Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21622540_1.fastq.gz | Fastqsanger.gz | |||
| SRR21622540_2.fastq.gz | Fastqsanger.gz | |||
| SRR21622541_1.fastq.gz | Fastqsanger.gz | |||
| SRR21622541_2.fastq.gz | Fastqsanger.gz | |||
| SRR21622542_1.fastq.gz | Fastqsanger.gz |
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Project description:We conducted comparative proteomic sequencing of Akkermansia muciniphila (Akk) and its extracellular vesicles (Akk-EVs) to identify functional protein components within Akk-EVs responsible for alleviating disease progression
2026-06-08 | PXD062069 | Pride
Project description:Akkermansia muciniphila (Akk) associated with multiple metabolic diseases and administration of Akk can improve the metabolic disorders. However, little is known about the effect of Akk on jejunal epithelial cells which absorb lipid and interact with oral administrated Akk. We oral administrated Akk to mice and measured the lipid absorption and gene expression in small intestinal epithelial cells. The long-term effect of Akk treatment reduced lipid deposits in the liver and adipocytes with improved the glucose metabolism. This is particularly caused by reduced lipid absorption in jejunal epithelia. Akk feeding reduced the expression of those genes that regulate synthesis and cell cycles, characters of the host cell responding to energy deficiency. In fact, we detected increased AMPK-alpha phosphorylation levels in Akk-treated jejunal epithelial cells both in vivo and in vitro. Furthermore, activating AMPK inhibits lipids absorption in jejunum. Thus, we conclude that oral administration of Akk activates the AMPK pathway and represses the lipid absorption in jejunal epithelial cells, which contributes to the metabolic benefits of oral Akk administration.
2025-01-25 | GSE254234 | GEO
Project description:Doxorubicin (DOX) is considered as the major culprit in chemotherapy-induced cardiotoxicity, which limits its clinical application. Akkermansia muciniphila (AKK) shows a beneficial role as a probiotic in the treatment of metabolic syndrome. However, the changes of AKK during DIC and whether it mediates cardioprotective effects remains unclear. Cardiac transcriptomics certified by in vitro experiments demonstrated that AKK administration effectively improved mitochondrial function and alleviated DIC, by activation of PPARα/PGC1α signaling pathway. These findings provide a therapeutic strategy for DIC through supplementation with AKK.
2025-05-30 | GSE276172 | GEO
Project description:Fasting protects the small intestine epithelial cells from high-dose radiation injury, yet the mechanisms linking fasting to epithelial regeneration remain incompletely understood. Akkermansia muciniphila (AKK) is both necessary and sufficient for fasting-induced radioprotection. Selective depletion of AKK abolishes fasting-mediated preservation of SI stem cells, while recolonization restores epithelial integrity and survival. AKK produces the short-chain fatty acid propionate, which, together with host-derived β-hydroxybutyrate (β-OHB), induces histone H3 acetylation (H3K27ac, H3K9ac) and β-hydroxybutyrylation (H3K9bhb) in crypt epithelial cells, remodeling enhancer–promoter landscapes. CUT&Tag and single-cell ATAC-seq analyses show that fasting, in an AKK-dependent manner, expands a Clu⁺Olfm4⁺ “revival” stem cell (persister cells) population enriched for HNF, FOXA, GATA and KLF transcription factor motifs, establishing a pro-regenerative chromatin state that persists through injury-repair phases. CTCF and BORIS activities persist, suggesting a role in maintaining epigenetic memory for intestinal regeneration after radiation. This microbiota–metabolite–chromatin axis primes persister cells for rapid regeneration after damage and offers a strategy to protect normal tissues during radiation therapy.
2026-06-08 | GSE306673 | GEO
Project description:Fasting protects the small intestine epithelial cells from high-dose radiation injury, yet the mechanisms linking fasting to epithelial regeneration remain incompletely understood. Akkermansia muciniphila (AKK) is both necessary and sufficient for fasting-induced radioprotection. Selective depletion of AKK abolishes fasting-mediated preservation of SI stem cells, while recolonization restores epithelial integrity and survival. AKK produces the short-chain fatty acid propionate, which, together with host-derived β-hydroxybutyrate (β-OHB), induces histone H3 acetylation (H3K27ac, H3K9ac) and β-hydroxybutyrylation (H3K9bhb) in crypt epithelial cells, remodeling enhancer–promoter landscapes. CUT&Tag and single-cell ATAC-seq analyses show that fasting, in an AKK-dependent manner, expands a Clu⁺Olfm4⁺ “revival” stem cell (persister cells) population enriched for HNF, FOXA, GATA and KLF transcription factor motifs, establishing a pro-regenerative chromatin state that persists through injury-repair phases. CTCF and BORIS activities persist, suggesting a role in maintaining epigenetic memory for intestinal regeneration after radiation. This microbiota–metabolite–chromatin axis primes persister cells for rapid regeneration after damage and offers a strategy to protect normal tissues during radiation therapy.
2026-06-08 | GSE306577 | GEO
Project description:To investigate whether Akkermansia muciniphila (AKK) bacteria affects colitis by regulating the ferroptosis signaling pathway, an mouse model of colitis was constructed, and the mice were administered with AKK and the ferroptosis agonist Erastin. HE staining and transmission electron microscopy were used to observe the pathological and microstructural changes of mouse colon tissues. The number of goblet cells was examined using alcian blue staining. The expression levels of oxidative stress-related indicators and ferroptosis-related proteins were detected by ELISA, western blot and immunohistochemisty analyses. Transcriptome and non-targeted metabolome sequencing were carried out to screen for differentially expressed genes and metabolites. Immunofluorescence double staining was used to detect the co-localization of cell adhesion-related indicators.16S microbiota sequencing was performed on mouse feces. Erastin caused damage to colon tissues, decreased the expression of ZO-1 and E-Cadherin, and increased the expression of oxidative stress and ferroptosis-related indicators. The species-abundance was increased after AKK treatment, while it was decreased after treatment with AKK bacteria+Erastin. AKK alleviated inflammatory cell infiltration, reduced organelle damage, and decreased the number of goblet cells in mice with colitis. MDA, ROS, and Fe2+ levels in colitis tissues were increased, but they were decreased after AKK bacteria treatment. The expression of GPX4 and SLC7A11 was decreased, while ACSL4 was increased. After intervention with AKK bacteria, the trend of changes in the above indicators was reversed, and 19 differential pathways were enriched. In conclusion, AKK bacteria can treat colitis in mice, and its mechanism may be related to regulating the ferroptosis signaling pathway.
2025-09-23 | GSE308591 | GEO