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Tytuł pozycji:

MiR-15p-5p Mediates the Coordination of ICAM-1 and FAK to Promote Endothelial Cell Proliferation and Migration.

Tytuł:
MiR-15p-5p Mediates the Coordination of ICAM-1 and FAK to Promote Endothelial Cell Proliferation and Migration.
Autorzy:
Gu W; Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai StreetAnhui Province, Bengbu, 233030, China.; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China.
Zhang L; Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai StreetAnhui Province, Bengbu, 233030, China.; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China.
Zhang X; Department of Basic Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Hubei Province, Wuhan, 430070, China.
Wang B; Department of Basic Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Hubei Province, Wuhan, 430070, China.
Shi X; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China.
Hu K; Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai StreetAnhui Province, Bengbu, 233030, China.; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China.
Ye Y; Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai StreetAnhui Province, Bengbu, 233030, China.; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China.
Liu G; Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, 2600 Donghai StreetAnhui Province, Bengbu, 233030, China. .; Anhui Province Key Laboratory of Translational Cancer Research, Bengbu Medical College, Anhui Province, Bengbu, 233030, China. .
Źródło:
Inflammation [Inflammation] 2022 Jun; Vol. 45 (3), pp. 1402-1417. Date of Electronic Publication: 2022 Jan 26.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 1999- : New York, NY : Kluwer Academic/Plenum Publishers
Original Publication: New York, Plenum Press.
MeSH Terms:
Cell Movement*
Intercellular Adhesion Molecule-1*/genetics
Intercellular Adhesion Molecule-1*/metabolism
MicroRNAs*/genetics
MicroRNAs*/metabolism
3' Untranslated Regions ; Animals ; Cell Proliferation ; Endothelial Cells/metabolism ; Focal Adhesion Protein-Tyrosine Kinases ; Inflammation/genetics ; Mice
References:
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Grant Information:
31372418 National Natural Science Foundation of China; 82104178 National Natural Science Foundation of China; BYKC201903 Bengbu Medical College Scientific and Technology Self-Innovation Foundation Program; Research Project of Anhui Educational Committee Natural Science Research Project of Anhui Educational Committee
Contributed Indexing:
Keywords: FAK; ICAM-1; cell proliferation; inflammation; miR-15b-5p
Substance Nomenclature:
0 (3' Untranslated Regions)
0 (MicroRNAs)
126547-89-5 (Intercellular Adhesion Molecule-1)
EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
Entry Date(s):
Date Created: 20220126 Date Completed: 20220516 Latest Revision: 20220531
Update Code:
20240105
DOI:
10.1007/s10753-022-01630-3
PMID:
35079920
Czasopismo naukowe
Intercellular adhesion molecule-1 (ICAM-1) in endothelial cells is critical for neutrophil adhesion and transmigration across the endothelium. Focal adhesion kinase (FAK), which controls the turnover of focal adhesion to regulate cell adhesion and migration, plays a role in the resolution of inflammation. However, the coordinated involvement of ICAM-1 and FAK during endothelial inflammation has yet to be elucidated. This study reports that, as part of an inflammatory response, ICAM-1 controls FAK expression in endothelial cells via the microRNA miR-15b-5p. Induction of lung injury by lipopolysaccharide (LPS) resulted in higher levels of FAK expression in inflammatory tissues, while in ICAM-1 knockout mice, FAK expression was reduced in the lungs. FAK expression was also reduced in endothelial cells following ICAM-1 siRNA downregulation. Furthermore, ICAM-1 inhibited miR-15b-5p expression while increasing FAK mRNA and protein expression via binding of miR-15b-5p to the 3' untranslated region (UTR) of FAK. ICAM-1 inhibited miR-15b-5p promoter activity and hence reduced miR-15b-5p expression. FAK increased endothelial cell proliferation and migration, whereas miR-15b-5p inhibited cell proliferation and migration. These findings indicate that the inflammatory molecule ICAM-1 regulates FAK expression via miR-15b-5p levels, which in turn controls endothelial cell proliferation and migration.
(© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

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