Unspecific interaction was analyzed between native 125I-lipoproteins of low density (LDL) as well as 125I-LDL, maintained in rabbit circulation during 4 hrs, and fibroblasts and macrophages. Alterations in properties of the LDL, occurred in blood, were accompanied by an increase in their affinity towards macrophages and a decrease in the affinity to fibroblasts. In vivo effect of HDL on catabolism of LDL was manifested as inhibition of extracellular modification of LDL and elimination of them from circulation, and in vitro--as inhibition of the native LDL capture by fibroblasts and, especially, by macrophages. In vivo inhibitory effect of HDL on modification of LDL, which are captured by cells (including arterial endothelial cells) by means of unspecific endocytosis, appears to be one of mechanisms in the antiatherogenic action of HDL.
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Oncol Rev
January 2025
Department of Histology, "Iuliu Hatieganu" University of Medicine and Pharmacy Cluj-Napoca, Cluj-Napoca, Romania.
Introduction: Breast cancer is the most common form of cancer diagnosed worldwide and the leading cause of death in women globally, according to Globocan 2020. Hence, investigating novel pathways implicated in cancer progression and metastasis could lead to the development of targeted therapies and new treatment strategies in breast cancer. Recent studies reported an interplay between the receptor for advanced glycation end products (RAGE) and its ligands, S100 protein group, advanced glycation end products (AGEs) and high-mobility group box 1 protein (HMGB1) and breast cancer growth and metastasis.
View Article and Find Full Text PDFSingle-cell RNA sequencing studies have revealed the heterogeneity of cell states present in the rheumatoid arthritis (RA) synovium. However, it remains unclear how these cell types interact with one another and how synovial microenvironments shape observed cell states. Here, we use spatial transcriptomics (ST) to define stable microenvironments across eight synovial tissue samples from six RA patients and characterize the cellular composition of ectopic lymphoid structures (ELS).
View Article and Find Full Text PDFCell Rep
January 2025
School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China; State Key Laboratory of Advanced Medical Materials and Devices, ShanghaiTech University, Shanghai 201210, China. Electronic address:
Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by excess accumulation of the extracellular matrix (ECM). The role of macrophage-fibroblast crosstalk in lung fibrogenesis is incompletely understood. Here we found that fibroblast growth factor-inducible molecule 14 (Fn14), the receptor for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is highly induced in myofibroblasts in the lungs of IPF patients and the bleomycin-induced lung fibrosis model.
View Article and Find Full Text PDFFEBS J
January 2025
Department of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, China.
TNFAIP3-interacting protein 1 (TNIP1; also known as ABIN-1) is a ubiquitin-binding protein that suppresses death-receptor- or Toll-like receptor-mediated apoptosis and necroptosis; however, it remains unclear whether ABIN-1 is capable of regulating pyroptosis. In the present study, we found that, in mouse embryonic fibroblasts and macrophages, ABIN-1 deficiency sensitized cells to poly(I:C) + TAK1 inhibitor 5Z-7-oxozeaenol-induced pyroptosis besides apoptosis and necroptosis. The sensitizing effect of ABIN-1 deficiency on pyroptosis depended on caspase-8 and its adaptor molecule FAS-associated death domain protein.
View Article and Find Full Text PDFCell Death Dis
January 2025
Department of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Cancer-associated fibroblasts (CAFs) play important roles in the occurrence and development of hepatocellular carcinoma (HCC) and are a key component of the immunosuppressive microenvironment. However, the origin of CAFs has not been fully elucidated. We employed single-cell sequencing technology to identify the dynamic changes in different subsets of fibroblasts at different time points in rat primary HCC model.
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