Dataset Information

Untargeted metabolites of supernatant of wild-type and Nlrp3-/- bone marrow-derived macrophages with or without LPS and ATP costimulation

ABSTRACT: Untargeted metabolites of supernatant of wild-type and Nlrp3-/- bone marrow-derived macrophages without stimulation or with 4 hours of LPS preconditioning and subsequently 30 min of ATP stimulation.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS12152 | MetaboLights | 2025-07-08

REPOSITORIES: MetaboLights

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Publications

The P2X7R/NLRP3 inflammasome axis suppresses enthesis regeneration through inflammatory and metabolic macrophage-stem cell cross-talk.

Gao Haihan H Wang Liren L Lyu Yangbao Y Jin Haocheng H Lin Zhiqi Z Kang Yuhao Y Li Ziyun Z Zhang Xueying X Jiang Yuhan Y Zhang Guoyang G Tao Zaijin Z Zhang Xiaofeng X Yang Bin B Bai Xingyu X Ma Xin X Liu Shen S Jiang Jia J

Science advances 20250425 17

The regeneration of the enthesis remains a formidable challenge in regenerative medicine. However, key regulators underlying unsatisfactory regeneration remain poorly understood. This study reveals that the purinergic receptor P2X7 (P2X7R)/Nod-like receptor family protein 3 (NLRP3) inflammasome axis suppresses enthesis regeneration by amplifying IL-1β-mediated inflammatory cross-talk and suppressing docosatrienoic acid (DTA) metabolic cross-talk. NLRP3 inflammasomes were activated in macrophages ...[more]

PMID: 40279432

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Project description:To recruit phagocytes, apoptotic cells characteristically release ATP, which functions as a “danger” signal. Here, we found that the culture supernatant of apoptotic cells activated the macrophages to express anti-inflammatory genes such as NR4A and Thbs1. A high level of AMP accumulated in the apoptotic cell supernatant in a Pannexin1-dependent manner. A nucleotidase inhibitor and A2a adenosine receptor antagonist inhibited the apoptotic supernatant-induced gene expression, suggesting AMP was metabolized to adenosine by an ecto-5’-nucleotidase expressed on macrophages, to activate the macrophage A2a adenosine receptor. Intraperitoneal injection of zymosan into AdoR A2a- or Panx1-deficient mice produced high, sustained levels of inflammatory mediators in the peritoneal lavage. These results indicated that AMP from apoptotic cells suppresses inflammation as a “calm down” signal. If apoptotic cells produce “danger” or “anti-danger” signal(s), we rationalized that such signals would activate gene expression in macrophages. To investigate this possibility, we examined the effect of the culture supernatant from apoptotic cells on macrophage gene expression by using microarrays. For mouse BMDMs, bone marrow cells from female C57BL/6J mice at 8 weeks of age were cultured for more than 7 days with DMEM containing 10% FCS supplemented with mouse M-CSF. We used adherent cells as BMDMs in the study. W3 cells, mouse T cell line expressing Fas, were treated with human Fas ligand at 37°C for 30 min to induce apoptosis. The cells were then washed and re-suspended at a concentration of 1 × 107 cells/ml with RPMI containing 1% FCS, and further incubated for 60 min at 37°C. Following Fas ligand treatment, more than 90% of the W3 cells were Annexin V positive, and only small percentage were positive for both Annexin V and propidium iodide (PI). The culture supernatant was collected from apoptotic W3 cells. Next, BMDMs were incubated with medium (BMDMs-Medium) or apoptotic W3 cell supernatant (BMDMs-Apoptotic cell supernatant) for 1 h. Total RNA was extracted from the cells and hybridized on Affymetrix microarrays.

			Action	DRS
	MWBD241048a_mix01.mzML	Mzml
	MWBD241048a_mix02.mzML	Mzml
	MWBD241048a_mix03.mzML	Mzml
	MWBD241048a_mix04.mzML	Mzml
	NEG_MWBD241048a_mix01.mzML	Mzml