Principal investigator
Name:
Christopher L. AntosAssociate Professor , PhD, Associate Professor
Position:
Affiliation:
School of Life Science and Technology
Honor:
Group Introduction
Research Area:
Heart and Appendage Regeneration
Research Interests:
The Antos group researches tissue regeneration. To understand the biology of regeneration, Dr. Antos is interested in answering three fundamental questions: 1. How are cells at the site of injury induced to regenerate lost tissues? 2. How are cells involved in regeneration controlled to produce the correct pattern? 3. What stops regeneration once the appropriate size is reached? These questions are highly relevant to tissue bioengineering and to the stem cell biology of repair or reconstruction of human tissues. The Antos lab uses the zebrafish to answer these questions, because the zebrafish will regenerate many of its organs, including heart and appendages. Therefore, the lab can describe and dissect the cell and molecular mechanisms involved in the fish’s regeneration abilities and relate them to the limits on mammalian regeneration.
Appendage Regeneration: Although the zebrafish fins have different architectures to the mammalian limbs, they contain almost all the same tissue types (bone, mesenchyme, joints, skin, melanocytes, etc.). These tissues just are arranged in a different pattern. Unlike mammalian limbs, after partial loss, the zebrafish fin will regenerate completely. Because the zebrafish can be researched with the current cell, genetic and molecular research tools, this regeneration model allows the Antos lab to assess the mechanisms involved in how to start, pattern and stop the stem and progenitor cells involved in regenerating appendages.
Heart Regeneration: Healthy heart physiology requires coordinated Ca2+ handling across the syncytial cardiac muscle. While single-cell cardiomyocyte experiments in culture indicate how individual cardiomyocytes alter their Ca2+subcellular distribution and handling properties, they are limited in addressing the syncytial nature of the cardiomyocytes in the heart in vivo. Thus, experimental dissection at the organ, cell and molecular levels are needed to understand how known and to-be-discovered mechanisms regulate cardiac physiology during heart regeneration in vivo. The Antos lab is therefore using all the current cell and molecular methods, including real-time in vivo zebrafish heart imaging, to address fundamental questions about cardiac injury, regeneration and function.
Representative Publications (*First Author, # Corresponding Author)
- 1. Kolanowski, Tomasz J.*; Antos, Christopher L.; Guan, Kaomei#.Making human cardiomyocytes up to date: Derivation, maturation state and perspectives.INTERNATIONAL JOURNAL OF CARDIOLOGY. 15 Aug 2017. 241:379-386.
- 2. Neef, Stefan*; Heijman, Jordi; Otte, Kristian; Dewenter, Matthias; Saadatmand, Ali R.; Meyer-Roxlau, Stefanie; Antos, Christopher L.; Backs, Johannes; Dobrev, Dobromir; Wagner, Michael; Maier, Lars S.; El-Armouche, Ali#.Chronic loss of inhibitor-1 diminishes cardiac RyR2 phosphorylation despite exaggerated CaMKII activity.NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY. 2017. 390(8):857-862.
- 3. Kujawski, Satu*; Lin, Weilin; Kitte, Florian; Boermel, Mandy; Fuchs, Steffen; Arulmozhivarman, Guruchandar; Vogt, Sebastian; Theil, Denise; Zhang, Yixin; Antos, Christopher L.#.Calcineurin Regulates Coordinated Outgrowth of Zebrafish Regenerating Fins.DEVELOPMENTAL CELL. 2014. 28(5):573-587.
- 4. Kizil, Caghan*; Kuechler, Beate; Yan, Jia-Jiun; Oezhan, Guenes; Moro, Enrico; Argenton, Francesco; Brand, Michael; Weidinger, Gilbert; Antos, Christopher L.#.Simplet/Fam53b is required for Wnt signal transduction by regulating beta-catenin nuclear localization.DEVELOPMENT. 2014. 141(18):3529-3539.
- 5. Kizil, Caghan*; Otto, Georg W.; Geisler, Robert; Nuesslein-Volhard, Christiane; Antos, Christopher L.#.Simplet controls cell proliferation and gene transcription during zebrafish caudal fin regeneration.DEVELOPMENTAL BIOLOGY. 2009. 325(2):329-340.
- 6. Lopez-Rodriguez, C*; Antos, CL; Shelton, JM; Richardson, JA; Lin, FM; Novobrantseva, TI; Bronson, RT; Igarashi, P; Rao, A; Olson, EN#.Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression.PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2004. 101(8):2392-2397.
- 7. Antos, CL*; McKinsey, TA; Dreitz, M; Hollingsworth, LM; Zhang, CL; Schreiber, K; Rindt, H; Gorczynski, RJ; Olson, EN#.Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors.JOURNAL OF BIOLOGICAL CHEMISTRY. 2003. 278(31):28930-28937.
- 8. Antos, CL*; McKinsey, TA; Frey, N; Kutschke, W; McAnally, J; Shelton, JM; Richardson, JA; Hill, JA; Olson, EN#.Activated glycogen synthase-3 beta suppresses cardiac hypertrophy in vivo.PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 2002. 99(2):907-912.
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