Health Medical

Researchers Discovered the Role of a Novel Protein In Scar Tissue Formation

Image Credits: Wikipedia

Researchers at Osaka University have discovered a novel protein that performs a vital role in the formation of scar tissue while healing an injured organ. When tissues get injured, they can heal themselves. Many tissues of the body have the extra ability to heal a wound. The process of wound healing is complex and sometimes during the healing process, something goes wrong which results in the excess formation of connective tissue around the wound area. The excess formation of connective tissue is called Fibrosis which leads to the loss of function in an organ.

The findings of this new study are published in Immunity. Researchers showed the role of the protein named Rbm7, which initiates the death of cells during tissue injury. This protein also recruits some particular type of immune system cells which induces the formation of tissue fibrosis. 

There can be multiple reasons for tissue injury such as trauma, infections and side effects of the drug. The tissue responds in a similar fashion during all the cases i.e. Formation of new tissues during the healing process and replacement of injured tissue by new tissues.

Apparently, the process looks simple and straightforward, but it has a complex interaction between immune cells and tissues. Researchers described that a large number of molecular actors have been involved in this process but the exact mechanism of formation of tissue fibrosis and its prevention is not clearly understood.

Must Read: Tissue Plasminogen Activator (tPA) May Treat Respiratory Failure In COVID-19

Shizuo Akira, a corresponding author of the study said that Fibrosis is a serious and complicated phenomenon that permanently deteriorates the function of injured tissue. The main aim of our study is to discover the exact mechanism that how tissue fibrosis develops and impairs the function of the organ. Also, want to find a new possible avenue for treating tissue fibrosis.

To materialize their goal, researchers induce a chemotherapeutic drug known as bleomycin in rodents which stimulate lung fibrosis. They observed that a level of protein Rbm7 has increased slowly in the fibrotic lungs. The function of Rbm7 is still unknown.

After observing the rodent models, researchers examined the human samples which were taken from clinical patients having lung fibrosis. They found that the level of Rbm7 protein is also high in human specimens with lung fibrosis.

Kiyoharu Fukushima who is the lead author of the study said that the mice who lack the Rbm7 protein develop a less severe form of lung fibrosis as compared to the one which has the protein. This discovery is becoming more interesting because researchers want to study the molecular basis of the protein Rbm7 for its pro-fibrotic action.

Researchers showed that there is a relationship between the injured tissue cells and a particular type of immune cell. The interaction between both of these cells is known as segregated nucleus-containing atypical monocytes (SatMs) as it plays a central role in the onset of fibrosis. When tissue undergoes damage such as trauma, infection or through drug bleomycin, then it increases the production level of proteinRbm7, which ultimately leads to death of the tissue.

In response to this, the molecules that stimulate the SatMs are secreted, which permanently replace the injured tissue region by scar tissue. 

 Still, there is no treatment available for the fibrosis that has an unknown origin. The goal is to alleviate the symptoms and to slow down the disease progression. In the advance stages, palliative care will be offered to the patient.

Akira further added that the results of the study are remarkable which shows how single protein induces the formation of fibrosis and how it impairs the function of an organ? Through targeting the protein Rmb7, it will be possible to treat and prevent Fibrosis in the future.

  

 

About the author

Aimen Ramzi

Add Comment

Click here to post a comment

Your email address will not be published. Required fields are marked *