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Background: Our previous work revealed the high expression of fibrinogen alpha chain (FGA) in patients with endometriosis (EM) and that it could promote the migration and invasion of endometrial stromal cells. Angiogenesis is the key condition for the development of EM. This study was aimed to elucidate the role of FGA in endometrial stromal cells involved in angiogenesis in EM.

Methods: Immunohistochemistry was used to detect the microvessel density (MVD) and VEGF expression in the eutopic endometrium samples from EM and non-EM. The conditioned medium (CM) of human primary eutopic endometrial stromal cells (EuESC) and immortalized endometrial stromal cell line hEM15A with FGA knockdown were collected and used to treat human umbilical vein endothelial cells (HUVECs). Then, tube formation assay, EdU assay, wound assay, transwell assay and flow cytometry assays were performed to assess the function of HUEVCs in vitro . The angiogenic capability of HUVECs was further measured using a matrigel plug assay with BALB/c nude mice in vivo . Immunofluorescence was used to detect the expression of F-actin and VE-cadherin. RT-PCR and western blotting were used to detect the expression of angiogenesis-related factors in endometrial stromal cells and downstream signalling pathways in HUVECs.

Results: MVD and VEGF expression in the eutopic endometrium of EM patients were significantly higher than those in the normal endometrium of non-EM patients, and the increased MVD in EM indicates an increased risk of recurrence. Functionally, we found that CM of endometrial stromal cells with FGA knockdown could inhibit HUEVCs migration and tube formation in vitro and in vivo , while having no significant effect on HUVECs proliferation, apoptosis and cell cycle. Mechanically, the expression of VEGFA, PDGF, FGF-B, VEGF, MMP-2 and MMP-9 was reduced in hEM15A cells with FGA knockdown. CM of hEM15A cells with FGA knockdown reduced the number of microfilaments and pseudopodia, as well as the expression of VE-cadherin, and inhibited the activity of VEGFR2 and the FAK signalling pathway in HUVECs.

Conclusion: Our study demonstrated FGA could enhance the interaction between endometrial stromal cells and HUVECs via the potential VEGA-VEGFR-FAK signalling axis and promote EM angiogenesis, revealing a promising therapeutic approach for EM.

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Titel:	FGA Controls VEGFA Secretion to Promote Angiogenesis by Activating the VEGFR2-FAK Signalling Pathway.
Autor/in / Beteiligte Person:	Li, H ; Cai, E ; Cheng, H ; Ye, X ; Ma, R ; Zhu, H ; Chang, X
Link:	Full Text Finder (Volltext)
Zeitschrift:	Frontiers in endocrinology, Jg. 13 (2022-04-13), S. 791860
Veröffentlichung:	[Lausanne : Frontiers Research Foundation], 2022
Medientyp:	academicJournal
ISSN:	1664-2392 (print)
DOI:	10.3389/fendo.2022.791860
Schlagwort:	Animals Extracellular Matrix Proteins Female Human Umbilical Vein Endothelial Cells Humans Mice Mice, Nude Signal Transduction Endometriosis Fibrinogen metabolism Vascular Endothelial Growth Factor A genetics
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article Language: English [Front Endocrinol (Lausanne)] 2022 Apr 13; Vol. 13, pp. 791860. <i>Date of Electronic Publication: </i>2022 Apr 13 (<i>Print Publication: </i>2022). MeSH Terms: Endometriosis* ; Vascular Endothelial Growth Factor A* / genetics ; Fibrinogen / *metabolism ; Animals ; Extracellular Matrix Proteins ; Female ; Human Umbilical Vein Endothelial Cells ; Humans ; Mice ; Mice, Nude ; Signal Transduction References: Angiogenesis. 2019 May;22(2):311-323. (PMID: 30539314) ; Nat Rev Cancer. 2008 Aug;8(8):579-91. (PMID: 18596824) ; Ann Lab Med. 2020 Sep;40(5):390-397. (PMID: 32311852) ; FASEB J. 2016 Oct;30(10):3515-3526. (PMID: 27402674) ; Ultrasound Med Biol. 2018 Jul;44(7):1460-1467. (PMID: 29706409) ; Int J Mol Sci. 2016 Nov 01;17(11):. (PMID: 27809279) ; Chin Med J (Engl). 2015 Feb 20;128(4):520-7. (PMID: 25673457) ; Stem Cell Res Ther. 2018 Jul 4;9(1):176. (PMID: 29973254) ; Ann N Y Acad Sci. 2001;936:406-25. (PMID: 11460495) ; Cell. 2011 Sep 16;146(6):873-87. (PMID: 21925313) ; Biol Reprod. 2020 Oct 5;103(4):779-790. (PMID: 32697296) ; Nat Rev Drug Discov. 2009 Mar;8(3):235-53. (PMID: 19247306) ; Res Pract Thromb Haemost. 2019 Mar 04;3(2):161-172. (PMID: 31011700) ; Nat Commun. 2016 Jun 29;7:11996. (PMID: 27353863) ; Med Sci Monit. 2011 Apr;17(4):RA92-9. (PMID: 21455119) ; Reprod Biomed Online. 2019 Dec;39(6):893-904. (PMID: 31740226) ; Clin Proteomics. 2019 Apr 23;16:17. (PMID: 31043929) ; Hum Reprod Update. 2012 Nov-Dec;18(6):682-702. (PMID: 22718320) ; Chin Med J (Engl). 2007 Jul 20;120(14):1241-6. (PMID: 17697575) ; Environ Health Perspect. 2018 Dec;126(12):127004. (PMID: 30675821) ; Fertil Steril. 2016 Apr;105(4):1093-101. (PMID: 26769301) ; Nat Rev Mol Cell Biol. 2016 Oct;17(10):611-25. (PMID: 27461391) ; J Extracell Vesicles. 2020 Apr 14;9(1):1750202. (PMID: 32363013) ; Front Oncol. 2019 Dec 06;9:1370. (PMID: 31921634) ; JAMA. 2018 Dec 25;320(24):2608. (PMID: 30575883) ; Expert Opin Biol Ther. 2003 Oct;3(7):1105-20. (PMID: 14519075) ; Nat Rev Endocrinol. 2019 Nov;15(11):666-682. (PMID: 31488888) ; Biomed Pharmacother. 2018 Oct;106:163-174. (PMID: 29958140) ; Int J Mol Med. 2019 Feb;43(2):945-955. (PMID: 30569127) ; Hum Reprod. 2016 Apr;31(4):734-49. (PMID: 26908845) ; J Biochem. 2000 Oct;128(4):705-10. (PMID: 11011154) ; Mol Hum Reprod. 2017 Mar 1;23(3):187-198. (PMID: 28158750) ; N Engl J Med. 2020 Mar 26;382(13):1244-1256. (PMID: 32212520) ; Am J Pathol. 1927 Mar;3(2):93-110.43. (PMID: 19969738) ; Hum Reprod. 1998 Mar;13(3):715-9. (PMID: 9572440) ; J Proteome Res. 2010 Aug 6;9(8):3781-8. (PMID: 20557135) ; Eur J Obstet Gynecol Reprod Biol. 2016 Sep;204:88-98. (PMID: 27541444) ; Mol Cancer. 2015 Apr 17;14:86. (PMID: 25890345) ; Hum Reprod Update. 2018 Mar 01;24(2):207-224. (PMID: 29377994) ; Mol Med Rep. 2018 Oct;18(4):3727-3736. (PMID: 30106150) ; PLoS Med. 2008 Jan 29;5(1):e19. (PMID: 18232728) ; J Cell Physiol. 2019 Nov;234(11):19384-19392. (PMID: 31004368) ; F1000Res. 2019 Apr 23;8:. (PMID: 31069056) ; J Biol Chem. 1997 Feb 21;272(8):5360-6. (PMID: 9030612) ; Cells. 2019 Dec 15;8(12):. (PMID: 31847469) Contributed Indexing: Keywords: VEGFA-VEFGR2 pathway; angiogenesis; endometriosis; endothelial cells; fibrinogen alpha chain (FGA) Substance Nomenclature: 0 (Extracellular Matrix Proteins) ; 0 (FGA protein, human) ; 0 (VEGFA protein, human) ; 0 (Vascular Endothelial Growth Factor A) ; 9001-32-5 (Fibrinogen) Entry Date(s): Date Created: 20220502 Date Completed: 20220503 Latest Revision: 20220716 Update Code: 20240513 PubMed Central ID: PMC9043601

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FGA Controls VEGFA Secretion to Promote Angiogenesis by Activating the VEGFR2-FAK Signalling Pathway.