Jan Lammerding

BIOGRAPHY

ACADEMIC POSITIONS:
Assistant Professor, Department of Biomedical Engineering, Weill Institute for Cell and Molecular Biology, Cornell University

EDUCATION:
• BE 1997 Thayer School of Engineering, Dartmouth College, Hanover, NH
• Dipl Ing 1999 Department of Mechanical Engineering, RWTH Aachen, Aachen, Germany
• PhD 2004 Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA
• Postdoctoral Fellow, Harvard Medical School/Brigham and Women’s Hospital, Boston, MA

PREVIOUS APPOINTMENTS:
• 2005-2008 Instructor in Medicine/Associate Biophysicist, Department of Medicine, Harvard Medical School/Brigham and Women’s Hospital, Boston, MA
• 2008-2010 Lecturer, Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA
• 2008-2011 Assistant Professor, Department of Medicine, Harvard Medical School/Brigham and Women’s Hospital, Boston, MA

MEMBERSHIPS:
• American Heart Association
• American Society for Cell Biology
• Biomedical Engineering Society

HONORS/AWARDS:
• 2006 Hearst Young Researchers Award, Brigham and Women’s Hospital, Department of Medicine
• 2008 Lerner Symposium Young Investigator Award, Brigham and Women’s Hospital, Department of Medicine, Cardiovascular Division
• 2009 Cardiovascular Leadership Group Investigation Award, Brigham and Women’s Hospital, Department of Medicine, Cardiovascular Division

RESEARCH INTERESTS:
The research in the Lammerding lab is focused on subcellular mechanics and the cellular response to mechanical stimulation. Combining sophisticated engineering tools such as magnetic tweezers and microfluidics with high resolution microscopy and traditional molecular biology assays, the Lammerding lab is developing new tools to characterize the biophysical properties of cells and how they can modulate cellular function. One particularly focus is the cell nucleus and the proteins that form the nuclear envelope. Mutations in these proteins cause a variety of human diseases, including muscular dystrophy, dilated cardiomyopathy, and progeria, a rare premature aging disease. One of the perplexing questions has been why many of the mutations affect only specific tissues, particularly muscles and tendons, even though the mutant proteins are expressed throughout the body. The Lammerding lab was able to demonstrate that lamins, which form a dense protein network on the inner side of the nuclear membrane, are the main determinants of nuclear stiffness and stability. Functional loss of lamins leaves cells with irregularly shaped and more fragile nuclei, thereby rendering the cells more susceptible to damage in mechanically active tissues such as muscle and providing a potential explanation for the tissue-specific phenotypes. In a surprising discovery, the Lammerding lab found that lamins can also modulate mechanotransduction signaling, i.e. the cellular response to mechanical stimulation, the same mechanism that is responsible for the muscle growth after rigorous exercise.

Building on these findings, the Lammerding lab is currently exploring the role of lamins in stem cell differentiation, as the fate of these cells is strongly influenced by feedback from their mechanical microenvironment. Recently, the Lammerding lab has also begun to explore the role of nuclear mechanics in cancer. Cancer cells are often identified by abnormally shaped nuclei, and more deformable nuclei could provide an advantage to cancer cells migrating through dense tissues or entering an existing blood vessel. The Lammerding lab is pursuing a multi-scale approach, ranging from experiments on isolated nuclei to studies on mouse models of the human diseases.

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