The outcome of a laboratory study is that the human endothelial cells (cells that make up the lining of blood vessels) can be genetically altered by using the CRISPR/Cas9 system gene editing system. CRISPRs (clustered regularly interspaced short palindromic repeats) are segments of prokaryotic DNA containing short repetitions of base sequences. In the past two years, researchers have reported a number of successes using CRISPR/Cas systems for gene editing (this means adding, disrupting or changing the sequence of specific genes). This has been practiced in different species.
In a new development, scientists at Yale University have reported the novel use of the CRISPR/Cas9 technique for working with human endothelial cells. With the study, The Scientist reports, researchers managed to infect cultured endothelial cells with a specific virus. The virus contained within it instructions for a Cas9 enzyme. The enzyme was constructed to wipe-out a gene termed CIITA. This gene functions to code for “a factor that controls the expression of class II major histocompatibility complex molecules.” The major histocompatibility complex controls a major part of the immune system.
Once the researchers treated the cells with virus,the laboratory study removed both copies of the gene from up to 40 percent of the cells. The outcome was that the cells lacking CIITA were no longer capable of producing the immune reaction that leads to the activation of T cells. This is the type of immune response that would occur when pathogens enter the bloodstream.
This type of study might seem a little abstract. However, the reasoning behind the study is that the information will help researchers learn about the way that blood vessels function. In the longer term, researchers hope that they can discover how tissues might be healed and whether this can be done artificially in the laboratory. Here the newly reported success is a step forwards.
The study has been published in the journal Circulation Research. The study is titled “Efficient Gene Disruption in Cultured Primary Human Endothelial Cells by CRISPR/Cas9.”
