Results 51 to 60 of about 1,133,037 (342)
Expression of factor V by resident macrophages boosts host defense in the peritoneal cavity [PDF]
, 2019 Macrophages resident in different organs express distinct genes, but understanding how this diversity fits into tissue-specific features is limited. Here, we show that selective expression of coagulation factor V (FV) by resident peritoneal macrophages ...
Broze, George J +12 more
core +1 more source
Macrophage-derived upd3 Cytokine causes impaired glucose homeostasis and reduced lifespan in drosophila fed a lipid-rich diet [PDF]
, 2014 Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that ...
Dionne, MS +5 more
core +1 more source
Mechanisms of parasite‐mediated disruption of brain vessels
FEBS Letters, EarlyView.Parasites can affect the blood vessels of the brain, often causing serious neurological problems. This review explains how different parasites interact with and disrupt these vessels, what this means for brain health, and why these processes matter. Understanding these mechanisms may help us develop better ways to prevent or treat brain infections in ...
Leonor Loira +3 more
wiley +1 more source
CD5L promotes M2 macrophage polarization through autophagy-mediated upregulation of ID3 [PDF]
, 2018 CD5L (CD5 molecule-like) is a secreted glycoprotein that controls key mechanisms in inflammatory responses, with involvement in processes such as infection, atherosclerosis, and cancer.
Amézaga, Núria +7 more
core +2 more sources
Molecular Oncology, EarlyView.This study indicates that Merkel cell carcinoma (MCC) does not originate from Merkel cells, and identifies gene, protein & cellular expression of immune‐linked and neuroendocrine markers in primary and metastatic Merkel cell carcinoma (MCC) tumor samples, linked to Merkel cell polyomavirus (MCPyV) status, with enrichment of B‐cell and other immune cell
Richie Jeremian +10 more
wiley +1 more source
Angiotensin type-2 (AT-2)-receptor activation reduces renal fibrosis in cyclosporine nephropathy: evidence for blood-pressure independent effect [PDF]
, 2016 Compound 21 (C21), selective agonist of AT2 receptors, shows antinflammatory effects in hypertension and nephroprotection in diabetes. The aim of this study was to evaluate the effects of C21 in cyclosporine nephropathy, which is characterized mainly by ...
Carletti, R +5 more
core +1 more source
International Journal of Molecular Sciences, 2022 Immunological memory is a crucial part of the immune defense that allows organisms to respond against previously encountered pathogens or other harmful factors. Immunological memory is based on the establishment of epigenetic modifications of the genome.
Malgorzata Kloc +3 more
openaire +2 more sources
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
Molecular Oncology, EarlyView.This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici +8 more
wiley +1 more source
The effects of exogenous lipid on THP-1 cells : an in vitro model of airway aspiration? [PDF]
, 2017 Chronic inflammatory diseases of the airways are associated with gastro-oesophageal reflux (GOR) and aspiration events. The observation of lipid laden macrophages (LLM) within the airway may indicate aspiration secondary to GOR.
Adams +6 more
core +2 more sources
Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine
Molecular Oncology, EarlyView.The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu +18 more
wiley +1 more source