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Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [RNA-Seq]

ABSTRACT: Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [RNA-Seq]

PROVIDER: PRJNA1257421 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33388867_1.fastq.gz	Fastqsanger.gz
	SRR33388867_2.fastq.gz	Fastqsanger.gz
	SRR33388868_1.fastq.gz	Fastqsanger.gz
	SRR33388868_2.fastq.gz	Fastqsanger.gz
	SRR33388869_1.fastq.gz	Fastqsanger.gz

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Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis

Project description:Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis

| PRJNA1256771 | ENA

Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis

Project description:Patho-mechanistic origins and disease dynamics of ulcerative colitis are still poorly understood. The actin crosslinker Filamin A (FLNA) impacts cellular responses through interaction with numerous, cytosolic proteins. FLNA exists in two forms that differ only in a single amino acid: genome-encoded FLNAQ, and FLNAR - generated by post-transcriptional A-to-I editing. In the intestinal tract, FLNA is edited in fibroblasts, smooth muscle- and endothelial cells and we identified the FLNA editing status as a key determinant of colitis severity. FLNA editing was highest in healthy colons, and reduced during acute murine and human colitis. Mice that exclusively express edited FLNAR and do not downregulate editing upon challenge were highly resistant to DSS-induced colitis, whereas fully unedited FLNAQ animals developed severe inflammation. While the genetic induction of FLNA editing influenced the transcriptional states of intestinal structural cells and microbiome composition, we found that edited FLNAR exerts protection specifically via its influence on myeloid immune cells, which are not edited under physiological conditions. The introduction of a fixed FLNAR editing state, did not hamper normal cell migration but reduced macrophage inflammation and rendered neutrophils less prone to NETosis. We thus conclude that loss of FLNA editing correlates with colitis severity and targeted FLNA editing of myeloid cells might serve as novel therapeutic approach in intestinal inflammation.

2025-04-29 | GSE295910 | GEO

Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [RNA-Seq]

Project description:Patho-mechanistic origins and disease dynamics of ulcerative colitis are still poorly understood. The actin-crosslinker Filamin A (FLNA) impacts cellular responses through interaction with cytosolic proteins. FLNA exists in two forms that differ only in one amino acid: genome-encoded FLNAQ and FLNAR - generated by post-transcriptional A-to-I editing. FLNA is edited in fibroblasts, smooth muscle- and endothelial cells in the colon. We identified the FLNA editing status as a key determinant of colitis severity. FLNA editing was highest in healthy colons and reduced during acute murine and human colitis. Mice that exclusively express edited FLNAR and do not downregulate editing upon challenge were highly resistant to DSS-induced colitis, whereas fully unedited FLNAQ animals developed severe inflammation. While the genetic induction of FLNA editing influenced transcriptional states of structural cells and the microbiome composition, we found that FLNAR exerts protection specifically via its influence on myeloid cells, which are not edited under physiological conditions. Introducing fixed, fully edited FLNAR did not hamper normal cell migration but reduced macrophage inflammation and rendered neutrophils less prone to NETosis. In conclusion, loss of FLNA editing correlates with colitis severity, and targeted FLNA editing of myeloid cells might serve as a novel therapeutic approach in intestinal inflammation.

2025-05-03 | GSE296059 | GEO

Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [scRNA-Seq]

2025-05-03 | GSE296058 | GEO

Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [scRNA-Seq]

Project description:Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis [scRNA-Seq]

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Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Disease Activity in Ulcerative Colitis

Project description:TUDCA Reduces Ulcerative Colitis Severity

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Paneth cell SIRT1 deficiency protects against DSS-induced colitis

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Alistipes putredinis protects DSS-induced colitis through mediating immune tolerance

Project description:Alistipes putredinis protects DSS-induced colitis through mediating immune tolerance

| PRJNA1037524 | ENA

Polydatin protects against DSS-induced ulcerative colitis via Nrf2/Slc7a11/Gpx4-dependent inhibition of ferroptosis signalling activation

Project description:Ulcerative colitis (UC), a form of inﬂammatory bowel disease, is characterized by a Q7 recurrent and persistent nonspeciﬁc inﬂammatory response. Polydatin (PD), a natural stilbenoid polyphenol with potent properties, exhibits unexpected beneﬁcial effects beyond its well-documented anti-inﬂammatory and antioxidant activities. In this study, we presented evidence that PD confers protection against dextran sodium sulfate (DSS)-induced ulcerative colitis. Our ﬁndings demonstrated that PD mitigated the DSS-induced increases in proinﬂammatory cytokines (IL-6, TNF-α, and IL-1β), alleviated colon length shortening, reduced morphological damage to the intestinal mucosa, and preserved tight junction proteins (TJ) occludin and Zonula occludens-1 (ZO-1) in both Caco-2 cells and murine models of colitis. Results from bulk RNA sequencing and differential gene analysis suggested a potential role for ferroptosis in the protective mechanisms of PD against UC. Further investigations revealed that PD modulated the expression levels of several ferroptosis-related proteins and transcription factors within the DSS-induced colitis model. Notably, treatment with PD enhanced nuclear translocation of Nrf2, which inhibits ferroptosis while ameliorating oxidative stress through upregulation of Slc7a11 and Gpx4 expression. Additionally, erastin—a known inducer of ferroptosis—reversed the protective effects conferred by PD in the DSS-induced colitis model by downregulating Slc7a11 expression. These ﬁndings underscore that PD protects against DSS-induced ulcerative colitis via the Nrf2/ Slc7a11/Gpx4 signaling axis, highlighting its potential as a novel therapeutic agent for UC.

2025-01-07 | GSE285956 | GEO

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