The role of ELAM-1 in the adhesion of monocytes to HUVEC, activated for 4h with TNF, was studied using MoAb ENA2 directed against ELAM-1. In a standard adhesion assay at 37 degrees C, F(ab')2 fragments of ENA2 did not, or weakly inhibited adhesion. When metabolic activity of the monocytes was reduced by (i) fixing the monocytes, (ii) performing the adhesion assay at 4 degrees C, and (iii) combining the forementioned conditions, the adhesion of the monocytes was strongly blocked by ENA2 and less effective or not by MoAb IB4 anti-CD18. The pattern of adhesion of monocytes to HUVEC, activated with TNF assessed at 4 degrees C, paralleled ELAM-1 expression on the endothelial cells. Maximal inhibitory effect of ENA2 on adhesion was shown 5 h after activation of HUVEC, at which ELAM-1 expression was also maximal. Adhesion assessed at 37 degrees C remained enhanced for at least 24 h, whereas the inhibitory effect of ENA2 followed ELAM-1 expression. Specific involvement of ELAM-1 was also confirmed using ELAM-1 transfected COS cells. These results indicated that monocytes express a counter structure for ELAM-1 and that this counter structure is involved in adhesion.
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http://dx.doi.org/10.1111/j.1365-3083.1992.tb02866.x | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Immunology, School of Medicine, UConn Health, Farmington, CT 06030.
Monocytes are critical in controlling tissue infections and inflammation. Monocyte dysfunction contributes to the inflammatory pathogenesis of cystic fibrosis (CF) caused by CF transmembrane conductance regulator (CFTR) mutations, making CF a clinically relevant disease model for studying the contribution of monocytes to inflammation. Although CF monocytes exhibited adhesion defects, the precise mechanism is unclear.
View Article and Find Full Text PDFExp Cell Res
January 2025
Department of Internal Medicine, Hebei Medical University, Shijiazhuang 050017, Hebei, China; Department of Cardiology, Hebei General Hospital, Shijiazhuang 050051, Hebei, China. Electronic address:
SRY-Box Transcription Factor-11 (SOX11) is a transcriptional regulatory factor that plays a crucial role in inflammatory responses. However, its involvement in atherosclerosis (AS), a cardiovascular disease driven by endothelial cell inflammation, remains unknown. This study aims to elucidate the role of SOX11 in AS.
View Article and Find Full Text PDFSci Rep
January 2025
Division of Liver Surgery, Department of General Surgery, West China Hospital, Si Chuan University, Chengdu, 610041, China.
Chemokine (C-X3-C motif) Receptor 1 (CX3CR1) primarily mediates the chemotaxis and adhesion of immune cells. However, its role in hepatitis C virus (HCV)-induced early-stage liver cirrhosis remains unexplored. GSE15654 was downloaded from the GEO database.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
College of Life Sciences and Biotechnology, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea.
Bone marrow stromal antigen 2 (BST2) is a host-restriction factor that plays multiple roles in the antiviral defense of innate immune responses, including the inhibition of viral particle release from virus-infected cells. BST2 may also be involved in the endothelial adhesion and migration of monocytes, but its importance in the immune system is still unclear. Immune cell adhesion and migration are closely related to the initiation of immune responses.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Department of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Beyond dyslipidemia, inflammation contributes to the development of atherosclerosis. However, intrinsic factors that counteract vascular inflammation and atherosclerosis remain scarce. Here we identify insulin-like growth factor binding protein 6 (IGFBP6) as a homeostasis-associated molecule that restrains endothelial inflammation and atherosclerosis.
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