Melatonin increases collagen content accumulation and Fibroblast Growth Factor-2 secretion in cultured human cardiac fibroblasts.
Cell cultures
Collagen
Connective tissue
Fibroblast
Glycosaminoglycan
Heart
Melatonin
Proliferation
Journal
Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
02
02
2023
accepted:
25
04
2023
revised:
24
04
2023
medline:
31
5
2023
pubmed:
16
5
2023
entrez:
15
5
2023
Statut:
ppublish
Résumé
The extracellular matrix serves as a scaffold for cardiomyocytes, allowing them to work in accord. In rats, collagen metabolism within a myocardial infarction scar is regulated by melatonin. The present study determines whether melatonin influences matrix metabolism within human cardiac fibroblast cultures and examines the underlying mechanism. The experiments were performed on cultures of cardiac fibroblasts. The Woessner method, 1,9-dimethylmethylene blue assay, enzyme-linked immunosorbent assay and quantitative PCR were used in the study. Melatonin treatment lowered the total cell count within the culture, elevated necrotic and apoptotic cell count as well as augmented cardiac fibroblast proliferation, and increased total, intracellular, and extracellular collagen within the fibroblast culture; it also elevated type III procollagen α1 chain expression, without increasing procollagen type I mRNA production. The pineal hormone did not influence matrix metalloproteinase-2 (MMP-2) release or glycosaminoglycan accumulation by cardiac fibroblasts. Melatonin increased the release of Fibroblast Growth Factor-2 (FGF-2) by human cardiac fibroblasts, but cardiotrophin release was not influenced. Within human cardiac fibroblast culture, collagen metabolism is regulated by melatonin. The profibrotic effect of melatonin depends on the elevation of procollagen type III gene expression, and this could be modified by FGF-2. Two parallel processes, viz., cell elimination and proliferation, induced by melatonin, lead to excessive replacement of cardiac fibroblasts.
Sections du résumé
BACKGROUND
BACKGROUND
The extracellular matrix serves as a scaffold for cardiomyocytes, allowing them to work in accord. In rats, collagen metabolism within a myocardial infarction scar is regulated by melatonin. The present study determines whether melatonin influences matrix metabolism within human cardiac fibroblast cultures and examines the underlying mechanism.
METHODS
METHODS
The experiments were performed on cultures of cardiac fibroblasts. The Woessner method, 1,9-dimethylmethylene blue assay, enzyme-linked immunosorbent assay and quantitative PCR were used in the study.
RESULTS
RESULTS
Melatonin treatment lowered the total cell count within the culture, elevated necrotic and apoptotic cell count as well as augmented cardiac fibroblast proliferation, and increased total, intracellular, and extracellular collagen within the fibroblast culture; it also elevated type III procollagen α1 chain expression, without increasing procollagen type I mRNA production. The pineal hormone did not influence matrix metalloproteinase-2 (MMP-2) release or glycosaminoglycan accumulation by cardiac fibroblasts. Melatonin increased the release of Fibroblast Growth Factor-2 (FGF-2) by human cardiac fibroblasts, but cardiotrophin release was not influenced.
CONCLUSION
CONCLUSIONS
Within human cardiac fibroblast culture, collagen metabolism is regulated by melatonin. The profibrotic effect of melatonin depends on the elevation of procollagen type III gene expression, and this could be modified by FGF-2. Two parallel processes, viz., cell elimination and proliferation, induced by melatonin, lead to excessive replacement of cardiac fibroblasts.
Identifiants
pubmed: 37188903
doi: 10.1007/s43440-023-00490-4
pii: 10.1007/s43440-023-00490-4
pmc: PMC10227126
doi:
Substances chimiques
Collagen
9007-34-5
Fibroblast Growth Factor 2
103107-01-3
Matrix Metalloproteinase 2
EC 3.4.24.24
Melatonin
JL5DK93RCL
Procollagen Type I
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
560-569Subventions
Organisme : Uniwersytet Medyczny w Lodzi
ID : 503/6-103-02/503-61-001-19-00
Informations de copyright
© 2023. The Author(s).
Références
Cytokine Growth Factor Rev. 2017 Dec;38:49-58
pubmed: 28967471
Exp Physiol. 1998 Sep;83(5):585-93
pubmed: 9793779
Cytobios. 1999;100(393):49-55
pubmed: 10643644
Cell Mol Life Sci. 2014 Aug;71(16):2997-3025
pubmed: 24554058
FASEB J. 2020 Apr;34(4):5282-5298
pubmed: 32067273
Ann Anat. 2020 Nov;232:151564
pubmed: 32603827
FASEB J. 2006 Feb;20(2):269-76
pubmed: 16449799
Neuro Endocrinol Lett. 2015;36(3):187-92
pubmed: 26313381
Annu Rev Biochem. 1978;47:385-417
pubmed: 354500
Hypertension. 2019 Mar;73(3):602-611
pubmed: 30612490
Biochim Biophys Acta Mol Basis Dis. 2022 Jan 1;1868(1):166281
pubmed: 34610472
Biochim Biophys Acta. 1999 Oct 18;1472(1-2):206-14
pubmed: 10572942
J Pineal Res. 2008 Oct;45(3):285-90
pubmed: 18384532
Int J Mol Sci. 2021 Nov 10;22(22):
pubmed: 34830026
J Physiol Pharmacol. 2011 Feb;62(1):29-35
pubmed: 21451207
Trends Endocrinol Metab. 2008 Jan;19(1):17-24
pubmed: 18155917
Acta Histochem. 2021 Apr;123(3):151700
pubmed: 33667778
J Am Heart Assoc. 2019 Feb 5;8(3):e011155
pubmed: 30686096
Pharmacol Rep. 2012;64(6):1442-54
pubmed: 23406755
Molecules. 2021 Aug 20;26(16):
pubmed: 34443626
Connect Tissue Res. 2010 Dec;51(6):491-6
pubmed: 20388018
J Pineal Res. 1999 Sep;27(2):106-10
pubmed: 10496146
Molecules. 2021 Aug 31;26(17):
pubmed: 34500708
Curr Drug Targets Cardiovasc Haematol Disord. 2003 Mar;3(1):1-30
pubmed: 12769643
Neuro Endocrinol Lett. 2002 Apr;23 Suppl 1:50-4
pubmed: 12019352
Acta Biochim Biophys Sin (Shanghai). 2021 Oct 12;53(10):1333-1341
pubmed: 34343226
Int J Biol Macromol. 2022 Feb 1;197:103-110
pubmed: 34968534
Mol Pharmacol. 2000 Nov;58(5):967-75
pubmed: 11040043
J Cell Physiol. 2010 Nov;225(3):631-7
pubmed: 20635395
J Pineal Res. 2021 Jan;70(1):e12686
pubmed: 32730639
Eur J Pharmacol. 2017 Mar 5;798:57-65
pubmed: 28011346
Antioxidants (Basel). 2020 Jun 22;9(6):
pubmed: 32580481
J Cell Mol Med. 2020 Dec;24(23):13853-13862
pubmed: 33124775
J Mater Sci Mater Med. 2005 Jun;16(6):581-5
pubmed: 15928875
J Cell Mol Med. 2021 Feb;25(3):1480-1492
pubmed: 33369155
J Physiol Pharmacol. 1996 Dec;47(4):621-7
pubmed: 9116329
Chin Med J (Engl). 2018 Sep 05;131(17):2089-2096
pubmed: 30127219