guest ::
| Home > Publications database > Heme oxygenase-1 modulates CD62E-dependent endothelial cell-monocyte interactions and mitigates HLA-I-induced transplant vasculopathy in mice. |
| Home > Publications database > Heme oxygenase-1 modulates CD62E-dependent endothelial cell-monocyte interactions and mitigates HLA-I-induced transplant vasculopathy in mice. |
| Journal Article | DKFZ-2025-00625 |
; ; ; ; ; ; ; ;
2025
Frontiers Media
Lausanne
This record in other databases: 
Please use a persistent id in citations: doi:10.3389/fimmu.2025.1447319
Abstract: The main risk factor for developing transplant vasculopathy (TV) after solid organ transplantation is de-novo production of donor-specific antibodies (DSAs) binding to endothelial cells (ECs) within the graft's vasculature. Diverse leukocyte populations recruited into the vessel wall via activated ECs contribute to vascular inflammation. Subsequent smooth muscle cell proliferation results in intima hyperplasia, the pathophysiological correlate of TV. We demonstrated that incubating aortic EC with anti-HLA-I antibodies led to increased monocyte adhesion to and transmigration across an EC monolayer. Both occurred in a CD62E-dependent fashion and were sensitive toward the anti-inflammatory enzyme heme oxygenase (HO)-1 modulation. Using a murine heterotopic aortic transplantation model, we demonstrated that anti-MHC I antibody-induced TV is ameliorated by pharmacologically induced HO-1 and the application of anti-CD62E antibodies results in a deceleration of developing TV. HO-1 modulation is a promising therapeutic approach to prevent leukocyte recruitment and subsequent intima hyperplasia in TV and thus precludes organ failure.
Keyword(s): Animals (MeSH) ; Heme Oxygenase-1: metabolism (MeSH) ; Mice (MeSH) ; Endothelial Cells: immunology (MeSH) ; Endothelial Cells: metabolism (MeSH) ; Monocytes: immunology (MeSH) ; Monocytes: metabolism (MeSH) ; Graft Rejection: immunology (MeSH) ; Humans (MeSH) ; Histocompatibility Antigens Class I: immunology (MeSH) ; Histocompatibility Antigens Class I: metabolism (MeSH) ; Cell Communication: immunology (MeSH) ; Mice, Inbred C57BL (MeSH) ; Male (MeSH) ; Disease Models, Animal (MeSH) ; Cell Adhesion: immunology (MeSH) ; Vascular Diseases: immunology (MeSH) ; Vascular Diseases: etiology (MeSH) ; Vascular Diseases: pathology (MeSH) ; Vascular Diseases: metabolism (MeSH) ; accommodation ; adhesion ; anti-HLA-1 antibodies ; chronic rejection ; endothelial cells ; heme oxygenase-1 ; monocyte transmigration ; transplantation ; Heme Oxygenase-1 ; Histocompatibility Antigens Class I
; 
; 
; Article Processing Charges ; Clarivate Analytics Master Journal List ; DOAJ Seal ; Essential Science Indicators ; Fees ; IF >= 5 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection
|
The record appears in these collections: |
