A study was made to characterize the effects of living Trypanosoma brucei brucei and its products on prostaglandin D2 (PGD2) and PGE2 production by fibroblasts and astrocytes. Cultured fibroblasts were prepared from Microtus agrestis embryos and astrocyte cultures were prepared from neonatal rats. The cultures were maintained in low-endotoxin or defined media (i.e. endotoxin-free). The PG production was compared with and studied in combination with a defined lipopolysaccharide (LPS) from Escherichia coli. Living T. b. brucei were without effect on PG production. Preparations of T. b. brucei prepared by freeze-thawing and sonication produced dose- and time-dependent increases in PGD2 and PGE2 synthesis by both cell types. LPS caused a similar pattern of increases. The combination of parasite products with LPS caused synergistic production to levels higher than the maximal production by each mitogen alone. The findings have important implications for several pathological features that accompany trypanosomiasis.
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http://dx.doi.org/10.1007/BF00932678 | DOI Listing |
Cells
January 2025
Department of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON M5S 3E1, Canada.
In neurons, the acquisition of a polarized morphology is achieved upon the outgrowth of a single axon from one of several neurites. Small extracellular vesicles (sEVs), such as exosomes, from diverse sources are known to promote neurite outgrowth and thus may have therapeutic potential. However, the effect of fibroblast-derived exosomes on axon elongation in neurons of the central nervous system under growth-permissive conditions remains unclear.
View Article and Find Full Text PDFDemyelination, or the loss of myelin in the central nervous system (CNS) is a hallmark of multiple sclerosis (MS) and occurs in various forms of CNS injury and neurodegenerative diseases. The regeneration of myelin, or remyelination, occurs spontaneously following demyelination. The lysophosphatidylcholine (LPC)-induced focal demyelination model enables investigations into the mechanisms of remyelination, providing insight into the molecular basis underlying an evolving remyelinating microenvironment over a tractable time course.
View Article and Find Full Text PDFbioRxiv
December 2024
Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX,77030, USA.
It is becoming more broadly accepted that human-based models are needed to better understand the complexities of the human nervous system and its diseases. The recently developed human brain organotypic culture model is one highly promising model that requires the involvement of neurosurgeons and neurosurgical patients. Studies have investigated the electrophysiological properties of neurons in such human tissues, but the maintenance of other cell types within explanted brain remains largely unknown.
View Article and Find Full Text PDFProgrammed cell death (apoptosis) is essential part of the process of tissue regeneration that also plays role in the mechanism of pathology. The phenomenon of fast and transient permeability of mitochondrial membranes by various triggers, known as permeability transition pore (mPTP) leads to the release of proapoptotic proteins and acts as an initial step in initiation of apoptosis. However, a role for mPTP was also suggested for physiology and it is unclear if there is a threshold in number of mitochondria with mPTP which induces cell death and how this mechanism is regulated in different tissues.
View Article and Find Full Text PDFCell Rep
January 2025
Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Neurogenic microRNAs 9/9 and 124 (miR-9/9-124) drive the direct reprogramming of human fibroblasts into neurons with the initiation of the fate erasure of fibroblasts. However, whether the miR-9/9-124 fate erasure logic extends to the neuronal conversion of other somatic cell types remains unknown. Here, we uncover that miR-9/9-124 induces neuronal conversion of multiple cell types: dura fibroblasts, astrocytes, smooth muscle cells, and pericytes.
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