Bio Wilhelm E. Jahnen-Dechent is Director of the Institute for Biointerface Science in the Helmholtz Institute for Biomedical Engineering at RWTH Aachen. He received his habilitation and venia legendi in Physiological Chemistry and Pathobiochemistry at the Medical Faculty of Johannes Gutenberg University Mainz in 1999. He graduated as Ph.D. in Biochemistry from the University of Cologne in 1986 after completing his thesis work at the Max-Planck-Institute for Plant Breeding from 1983-1986. He did postdoctoral research as a Fellow of the Deutsche Forschungsgemeinschaft and the Max-Planck Society at the Plant Cell Biology Research Centre, Melbourne University, at the Joint Protein Structure Laboratory of the Ludwig Institute for Cancer Research and the Walter and Eliza Hall Institute in Melbourne, and at the Department of Plant and Soil Sciences at University of Massachusetts, Amherst. He studied Biology with majors in Botany, Biochemistry, Genetics and Microbiology at Johannes-Gutenberg-University Mainz from 1977-1983.
Professor Jahnen-Dechent has published over 200 peer-reviewed research papers on the structure and function of proteins in highly diverse areas including plant pathogen defense, fertility research, and cell-materials interaction in medicine and biotechnology. His work has been cited more than 18,000-fold resulting in an h-index of 63 (Google Scholar). He has won the Otto-Hahn-Medal of the Max-Planck Society for his PhD work. His work centers on the function of fetuin family serum proteins as prototypic blood proteins with high surface activity involved in mineral metabolism, blood coagulation and reproduction biology. Practical consequences of this research include the potential toxicity and clearing of nanoparticles with medical applications, the diagnosis and therapy of calcification disease and fertility control in humans.
Professor Jahnen-Dechent has chaired or assisted the organization of over 25 international scientific symposia to date, has given over 150 invited lectures, and serves as a regular reviewer of journals in the biomedical field, reviewing over 30 manuscripts annually. He is president emeritus of the German Society for Biomaterials and member of several institutional review boards. He co-founded the Swiss diagnostic company Calciscon AG (www.calciscon.com). Additionally, he actively consults with industries in applications of materials in biotechnologies and medicine.
GOOGLE SCHOLAR: Jahnen-Dechent
ORCID ResearcherID: A-7608-2011
LOOP ID 397183
Abstract The minerals calcium and phosphate are indispensable for the cellular metabolism of all living beings. Calcium is both a cellular messenger substance and an essential component in bones and teeth. Energy-rich phosphates are critically involved in energy metabolism and the regulation of signaling molecules. Both ions typically occur in millimolar concentrations in biological fluids. This causes a solubility and transport problem because calcium phosphates are difficult to dissolve in water and precipitate easily from supersaturated solutions. Nature has found a way to handle water-insoluble minerals in circulation by forming colloids with proteins. This is highly reminiscent of cholesterol transport, which is mediated by lipoprotein particles, colloidal complexes of lipids and proteins. We introduced the concept of calciprotein particles or CPP as carriers of otherwise insoluble calcium phosphates. We study their synthesis, metabolism and their role in physiological mineralization and in pathological calcification. Mineralization in vertebrates is restricted to bones and teeth. Mineral concentration throughout the body is similarly high and therefore mineralization proceeds once started. For this reason, all other tissues must be actively protected against accidental or pathological mineralization commonly called calcification. Calcification is a frequent bystander phenomenon in dystrophic tissue remodeling. Ectopic calcification results when mineral deposition exceeds clearance, which is common in chronic metabolic and degenerative diseases. Fetuin-A/α2-HS glycoprotein (genetic symbol AHSG) is an important regulator of mineralized matrix metabolism. Fetuin-A acts as a »mineral chaperone« stabilizing mineral precursors and mediating clearance of excess mineral as protein-mineral complexes. Fetuin-A deficient mice develop severe calcification impairing heart, lung and kidney function as well as reproduction. Fetuin-A deficiency in humans is associated with all-cause as well as cardiovascular mortality. I will present an update of our most recent Fetuin-A related research. I will translate lessons learned from animal and cell culture models into practical approaches for tissue engineering of mineralized tissues and for the prevention of calcification in soft tissues.
Literature
1. Rudloff S, Janot M, Rodriguez S, Dessalle K, Jahnen-Dechent W and Huynh-Do U. Fetuin-A is a HIF target that safeguards tissue integrity during hypoxic stress. Nature Com. 2021;12: 549-16.
2. Jahnen-Dechent W, Büscher A, Koeppert S, Heiss A, Kuro-o M and Smith ER. Mud in the blood the role of protein-mineral complexes and extracellular vesicles in biomineralisation and calcification 2020:107577.
3. Herrmann M, Babler A, Moshkova I, Gremse F, Kiessling F, Kusebauch U, Nelea V, Kramann R, Moritz RL, McKee MD and Jahnen-Dechent W. Lumenal calcification and microvasculopathy in fetuin-A-deficient mice lead to multiple organ morbidity. PLoS ONE. 2020;15:e0228503.
4. Babler A, Schmitz C, Buescher A, Herrmann M, Gremse F, Gorgels T, Floege J and Jahnen-Dechent W. Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate. PLoS ONE. 2020;15:e0228938.
5. Köppert S, Büscher A, Babler A, Ghallab A, Buhl EM, Latz E, Hengstler JG, Smith ER and Jahnen-Dechent W. Cellular Clearance and Biological Activity of Calciprotein Particles Depend on Their Maturation State and Crystallinity. Frontiers Immunol. 2018;9:1991.
6. Herrmann M, Schäfer C, Heiss A, Gräber S, Kinkeldey A, Büscher A, Schmitt MMN, Bornemann J, Nimmerjahn F, Herrmann M, Helming L, Gordon S and Jahnen-Dechent W. Clearance of fetuin-A--containing calciprotein particles is mediated by scavenger receptor-A. Circ Res. 2012;111:575-584.
7. Jahnen-Dechent W, Heiss A, Schäfer C and Ketteler M. Fetuin-A regulation of calcified matrix metabolism. Circ Res. 2011;108:1494-1509.
8. Schäfer C, Heiss A, Schwarz A, Westenfeld R, Ketteler M, Floege J, Müller-Esterl W, Schinke T and Jahnen-Dechent W. The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification. J Clin Invest. 2003;112:357-366.
9. Ketteler M, Bongartz P, Westenfeld R, Wildberger JE, Mahnken AH, Böhm R, Metzger T, Wanner C, Jahnen-Dechent W and Floege J. Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study. Lancet. 2003;361:827-833.
10. Heiss A, DuChesne A, Denecke B, Grötzinger J, Yamamoto K, Renné T and Jahnen-Dechent W. Structural basis of calcification inhibition by alpha 2-HS glycoprotein/fetuin-A. Formation of colloidal calciprotein particles. J Biol Chem. 2003;278:13333-13341.
Website Prof. Dr. Wilhelm E. Jahnen-Dechent
Host Prof. Dr. Uyen Huynh-Do, Department of Nephrology, Hypertension and Clinical Pharmacology, University of Bern, Inselspital
