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Awards for researchers at MedUni Vienna's Karl Chiari Lab for Orthopaedic Biology

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(Vienna 13 January 2021) Daniela Weinmann and Mahmoud Elshamly from the Karl Chiari Lab for Orthopaedic Biology (Stefan Tögel's working group) at MedUni Vienna's Department of Orthopedics and Trauma Surgery have been awarded Science Prizes for their research projects. Daniela Weinmann was awarded the AFOR Science Prize, Mahmoud Elshamly the Science Prize of the Austrian Society for Spinal Surgery.

The Karl Chiari Lab for Orthopaedic Biology at MedUni Vienna's Department of Orthopedics and Trauma Surgery is studying the pathomechanisms of orthopaedic diseases with the aim of developing new concepts for their understanding and treatment. A main focus of their research activities is the glycobiology of osteoarthritis, a new research approach that looks at the interaction between glycans and glycan-binding proteins (e.g. galectins) and its role in arthritic cartilage degeneration.

Daniela Weinmann awarded AFOR Science Prize 2020
Every year, the Swiss association AFOR (Association For Orthopaedic Research) awards the AFOR Science Prize for outstanding papers from clinical or experimental research in the field of orthopaedics and traumatology. Daniela Weinmann received the prize for her paper entitled "Galectin-8 induces functional disease markers in human osteoarthritis and cooperates with galectin-1 and -3" [1], which was published in the leading journal "Cellular and Molecular Life Sciences“ (impact factor: 6.496).

This work was produced in the Karl Chiari Lab for Orthopaedic Biology in collaboration with the Center for Medical Statistics, Informatics and Intelligent Systems (Institute for Biosimulation and Bioinformatics), the Center for Anatomy and Cell Biology (Division of Cell and Developmental Biology) and the Department of Physiological Chemistry of Ludwig Maximilian University in Munich.

Galectin-8 induces arthritic cartilage degeneration
Osteoarthritis is a degenerative joint disease and is one of the main causes of physical impairment in older people. Nonetheless, the underlying disease mechanisms are still not fully understood. For several years now, the Karl Chiari Lab of Orthopaedic Biology has been pursuing a completely new approach in arthritis research and is focussing in particular on the glycobiological aspects of this disease.

Countless pieces of biological information are transmitted during physiological and pathological processes by the interaction of glycan structures (sugar structures) and galectins (sugar-binding proteins) in tissues and/or on cell surfaces. In previous studies, the researchers have already highlighted the relevance of glycobiological changes in arthritic articular cartilage and the functional importance of the interaction between certain galectins (galectin-1 and galectin-3) and glycan structures in the progression of osteoarthritis.

Amongst other things, they were able to show that the functional cooperation of galectin-1 and galcetin-3, which belong to two different structural groups of galectins, plays a significant role in inflammatory processes in arthritic tissue.

In the prize-winning study, which extends the concept of functional cooperation to include galectin-8 from the third structural group of galectins, they were first of all able to show that the presence of galectin-8 in cartilage cells is associated with the degree of degeneration of the cartilage tissue in osteoarthritis patients. It was further shown that galectin-8 is also secreted by cartilage cells, which in turn facilitates glycan-mediated binding to the cells and triggers a biological effect.

By means of cell-biological and bioinformatics analyses, the researchers also discovered that galectin-8 triggers a genetic programme in cartilage cells that is largely under the control of NF-κB, and which induces joint inflammation and cartilage breakdown. A comparison with the data for galectin-1 and -3 indicated that these cellular programmes overlap to a certain extent. Cell culture experiments with a combination of all three galectins confirmed this suspected functional cooperation between galectin-8 and galectin-1 and -3.

Hence, the study not only identified galectin-8 as an additional clinically relevant factor in arthritic cartilage degeneration but, for the first time, also studies galectins from all structural groups in the same model system (osteoarthritis). In future, this new approach, which, rather than considering the function of specific galectins in isolation, considers these as a network, might be of interest in other fields of research.

About Daniela Weinmann
Daniela Weinmann was born in 1987 in St. Pölten, where she graduated from the Commercial Academy in 2006. She then went on to study molecular biology at the University of Vienna from 2006 until 2012. Weinmann completed her dissertation in the Karl Chiari Lab of Orthopaedic Biology under the supervision of Stefan Tögel and went on to write her dissertation for the Medical University of Vienna's PhD course in "Bones and Joint Regeneration". Daniela Weinmann received the vfwf dissertation prize for her PhD thesis in January 2018. Since 2016, she has additionally been pursuing a course in human medicine at the Medical University of Vienna, where she has also been involved in teaching for several years. Daniela Weinmann is married and gave birth to a son in 2018.

