Side Lined by Soccer but a Key Player in the Research Field

Side Lined by Soccer but a Key Player in the Research Field

Dr Li Tieshi has an outstanding research and academic background. Currently, he is an assistant professor at the University of Nebraska. As an avid fan soccer fan, Dr Tieshi didn’t just watch from the side lines but enjoyed playing the game. Unfortunately, an injury to his right knee eleven years ago not only limited his participation but led to post-traumatic OA progression. The pain he experienced from this as well as the pain he saw in other family members with the same condition is a driving force inspiring this researcher to understand and treat OA.

The true empathy resulting from personal experience of OA, as well as the wealth of knowledge in biochemistry, molecular biology, immunology, stem cell biology and skeletal biology of this researcher made him an ideal candidate to receive support from ANRF. Dr Tieshi strongly believes that being awarded an ANRF grant was key in establishing his research career. Additionally, the pilot study undertaken with the funds from ANRF ensured that Dr Tieshi was in a position to be competitive for additional federal grants and other funding opportunities.

Interleukin 36α is a cytokine (a substance secreted by the immune cells that effect other cells), that has pro-inflammatory effects. Interleukin 36 α has been found to play a significant role in the pathogenesis of a number of diseases including psoriatic arthritissystemic lupus erythematosusinflammatory bowel disease and ulcerative colitis.  Dr Tieshi has focused his research on this cytokine and the part it may play in OA progression and the pain associated with it. It is believed that the effects of Interleukin 36α occurs via accelerating chondrocyte (cells only found in healthy cartilage) hypertrophy and final maturation, triggering catabolic processes, immune responses and activation of peripheral nociceptors (sensory neurons that transmit messages of potential threats).

The best laid schemes o’ Mice an’ Men

In order to confirm this and better understand the role of interleukin 36α Dr Tieshi created a post-traumatic OA mouse model. OA was induced by surgically destabilizing the medial meniscus (a fibrocartilage band surrounding the knee). This was combined with intra-articular injections of proteins and the use of behavioural tests which allowed Dr Tieshi and his team to draw out some interesting findings. Thus far his research has delineated a novel role for IL36α in chondrocyte maturation, homeostasis, post-traumatic OA progression and OA-induced pain. Interleukin 36α treatment promotes chondrogenic maturation and induces expression of a number of substances involved in skeletal development and bone mineralization. Additionally, Dr Tieshi found that interleukin 36α treatment regulated human articular chondrocyte homeostasis by acting as a catabolic factor. Pharmacological inhibition of interleukin 36α signalling reduced OA progression as well as pain in mice, whereas hyperactivation exacerbated OA in the study mice and induced OA-like phenotypes in wild type mice.

There’s No Place Like Home(ostasis)

These findings are key to Dr Tieshi’s long term goal of elucidating how joint cells regulate and express genes involved in the processes of regeneration and degradation necessary to maintain joint homeostasis. It also provides a therapeutic target which can hopefully lead to more effective treatments with decreased pain associated with OA eventually allowing a level of normality relating to movement in patients.

Results of this work have been presented to the American Society for Bone and Mineral Research 2018 Annual Meeting and Orthopaedic Research Society 2019 Annual Meeting. Newly generated data is scheduled be presented to the American Society for Bone and Mineral Research 2019 Annual Meeting and the 4th International Chinese Musculoskeletal Research Conference.

Waging War and Winning Battles Against OA

Dr Tieshi is hopeful that in the future his research will determine the molecular mechanism of musculoskeletal development, homeostasis and trauma. Understanding novel mechanisms in these areas will lead to the development of translational pharmacological and cell-based therapies for adult musculoskeletal disorders. The ANRF grant is instrumental as a means to launch young scientist’s research careers, it is through their work that we slowly begin to win the battle of finding a cure for OA and related disorders. The proliferative nature of this disease means that we are all likely to be or know someone effected and as such research such as this will have far reaching effects. ANRF is extremely humbled to support this goal through the power of good quality collaborative research.


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ANRF
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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