TNFα induces matrix metalloproteinase-9 expression in monocytic cells through ACSL1/JNK/ERK/NF-kB signaling pathways.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
01 09 2023
01 09 2023
Historique:
received:
21
01
2023
accepted:
28
08
2023
medline:
4
9
2023
pubmed:
2
9
2023
entrez:
1
9
2023
Statut:
epublish
Résumé
Studies have established the association between increased plasma levels of matrix metalloproteinase (MMP)-9 and adipose tissue inflammation. Tumor necrosis factor α (TNFα) was elevated in obesity and is involved in the induction of MMP-9 in monocytic cells. However, the underlying molecular mechanism was incompletely understood. As per our recent report, TNFα mediates inflammatory responses through long-chain acyl-CoA synthetase 1 (ACSL1). Therefore, we further investigated the role of ACSL1 in TNFα-mediated MMP-9 secretion in monocytic cells. THP-1 cells and primary monocytes were used to study MMP-9 expression. mRNA and protein levels of MMP-9 were determined by qRT-PCR and ELISA, respectively. Signaling pathways were studied using Western blotting, inhibitors, and NF-kB/AP1 reporter cells. We found that THP-1 cells and primary human monocytes displayed increased MMP-9 mRNA expression and protein secretion after incubation with TNFα. ACSL1 inhibition using triacsin C significantly reduced the expression of MMP-9 in the THP-1 cells. However, the inhibition of β-oxidation and ceramide biosynthesis did not affect the TNFα-induced MMP-9 production. Using small interfering RNA-mediated ACSL1 knockdown, we further confirmed that TNFα-induced MMP-9 expression/secretion was significantly reduced in ACSL1-deficient cells. TNFα-mediated MMP-9 expression was also significantly reduced by the inhibition of ERK1/ERK2, JNK, and NF-kB. We further observed that TNFα induced phosphorylation of SAPK/JNK (p54/46), ERK1/2 (p44/42 MAPK), and NF-kB p65. ACSL1 inhibition reduced the TNFα-mediated phosphorylation of SAPK/JNK, c-Jun, ERK1/2, and NF-kB. In addition, increased NF-κB/AP-1 activity was inhibited in triacsin C treated cells. Altogether, our findings suggest that ACSL1/JNK/ERK/NF-kB axis plays an important role in the regulation of MMP-9 induced by TNFα in monocytic THP-1 cells.
Identifiants
pubmed: 37658104
doi: 10.1038/s41598-023-41514-6
pii: 10.1038/s41598-023-41514-6
pmc: PMC10474281
doi:
Substances chimiques
NF-kappa B
0
triacsin C
6M6D4602I5
Tumor Necrosis Factor-alpha
0
Matrix Metalloproteinase 9
EC 3.4.24.35
ACSL1 protein, human
EC 6.2.1.3
Coenzyme A Ligases
EC 6.2.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
14351Informations de copyright
© 2023. Springer Nature Limited.
Références
Cell Physiol Biochem. 2014;34(3):929-42
pubmed: 25200491
Cell Physiol Biochem. 2019;52(3):397-407
pubmed: 30845379
Oncogene. 1997 Apr 24;14(16):1995-8
pubmed: 9150367
Diabetes Metab Res Rev. 2019 Feb;35(2):e3087
pubmed: 30339734
Cell. 1998 May 1;93(3):411-22
pubmed: 9590175
J Clin Endocrinol Metab. 2010 Jun;95(6):2993-3001
pubmed: 20392866
Cell Metab. 2010 Jul 7;12(1):53-64
pubmed: 20620995
Cell Physiol Biochem. 2016;39(3):889-900
pubmed: 27497609
Semin Immunol. 2014 Jun;26(3):253-66
pubmed: 24958609
Clin Exp Allergy. 2000 Jan;30(1):48-55
pubmed: 10606930
J Inflamm Res. 2022 Jul 27;15:4291-4302
pubmed: 35923906
Int J Retina Vitreous. 2022 Jun 21;8(1):44
pubmed: 35729613
FEBS Lett. 1998 Sep 11;435(1):29-34
pubmed: 9755853
Metabolism. 2015 Apr;64(4):527-38
pubmed: 25633268
Endothelium. 2008 Jul-Aug;15(4):219-24
pubmed: 18663625
Future Lipidol. 2008;3(5):545-556
pubmed: 18978945
J Cell Physiol. 2004 Mar;198(3):417-27
pubmed: 14755547
J Periodontal Res. 2012 Apr;47(2):236-42
pubmed: 22035412
J Immunol. 2018 May 15;200(10):3599-3611
pubmed: 29632147
Adv Drug Deliv Rev. 2016 Apr 1;99(Pt B):180-185
pubmed: 26621196
J Cancer. 2016 Jan 01;7(1):42-9
pubmed: 26722359
Glia. 2002 Sep;39(3):279-91
pubmed: 12203394
Cell Physiol Biochem. 2019;52(4):908-921
pubmed: 30964608
Sci Rep. 2021 Apr 15;11(1):8259
pubmed: 33859296
Biol Reprod. 2010 Sep;83(3):481-7
pubmed: 20463356
Shock. 2001 Feb;15(2):135-42
pubmed: 11220642
J Biomed Sci. 2014 Feb 05;21:12
pubmed: 24502696
Cell Physiol Biochem. 2017;41(5):1993-2003
pubmed: 28419983
Arthritis Res. 2000;2(3):189-202
pubmed: 11094428
Biochem Biophys Res Commun. 2017 Jun 10;487(4):903-909
pubmed: 28465234
Sci Rep. 2020 Oct 1;10(1):16364
pubmed: 33004937
JCI Insight. 2020 Jun 4;5(11):
pubmed: 32369451
PLoS One. 2016 Oct 3;11(10):e0162667
pubmed: 27695085
J Immunol. 2000 Nov 15;165(10):5788-97
pubmed: 11067938
Mol Hum Reprod. 2006 Apr;12(4):225-32
pubmed: 16520344
J Mol Cell Cardiol. 2016 May;94:1-9
pubmed: 26995156
Biol Chem. 2006 Jan;387(1):69-78
pubmed: 16497166
J Biol Chem. 2013 Apr 5;288(14):9957-9970
pubmed: 23426369
Anticancer Res. 2014 Mar;34(3):1355-66
pubmed: 24596383
J Immunol. 2002 Aug 1;169(3):1401-9
pubmed: 12133965
Nat Rev Rheumatol. 2016 Jan;12(1):37-48
pubmed: 26633290
Oral Dis. 2017 Mar;23(2):199-209
pubmed: 27868311
Cells. 2022 Sep 15;11(18):
pubmed: 36139454
J Leukoc Biol. 2019 Oct;106(4):787-790
pubmed: 31269272
Atherosclerosis. 2005 Jan;178(1):207-15
pubmed: 15585220
J Neuroinflammation. 2012 Dec 13;9:268
pubmed: 23234315
Int J Mol Sci. 2021 Jul 19;22(14):
pubmed: 34299302
Int J Mol Sci. 2021 Sep 29;22(19):
pubmed: 34638857
Biomedicines. 2020 Oct 09;8(10):
pubmed: 33050324
Bratisl Lek Listy. 2005;106(3):127-32
pubmed: 16026148
Biomedicines. 2021 Oct 29;9(11):
pubmed: 34829801
Eur J Microbiol Immunol (Bp). 2011 Dec;1(4):302-10
pubmed: 24516737