 

Mahmoud Elshamly awarded Austrian Society for Spinal Surgery Science Prize 2020
Every year, the Austrian Society for Spinal Surgery awards a prize for a study placement of at least four weeks to authors of outstanding scientific publications.
This year, the prize went to Mahmoud Elshamly for his paper entitled "Galectins‐1 and ‐3 in Human Intervertebral Disc Degeneration: Non‐Uniform Distribution Profiles and Activation of Disease Markers Involving NF‐κB by Galectin‐1" [2], which was published in the Journal of Orthopedic Research (impact factor: 2.728). During a study placement funded by the prize, which he spent at the Spinal Centre of the Schön Klinik in Munich, Mahmoud Elshamly had the opportunity to work with Christoph Siepe to hone his skills in endoscopic spinal surgery.

This paper was produced at the Karl Chiari Lab for Orthopaedic Biology under the supervision of Stefan Tögel at the Department of Orthopedics and Trauma Surgery in collaboration with the Department of Physiological Chemistry of Ludwig Maximilian University in Munich.

Galectin-1 is associated with intervertebral disc degeneration
The statistics indicate that a large percentage of the population is currently suffering from back pain, often caused by degenerative changes to the intervertebral discs. As in the case of osteoarthritis of major joints, virtually nothing is known about the glycobiological links with the onset of degenerative disc changes.
The aim of this work was to assess the expression of galectin-1 and galectin-3 in intervertebral discs and its correlation with radiological and histological degenerative changes, as well as with mechanical load, and also to investigate the role of galectin-1 and -3 in the pathomechnisms of intervertebral disc degeneration.

The study included tissue samples from patients with degenerative conditions of the lumbar spine (spondylosis, deformity or spondylolisthesis). Immunohistochemical analyses showed that galectin-1 and galectin-3 are present in various parts of the degenerative intervertebral disc but have different distribution patterns. The expression of both galectins correlates with the radiologically and histologically determined degree of degeneration, whereby only galectin-3 correlated with the patient's age. The finding that the presence of galectin-1 and galectin-3 did not correlate with each other already points to a different functionality of the two galectins.
It was possible to show from cultivated intervertebral disc cells isolated from samples of patient tissue that both galectins are secreted from these cells and bound to glycan structures on the cell surfaces.

The effects of the binding of recombinant galectin-1 and galectin-3 were then investigated at mRNA and protein level. Interestingly, it was found that galectin-1 – but not galectin-3 – induces activation of the NF-κB signalling pathway and the expression of degeneration markers (IL-6, IL-8, MMP-1, MMP-3 and MMP-13).

This study substantiates the concept of the "sugar code" and its relevance in degenerative musculoskeletal diseases. The data support the functional difference in terms of intervertebral disc cells between galectin-1 and galectin-3, two representatives of the galectin family with different protein architecture and glycan specificity. The study found that galectin-1 stimulates inflammatory factors and matrix degrading enzymes. Follow-on studies are planned to look at other galectins, such as galectin-8 and to check the possibility of inhibiting galectin activity using new galectin variants.

About Mahmoud Elshamly
Mahmoud Elshamly was born in Egypt in 1987, where he graduated from the Salam Modern School in 2003. He then studied human medicine at the Ain Shams University in Cairo from 2004 until 2010. Elshamly completed his Master's thesis at Danube University in 2018 under the supervision of Josef Grohs and then went on to write his dissertation at the Medical University of Vienna in the Karl Chiari Lab for Orthopaedic Biology under the supervision of Stefan Tögel, as part of his PhD in "Bones and Joint Regeneration". He completed his specialist training to become a consultant in orthopaedics and traumatology in 2019 and was awarded a Diploma in Manual Medicine by the Austrian Medical Association. Mahmoud Elshamly is married and has one son.


References
[1] Weinmann D, Kenn M, Schmidt S, et al. Galectin-8 induces functional disease markers in human osteoarthritis and cooperates with galectins-1 and -3. Cell Mol Life Sci. 2018;75(22):4187-4205. doi:10.1007/s00018-018-2856-2.

[2] Elshamly M, Kinslechner K, Grohs JG, et al. Galectins-1 and -3 in Human Intervertebral Disc Degeneration: Non-Uniform Distribution Profiles and Activation of Disease Markers Involving NF-κB by Galectin-1. J Orthop Res. 2019;37(10):2204-2216. doi:10.1002/jor.24351.