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- 01GJ2R1AEEEHATB635NYAC5R8V classification A1.
- 01GJ2R1AEEEHATB635NYAC5R8V date "2022".
- 01GJ2R1AEEEHATB635NYAC5R8V language "eng".
- 01GJ2R1AEEEHATB635NYAC5R8V type journalArticle.
- 01GJ2R1AEEEHATB635NYAC5R8V hasPart 01GJ2R5KJMW74691NSK7KC7D2X.pdf.
- 01GJ2R1AEEEHATB635NYAC5R8V subject "Biology and Life Sciences".
- 01GJ2R1AEEEHATB635NYAC5R8V subject "Medicine and Health Sciences".
- 01GJ2R1AEEEHATB635NYAC5R8V doi "10.1038/s41467-022-28809-4".
- 01GJ2R1AEEEHATB635NYAC5R8V issn "2041-1723".
- 01GJ2R1AEEEHATB635NYAC5R8V issue "1".
- 01GJ2R1AEEEHATB635NYAC5R8V volume "13".
- 01GJ2R1AEEEHATB635NYAC5R8V abstract "Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process, which requires rapid responses via post translational modifications (PTM) of proteins. Protein arginine methyltransferase 7 (PRMT7) is an epigenetic factor that has the capacity to mono-methylate histones on arginine residues. Here we show that in chronic obstructive pulmonary disease (COPD) patients, PRMT7 expression is elevated in the lung tissue and localized to the macrophages. In mouse models of COPD, lung fibrosis and skin injury, reduced expression of PRMT7 associates with decreased recruitment of monocytes to the site of injury and hence less severe symptoms. Mechanistically, activation of NF-kappa B/RelA in monocytes induces PRMT7 transcription and consequential mono-methylation of histones at the regulatory elements of RAP1A, which leads to increased transcription of this gene that is responsible for adhesion and migration of monocytes. Persistent monocyte-derived macrophage accumulation leads to ALOX5 over-expression and accumulation of its metabolite LTB4, which triggers expression of ACSL4 a ferroptosis promoting gene in lung epithelial cells. Conclusively, inhibition of arginine mono-methylation might offer targeted intervention in monocyte-driven inflammatory conditions that lead to extensive tissue damage if left untreated. Chronic obstructive pulmonary disease is a progressive and incurable chronic condition that involves accumulation of inflammatory macrophages in the lung tissue. Authors here show in mouse models of lung disease that PRMT7, a protein arginine methyltransferase, is an important regulator of recruitment and the pro-inflammatory phenotype of macrophages.".
- 01GJ2R1AEEEHATB635NYAC5R8V author 358D04BC-F0EE-11E1-A9DE-61C894A0A6B4.
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- 01GJ2R1AEEEHATB635NYAC5R8V author urn:uuid:16036794-251f-4b54-9264-b344d03de45b.
- 01GJ2R1AEEEHATB635NYAC5R8V author urn:uuid:17779fdd-e7d6-4046-a448-48103d629770.
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- 01GJ2R1AEEEHATB635NYAC5R8V author urn:uuid:fc2ba957-df2d-49a1-9b6c-1fef381d8b2f.
- 01GJ2R1AEEEHATB635NYAC5R8V dateCreated "2022-11-17T12:11:52Z".
- 01GJ2R1AEEEHATB635NYAC5R8V dateModified "2024-11-28T00:15:24Z".
- 01GJ2R1AEEEHATB635NYAC5R8V name "The arginine methyltransferase PRMT7 promotes extravasation of monocytes resulting in tissue injury in COPD".
- 01GJ2R1AEEEHATB635NYAC5R8V pagination urn:uuid:03c3b825-2d1b-4fd5-bfff-5260034ca278.
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- 01GJ2R1AEEEHATB635NYAC5R8V type A1.