Inhibiting oncogenic proteins can prevent scleroderma fibrosis


Scleroderma is an autoimmune disease of connective tissue, which is characterized by hard and thickened skin, spontaneous scabs, and sometimes in other organs of the body. And it may also cause vascular disease and varying degrees of inflammation. Connective tissue is a network of tissues that connect and support muscles, joints, organs, and skin. A typical symptom of scleroderma is the Raynaud phenomenon, which is manifested as discoloration of the fingers or toes due to blood loss in the limbs, as seen in as many as 90% of patients. This disease occurs more frequently in women than in men.

The connective tissue of patients with scleroderma contains too much collagen, making the skin hard and tight. Experts believe that this may be because the human immune system has become too active, leading to excessive production and accumulation of collagen. However, the cause of scleroderma is still unknown, and there is currently no cure.

Sawalha, a professor in the department of rheumatology at the University of Michigan, incorporation with his team researched scleroderma at the molecular level to better understand the fibrosis process. And their study was published in the proceeding of the National Academy of Sciences.

The research team studied the molecule enhancer of aeste homolog 2, also known as EZH2, which is shown to be overexpressed in multiple carcinomas, such as breast cancer and prostatic cancer. This protein regulates gene expression through a process called epigenetic regulation that affects the modification of DNA and other proteins that attach to it. 

Sawalha and other researchers have previously identified the role of EZH2 in lupus, another autoimmune disease. EZH2 is overexpressed in lupus T cells, which makes these white blood cells active in lupus patients. They then extended their research to scleroderma, specifically looking at the role of EZH2 in fibroblasts and endothelial cells in this disease.
The team first worked with the Michigan medical scleroderma project to isolate cells from patients with scleroderma. They then extended their research to animal models to further examine the results found in human cells.

The main pathologic aspects of scleroderma are fibrosis and abnormal vascular function with increased or angiogenic deficits. They analyzed the cells and found that elevated EZH2 levels were responsible for the progression of scleroderma in patients with the disease.

After identifying the molecule, the team suppressed EZH2 in the cells and observed that increased fibrosis and vascular dysfunction in scleroderma could be corrected.

EZH2 is a molecule known to play a role in cancer patients, and EZH2 inhibitors have been developed and used in clinical trials for some cancers. Therefore, by reusing existing EZH2 inhibitors to treat scleroderma, they can more intuitively observe the clinical effects.

Since there is currently no effective treatment for scleroderma, this type of research is important for future research and trials.

The team said they would continue to study the disease at the molecular level and try to identify other therapeutic targets for these patients. 

Cite this article

CUSABIO team. Inhibiting oncogenic proteins can prevent scleroderma fibrosis. https://www.cusabio.com/c-20855.html
 

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