OSTEOARTHRITIS RESEARCH- Exploring Disease Development and New Ideas in Cartilage Regeneration

What is osteoarthritis?

OSTEOARTHRITIS RESEARCH- Exploring Disease Development and New Ideas in Cartilage Regeneration

This is the most common form of arthritis, affecting over 32 million Americans. Age and obesity are two of the biggest risk factors for developing the condition. Injury to a joint also increases the risk of developing the condition in that joint.

Jonathan Brunger (PhD) – Synthetically regulated cell-based therapeutics for targeted articular cartilage regenerative medicine

Reprogramming our cells to heal themselves

Progressive osteoarthritis (OA) leads to cartilage degradation, as no effective drug therapy currently exists this leads to surgeries, such as joint replacement, being necessary for many patients. It’s estimated that more than half of knee OA patients will receive total knee replacement over their lifetime. Although surgery offers relief, the benefits decrease over time as surgery does not fix the original problem of degraded cartilage. Dr Brunger hopes to be able to reprogram the cells involved in this degradation so that they start producing proteins that can in fact treat this underlying cause. Basically, cells will be taught how to produce their own medicine and treat themselves in the process. Wouldn’t it be great if our own cells could heal themselves?

Shouan Zhu (PhD) – Metabolic regulation of chondrocytes by Sirt5 and protein malonylation in osteoarthritis development

A relaxed cell is a functioning cell

Two factors that we know contribute to osteoarthritis are aging and obesity. What we don’t know yet is the exact effect these factors have on joint cells which leads to development OA. If we over eat and take in more energy than we use our cells start to be become stressed. If you are particularly stressed you don’t function quite as well as if you are calm and relaxed, neither do your cells. A special protein can help our cells to relax, a bit like offering our cells a massage to help them unwind so they function optimally once again. This protein gets less as we age so our cells stay stressed. Dr Zhu wants to know if obesity has a greater impact on our cellular stress and whether it leads to OA if there is less of this protein. Perhaps by answering this we can find new ways to help relax and soothe our cells to prevent the constant stress that leads to OA. 

Carl Ware Fellowship:

Dr. Michael Jurynec (PhD) – Analysis of the NOD-RIPK2 signaling pathway in osteoarthritis

Increased risk of OA if there is a diseased gene

By studying 200 families in which family members have severe or early-onset osteoarthritis Dr Jurynec has been able to identify a diseased version of a gene that contributes greatly to the risk of a person developing OA. Mice that were bred to have this diseased gene were far more susceptible to developing the condition. What he now wants to establish as an ANRF scholar is which cells are impacted by this diseased gene and how does it alter how they work. If this can be answered it can help to find a treatment that targets this diseased gene and lessen the effects of it which leads to the development and progression of OA.

 

Dr. Chenghai Zhang (PhD) – Investigating the role of gene Creb5 in lubricin expression during the development of osteoarthritis

Is your joints’ check engine light on?

Just as your car engine needs to have its oil checked so do our joints. Just as a car engine requires lubrication so that the parts slide smoothly over one another so do joints in the body. Cartilage cells produce a substance called lubricin, which is known to be essential for proper joint lubrication and maintenance. In OA cartilage begins to break down and bones end up rubbing against each other, causing inflammation, pain, and joint stiffness. Dr Zhang previously identified a molecule which regulates both the formation of joints and the production of lubricin thus ensuring the bones in the joint can glide over each other effortlessly. Dr Zhang wants to understand how this molecule achieves this and whether if it is given artificially, it prevents the joint damage that leads to OA.

 

Article Author
Arthritis National Research Foundation
arthritisresearch@curearthritis.org

The Arthritis National Research Foundation's mission is to provide initial research funding to brilliant, investigative scientists with new ideas to cure arthritis and related autoimmune diseases. Writing articles about the patients affected and the science being done to find a cure shows why we need to come together to #CureArthritis!

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