In a previous study, we noticed that some ascitic cells isolated from melanoma patients survive, proliferate, and differentiate into giant phagocytes after the other cells died. Similar phenomena were observed in the primary cultures of mouse lung and liver cells. In the present study, the effects of dying cells on abdominal exudate cells, and the biological characteristics of the differentiated cells were studied. The results indicate that necrotic cells induce CD14(-)/CD68(+) fraction of abdominal exudate cells to proliferate and differentiate into giant phagocytes; however, apoptotic cells had no such effect. Morphologic studies revealed that the large phagocytes possess characteristics of macrophages. Moreover, necrotic cells enhance the expression of CD14, CD68, CD80, and CD86, and the differentiated cells expressed high levels of CD68 and CD86. Our results indicate that necrotic cells induce CD14(-)/CD68(+) fraction of abdominal exudate cells to proliferate and differentiate, and the differentiated cells possess characteristics similar to macrophages.
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http://dx.doi.org/10.3109/08820139.2013.822388 | DOI Listing |
J Orthop Surg Res
January 2025
Department of Joint Osteopathy, Liuzhou Worker's Hospital, Liuzhou, Guangxi Province, 545000, China.
Alcoholic osteonecrosis of the femoral head (AIONFH) is caused by long-term heavy drinking, which leads to abnormal alcohol and lipid metabolism, resulting in femoral head tissue damage, and then pathological necrosis of femoral head tissue. If not treated in time in clinical practice, it will seriously affect the quality of life of patients and even require hip replacement to treat alcoholic femoral head necrosis. This study will confirm whether M2 macrophage exosome (M2-Exo) miR-122 mediates alcohol-induced BMSCs osteogenic differentiation, ultimately leading to the inhibition of femoral head necrosis.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
January 2025
Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, 240003, Nigeria.
Background: Glia mediated neuroinflammation and degeneration of inhibitory GABAergic interneurons are some of the hall marks of pyrethroid neurotoxicity. Here we investigated the sex specific responses of inflammatory cytokines, microglia, astrocyte and parvalbumin positive inhibitory GABAergic interneurons to λ-cyhalothrin (LCT) exposures in rats.
Methods: Equal numbers of male and female rats were given oral corn oil, 2 mg/kg.
Mol Med
January 2025
The First People's Hospital of Lin'an District, No. 360, Yikang Street, Jinnan Subdistrict, Lin'an District, Hangzhou, Zhejiang, 311300, China.
Background: Myocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.
View Article and Find Full Text PDFSci Rep
January 2025
General Hospital of Xinjiang Military Command, 359 North Friendship Road, Sayibak, Ürümqi, 830000, Xinjiang, China.
The inflammatory response of lung tissue and abnormal proliferation of pulmonary artery smooth muscle cells are involved in the pathogenesis of high-altitude pulmonary hypertension (HAPH). Halofuginone (HF), an active ingredient derivative of Chang Shan (Dichroa febrifuga Lour. [Hydrangeaceae]), has antiproliferative, antihypertrophic, antifibrotic, and other effects, but its protective effects on HAPH remains unclear.
View Article and Find Full Text PDFNat Commun
January 2025
College of Life Sciences, Shaanxi Normal University, 710119, Xi'an, China.
Ferroptosis is a form of iron-dependent programmed cell death, which is distinct from apoptosis, necrosis, and autophagy. Mitochondria play a critical role in initiating and amplifying ferroptosis in cancer cells. Voltage-Dependent Anion Channel 1 (VDAC1) embedded in the mitochondrial outer membrane, exerts roles in regulation of ferroptosis.
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