Role Of Macrophage Populations Research Articles

The Role of Macrophage Populations in Skeletal Muscle Insulin Sensitivity: Current Understanding and Implications.

Insulin resistance is a crucial factor in the development of type 2 diabetes mellitus (T2DM) and other metabolic disorders. Skeletal muscle, the body's largest insulin-responsive tissue, plays a significant role in the pathogenesis of T2DM due to defects in insulin signaling. Recently, there has been growing evidence that macrophages, immune cells essential for tissue homeostasis and injury response, also contribute to the development of skeletal muscle insulin resistance. This review aims to summarize the current understanding of the role of macrophages in skeletal muscle insulin resistance. Firstly, it provides an overview of the different macrophage populations present in skeletal muscle and their specific functions in the development of insulin resistance. Secondly, it examines the underlying mechanisms by which macrophages promote or alleviate insulin resistance in skeletal muscle, including inflammation, oxidative stress, and altered metabolism. Lastly, the review discusses potential therapeutic strategies targeting macrophages to improve skeletal muscle insulin sensitivity and metabolic health.

Early cellular events of renal fibrosis revealed by nanoparticle-based immunocytochemistry

Aim Visualisation of cellular events in early renal fibrosis is limited by the availability of probes to mark different cell types concurrently. By employing quantum dot (QD) nanoparticles to replace traditional organic fluorophores we can increase the range of cell markers available for light microscopy and extend their visualisation to the electron microscopy domain. The aim of this work was to assess the utility of QD probes for immuno-labelling of renal tissue showing inflammatory changes and early renal fibrosis. Methods Antibody conjugated QDs in various sizes were applied to air-dried frozen sections from routine renal biopsy tissue and viewed by widefield epifluorescence microscopy using LED excitation at 385 nm. Transmission electron microscopy was performed on adjacent tissue taken from the same biopsy. Results QD probes targeting CD68 (green 525 nm) and L1 calprotectin (red 655 nm) have been used as macrophage markers. No co-localisation was observed suggesting that CD68 + macro-macrophages and L1 calprotectin + macrophages represent independent populations in early fibrosis. Discussion QD immunolabelling has highlighted the role of macrophage populations in inflammatory infiltrates associated with early fibrosis. This approach may be up-scaled to employ seven different antibodies in different colours for simultaneous labelling of multiple cell types and detailed correlation studies.

The underlying roles of macrophage populations in myocardial fibrosis

Myocardial fibrosis is one of the main structural changes following cardiomyocyte injury such as infarction. Macrophages play a central role in the development of fibrotic lesions. In myocardial fibrosis, three different populations of macrophages are recognized: exudate macrophages, resident macrophages, and interstitial dendritic cells. Exudate macrophages, which are derived from blood monocytes and recruited into injured areas through chemoattractants and cell adhesion molecules, release various fibrogenic growth factors in early stages of the fibrosis. Transforming growth factor-beta and platelet-derived growth factors are proposed as the most probable growth factors produced by exudate macrophages to induce the modulation of fibroblasts towards myofibroblasts. Emerging evidence shows that macrophage-secreted nerve growth factor may also be involved in that process. The myofibroblasts are capable of producing extracellular matrix proteins which contribute to myocardial fibrosis. The exudate macrophages also participate in the induction ofapoptosis in injured myocytes and myofibroblasts in the fibrotic lesions. These apoptotic cells are phagocytized by exudate macrophages, and the macrophages themselves also disappear by apoptosis. The decrease in cellularity by apoptosis leads to the evolution of fibrous granulation tissues into scar tissues (reparative fibrosis). The resident macrophages particiapte exclusively in the late stages of the myocardial fibrosis, when their mitotic activity increases in the lesions; they are presumed to have the same roles as the exudate macrophages. In addition, the resident macrophages and interstitial dendritic cells both act as immune mediators to recruit T-lymphocytes into the lesions. In contrast to hepatic, pulmonary, and renal fibrosis, the roles of macrophage populations in myocardial fibrosis has not yet been extensively investigated. Biomedical Reviews 1999; 10: 89-105.