RIEGGER LAB
Our research
Understanding how injury, ageing, and inflammation shape cell fate,
tissue degeneration, and regeneration.
Das sind wir
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Our research focus in brief
Osteoarthritis (OA) is the most common joint disease and is characterized by progressive degeneration of articular cartilage, a tissue with very limited intrinsic repair capacity. Besides ageing, joint injury is a major risk factor for OAand can lead to post-traumatic osteoarthritis (PTOA), often affecting patients much earlier in life. As curative treatments are currently lacking, our research aims to uncover the cellular and molecular mechanisms that determine cartilage degeneration or repair after injury and to identify new therapeutic strategies for both acute tissue protection and regeneration.
A particular focus lies on the fate of surviving chondrocytes after trauma. Using our established ex vivo cartilage injury model, we investigate how injury-induced stress alters chondrocyte phenotype and function and how these changes contribute to extracellular matrix degeneration [1–3]. This approach has enabled us to identify potential therapeutic targets [4] and to evaluate novel treatment strategies [5,6]. We are also interested in the regenerative potential of cartilage-resident stem/progenitor cells, which respond to tissue injury through migration, proliferation, and immunomodulatory mechanisms [7].
References: [1] Riegger J and Brenner RE. Pathomechanisms of Posttraumatic Osteoarthritis: Chondrocyte Behavior and Fate in a Precarious Environment. Int J Mol Sci. 2020, 21:1560. [2] Riegger J and Brenner R. Evidence of necroptosis in osteoarthritic disease: Investigation of blunt mechanical impact as possible trigger in regulated necrosis. Cell Death Dis. 2019, 10:683. [3] Kirsch V, Ramge J-M, Schoppa A, Ignatius A, Riegger J. In Vitro Characterization of Doxorubicin-Mediated Stress-Induced Premature Senescence in Human Chondrocytes. Cells. 2022, 11(7): 1106. [4] Riegger J, Huber-Lang M and Brenner RE. Crucial role of the terminal complement complex in chondrocyte death and hypertrophy after cartilage trauma. Osteoarthritis Cartilage. 2020; 28(5):685-697. doi:10.1016/j.joca.2020.01.004. [5] Riegger J, Joos H, Palm HG, Friemert B, Reichel H, Ignatius A, Brenner RE. Striking a new path in reducing cartilage breakdown: combination of antioxidative therapy and chondroanabolic stimulation after blunt cartilage trauma. J Cell Mol Med. 2018, 22(1):77-88. [6] Riegger J, Joos H, Palm HG, Friemert B, Reichel H, Ignatius A, Brenner RE. Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine. Osteoarthritis Cartilage. 2016, 24(12):2171-80. [7] Riegger J, Palm HG, Brenner RE. The functional role of chondrogenic stem/ progenitor cells: Novel evidence for immunomodulatory properties and regenerative potentials after cartilage injury. Eur Cell Mater. 2018, 36:110-127.
Our ex vivo cartilage trauma model
After pulling out the "trigger", the weight falls down and gains energy due to gravity. By reaching the end of the guide rail, the kinetic energy is transmitted in the sample, which is placed in the sample slot under the "indenter". The support frame stabilizes the guide rail and thus guarantees a perfect vertical fall of the weight without loss of energy.
Our cooperations
Our lab has various national and internation collaboration partners. Internal collaborators: - Prof. Markus Huber-Lang (Institut für Klinische und Experimentelle Trauma-Immunologie) - Prof. Anita Ignatius (Institut für Unfallchirurgische Forschung und Biomechanik) - PD Christoph Schmidt (Institut für Naturheilkunde und Klinische Pharmakologie) - Prof. Jan Münch (Institut für Molekulare Virologie) External collaborators: - Prof. Frank Zaucke (Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Orthopädische Universitätsklinik Friedrichsheim/ Frankfurt) - Prof. Tonia Vincent (Kennedy Institute of Rheumatology, University of Oxford) - PD Dr. Konrad Fischer (Section Xenotransplantation, TUM - Technical University of Munich)
Our funding
Our research is currently funded by - European Social Fund and the Ministry of Science, Research and Arts Baden-Württemberg - German Research foundation (DFG) - Professorinnenprogramm III (University of Ulm) - Collaborative Research Centre (CRC) 1149 Ulm - German Ministry of Defence - German Society of Orthopedics and Orthopedic Surgery (DGOOC)
