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  NCX1 represents an ionic Na(+)sensing mechanism in macrophages

Neubert, P., Homann, A., Wendelborn, D., Baer, A.-L., Krampert, L., Trum, M., et al. (2020). NCX1 represents an ionic Na(+)sensing mechanism in macrophages. PLOS BIOLOGY, 18(6): e3000722. doi:10.1371/journal.pbio.3000722.

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 Creators:
Neubert, Patrick1, Author
Homann, Arne1, Author
Wendelborn, David1, Author
Baer, Anna-Lorena1, Author
Krampert, Luka1, Author
Trum, Maximilian1, Author
Schroeder, Agnes1, Author
Ebner, Stefan2, Author              
Weichselbaum, Andrea1, Author
Schatz, Valentin1, Author
Linz, Peter1, Author
Veelken, Roland1, Author
Schulte-Schrepping, Jonas1, Author
Aschenbrenner, Anna C.1, Author
Quast, Thomas1, Author
Kurts, Christian1, Author
Geisberger, Sabrina1, Author
Kunzelmann, Karl1, Author
Hammer, Karin1, Author
Binger, Katrina J.1, Author
Titze, Jens1, AuthorMueller, Dominik N.1, AuthorKolanus, Waldemar1, AuthorSchultze, Joachim L.1, AuthorWagner, Stefan1, AuthorJantsch, Jonathan1, Author more..
Affiliations:
1external, ou_persistent22              
2Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565159              

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Free keywords: SODIUM-CALCIUM EXCHANGE; ANTIBACTERIAL DEFENSE; NA+/CA2+ EXCHANGER; CA2+ ENTRY; EXPRESSION; PROTEIN; CELLS; INHIBITOR; AMILORIDE; CHANNELS
 Abstract: Inflammation and infection can trigger local tissue Na(+)accumulation. This Na+-rich environment boosts proinflammatory activation of monocyte/macrophage-like cells (M phi s) and their antimicrobial activity. Enhanced Na+-driven M phi function requires the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5), which augments nitric oxide (NO) production and contributes to increased autophagy. However, the mechanism of Na(+)sensing in M phi s remained unclear. High extracellular Na(+)levels (high salt [HS]) trigger a substantial Na(+)influx and Ca(2+)loss. Here, we show that the Na+/Ca(2+)exchanger 1 (NCX1, also known as solute carrier family 8 member A1 [SLC8A1]) plays a critical role in HS-triggered Na(+)influx, concomitant Ca(2+)efflux, and subsequent augmented NFAT5 accumulation. Moreover, interfering with NCX1 activity impairs HS-boosted inflammatory signaling, infection-triggered autolysosome formation, and subsequent antibacterial activity. Taken together, this demonstrates that NCX1 is able to sense Na(+)and is required for amplifying inflammatory and antimicrobial M phi responses upon HS exposure. Manipulating NCX1 offers a new strategy to regulate M phi function.

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Language(s): eng - English
 Dates: 2020
 Publication Status: Published online
 Pages: 21
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
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Title: PLOS BIOLOGY
Source Genre: Journal
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Publ. Info: 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA : PUBLIC LIBRARY SCIENCE
Pages: - Volume / Issue: 18 (6) Sequence Number: e3000722 Start / End Page: - Identifier: ISSN: 1544-9173