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Anderson, A. M.

Publications and source records attributed to Anderson, A. M..

2 recordsLinked to original sources

Temperature influences immune cell development and body length in purple sea urchin larvae

Anthropogenic climate change has increased the frequency and intensity of marine heatwaves that may broadly impact the health of marine invertebrates. Rising ocean temperatures lead to increases in disease prevalence in marine organisms; it is therefore critical to understand how marine heatwaves impact immune system development. The purple sea urchin (Strongylocentrotus purpuratus) is an ecologically important, broadcast-spawning, omnivore that primarily inhabits kelp forests in the northeastern Pacific Ocean. The S. purputatus lifecycle includes a relatively long-lived ([~]2 months) planktotrophic larval stage. Larvae have a well-characterized cellular immune system that is mediated, in part, by a subset of mesenchymal cells known as pigment cells. To assess the role of environmental temperature on the development of larval immune cells, embryos were generated from adult sea urchins conditioned at 14 {degrees}C. Embryos were then cultured in either ambient (14 {degrees}C) or elevated (18 {degrees}C) seawater. Results indicate find that larvae raised in an elevated temperature were slightly larger and had more pigment cells than those raised at ambient temperature. Further, the larval phenotypes varied significantly among genetic crosses, which highlights the importance of genotype in structuring how the immune system develops in the context of the environment. Overall, these results suggest that developmental temperature shapes the larval immune system and may adversely affect survival long-term.

ecology↗

Selective Removal of 7KC by a Novel Atherosclerosis Therapeutic Candidate Reverts Foam Cells to a Macrophage-like Phenotype

The removal of the toxic oxidized cholesterol, 7-ketocholesterol (7KC), from cells through the administration of therapeutics has the potential to treat atherosclerosis and various other pathologies. While cholesterol is a necessary building block for homeostasis, oxidation of cholesterol can lead to the formation of toxic oxysterols involved in various pathologies, the most prominent of which is 7KC, which is formed through the non-enzymatic oxidation of cholesterol. Oxidized LDL (oxLDL) particles, highly implicated in heart disease, contain high levels of 7KC, and molecular 7KC is implicated in the pathogenesis of numerous diseases, including multiple sclerosis, hypercholesterolemia, sickle cell anemia, and multiple age related diseases. Of particular interest is the role of 7KC in the progression of atherosclerosis, with several studies associating elevated levels of 7KC with the etiology of the disease or in the transition of macrophages to foam cells. This research aims to elucidate the molecular mechanisms of UDP-003, a novel therapeutic, in mitigating the harmful effects of 7KC in mouse and human monocyte and macrophage cell lines. Experimental evidence demonstrates that administration of UDP-003 can reverse the foam cell phenotype, rejuvenating these cells by returning phagocytic function and decreasing both reactive oxygen species (ROS) and intracellular lipid droplet accumulation. Furthermore, our data suggests that the targeted removal of 7KC from foam cells with UDP-003 can potentially prevent and reverse atherosclerotic plaque formation. UDP-003 has the potential to be the first disease-modifying therapeutic approach to treating atherosclerotic disease.

cell biology↗