonstrated that CIH caused aggravated atherosclerotic lesions and facilitated AS in apoE-/- mice treated with HFD. The gut bacteria was significantly varied in AS and AS+CIH mice compared with that in the control mice. Significantly perturbed GM profiles were detected in AS mice with and without CIH, with altered microbial α- and β- diversity and shifts in bacterial compositions at phylum and genus levels. While the difference between AS and AS+CIH was observed at different bacteria taxa levels. Aggravation of reduced Sutterella and increased Halomonas, Halomonadaceae and Oceanospirillales was noted in CIH-treated AS mice. The correlation of intestinal bacterial parameters with pathological changes in artery indicated complicated interactions under CIH-induced GM dysbiosis. Furthermore, the gut microbial functions in the potential ability of replication recombination and repair proteins, glycan biosynthesis and metabolism, as well as metabolism of cofactors and vitamins were identified to be further suppressed by CIH. Our findings demonstrated a causal effect of CIH on GM alterations in AS mice and suggested that the disordered GM features in AS development were deteriorated by CIH, which may be associated with AS aggravation. Preventative strategies targeting gut microbiome are highly recommended for intervention of OSA-related AS.

Project description:Atherosclerosis is the preliminary cause of coronary artery disease, one of the diseases that ac-count for the largest number of fatal mortalities. Physical activity is an effective strategy to restrain atherosclerosis from deterioration. Evidence indicated that the changes of proteomic profile is highly associated with the atherosclerosis development, but the mechanism behind the exercise for atherosclerosis amelioration has not yet been investigated from the proteomics perspective. Hence, the proteomic profiles could further elucidate the systematic effects of exercise interven-tion on ApoE knockout atherosclerotic model and high fat diet intervention. In current study, Apoeem1Narl/Narl mice were randomly allocated into a normal diet (ND), western diet (WD) and WD with 12 weeks exercise intervention (WD EX) groups. The plasm proteome between WD and WD EX demonstrate the significant difference, and ten major pathways, including cardiovascular disease (CVD)–hematological disease, cellular compromise–inflammatory response, protein synthesis, connective tissue disorders, cellular movement–immune cell tracking, inflammatory response, etc., were generated by the IPA analysis. The fourteen proteins (PROS, PROZ, C2, F5, C5, SERPINA 10, FGB, FGG, CFB, F12, CRP, CFHR1, HABP2, and PPIA) critically involved in CVD–hematological disease pathway showed significant difference among groups. The PROS, F5, C5, FGG, and CFB levels associated with thrombosis and atherosclerosis induced by WD were significantly decreased by exercise intervention in WD EX. Furthermore, the F5 and FGG were well-demonstrated the important roles for thrombosis of atherosclerotic pathogenesis but the complement factor C5 in the development of atherosclerosis is not fully understood. In current study, the exercise could significantly alleviate the significantly elevated C5 and inflammation induced by WD group in accordance to amelioration of atherosclerosis. Therefore, exercise could mitigate chemotaxis through the modulation of the C5 level and innate immunity, thereby alle-viating the pathogenesis of atherosclerosis in western-diet induced obese mice.

Dataset Information

Chronic intermittent hypoxia participates in the pathogenesis of atherosclerosis and perturbs the formation of intestinal microbiota

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets