Access: Lupus Research -- Animal Model
Research Summaries from 2011
New Experimental Molecule Neutralizes Lupus Autoantibodies
Humans and animals with lupus produce autoantibodies that can cause inflammation, as well as damage cells and organs of one’s own body. In particular, antibodies to double-stranded DNA contribute to organ damage. Researchers have long investigated the possibility of blocking the actions of lupus-related autoantibodies to reduce the extent of such damage. Typically, such research is first tested in animals to ensure efficacy and safety before being conducted in humans. Researchers at The Feinstein Institute for Medical Research have created a new experimental molecule to test its ability to inhibit lupus-related autoantibody attachment to ds-DNA isolated from mice, as well as to components of kidneys extracted from mice, and to living brain cells of mice. The results of these studies provide hope for the development of more specific, less toxic therapies for lupus. However, more animal research is needed before this molecule can be tested in living humans with lupus.
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MicroRNAs Common to Three Lupus Mouse Models
MicroRNAs are small pieces of genetic material. Specific blueprints in the DNA can be “turned off” by these microRNAs so that some proteins won’t be made. The role of microRNAs in lupus has recently been studied in mouse models of lupus. If common sets of microRNAs could be identified in different mouse models of lupus with different genetic backgrounds, then this would very likely increase their usefulness for the study of lupus in people. The researchers hoped to identify a set of microRNAs common to three different strains of mice that have been genetically modified in different ways to have lupus, making it more likely that something similar to these microRNAs might be found in substantial percentages of people.
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