miR-200a-3p improves neonatal necrotizing enterocolitis by regulating RIPK1.

{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:34956481", "kind": "science-record", "revision": 2, "content_hash": "sha256:547c0ded19bb2fe82be63f1eb0050721224eeed001a6bad6c3d656b95db5a7c5", "created_at": "2026-11-01T17:36:40Z", "updated_at": "2026-11-01T18:57:46Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "partial", "title": "miR-200a-3p improves neonatal necrotizing enterocolitis by regulating RIPK1.", "doi": null, "pmid": "34956481", "authors": ["Yulu Liu", "Zhansheng Wang", "Hua Huang", "Kaijun Shou"], "journal": "American journal of translational research", "year": 2021, "abstract": "BACKGROUND: Necrotizing enterocolitis (NEC) is an acquired disease, which mainly occurs in premature infants or sick newborns. microRNA (miR), as a common non-coding RNA in recent years, is found in many diseases. In this research, miR usefulin NEC is analyzed by GEO.\nMETHOD: The differentially expressed miRs in NEC were screened by analyzing GSE68054, and miR-200a-3p in IEC-6 cells induced by lipopolysaccharide (LPS) and serum of NEC children were detected by qRT-PCR. The role of miR-200a-3p in LPS-induced IEC-6 cells was tested using CCK-8, PI dyeing, and inflammatory cytokine detection. The direct downstream molecules of miR-200a-3p were identified using TargetScanHuman and verified by luciferase reporter gene assay. The mechanism of action was explored using western blot.\nRESULTS: miR-200a-3p in IEC-6 treated with NEC and LPS was significantly decreased. In vitro experiments revealed that miR-200a-3p mimetic could inhibit IL-6 and TNF-α in IEC-6 cells induced by LPS and reduce the positive rate of PI. In addition, it was determined that receptor-interacting protein kinase 1 (RIPK1) was a downstream molecule of miR-200a-3p, and overexpression of RIPK1 could aggravate LPS-induced IEC-6 injury, while miR-200a-3p mimics could alleviate the overexpression of RIPK1. miR-200a-3p mimics inhibited the elevation of necrosis-related molecules and the interaction between RIPK1 and RIPK3 in LPS-induced IEC-6 cells.\nCONCLUSION: miR-200a-3p can protect intestinal epithelial cells from LPS injury by inhibiting inflammation and necrosis mediated by RIPK1, which provides a possible target for NEC.", "claims": [{"id": "claim-data-access", "statement": "The differentially expressed miRs in NEC were screened by analyzing GSE68054, and miR-200a-3p in IEC-6 cells induced by lipopolysaccharide (LPS) and serum of NEC children were detected by qRT-PCR.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:34956481", "locator": "sections[0] \"Abstract\" paragraph 1", "quote": "The differentially expressed miRs in NEC were screened by analyzing GSE68054, and miR-200a-3p in IEC-6 cells induced by lipopolysaccharide (LPS) and serum of NEC children were detected by qRT-PCR."}], "state": "complete"}], "gaps": ["doi"]}, "experiment": {"state": "complete", "objective": "", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:34956481"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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