[phas-dept] Feb 16 (Thursday) 4 PM - Physics and Astronomy Colloquium

[Heungman Park]

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Spring 2017 Colloquium

Department of Physics & Astronomy

Feb 16, Thursday, 4-5 PM in Science Building 127

(coffee and cookies will be served at 3:50 PM)

Molecular biology

Cardiac-Inducing RNAs Direct the Differentiation of Stem Cells into Cardiomyocytes for Heart Repair
Dr. Larry Lemanski

Texas A&M University - Commerce

[https://lh4.googleusercontent.com/WUtt-LAoE7FK6zK6rbZOGNyeVJWGyhMAlPoCmv1el6wJGPX0ixNdvr1pYJ4SwMI06SufHvWDRpe--b2C4oMnoKR1T4MS6g5itMdPHuWQowjs5kTk_8mnt_Rd7ckwYOWaClvOC2Qi]

Larry F. Lemanski completed his B.S. degree (1966) with honors, in Biology and Chemistry, from the University of Wisconsin-Platteville and his M.S. (1968) and Ph.D. (1971) degrees from Arizona State University, Tempe, Arizona, U.S.A.  He was a postdoc at the University of Pennsylvania, and then he joined the medical faculty at the University of California, San Francisco. He became a full professor in the College of Medicine at the University of Wisconsin, Madison. After that, he joined the Upstate Medical University in Syracuse, New York, as Professor and Chairman of the Department of Anatomy and Cell Biology, became Associate Vice President for Research at Texas A&M University, Vice President for Research at Florida Atlantic University, and Senior Vice president for Research and Strategic Initiatives at Temple University, Philadelphia, Pennsylvania. He was recruited to Texas A&M University-Commerce as Provost and Vice President for Academic Affairs and has now transitioned to the position of Distinguished Research Professor and Founding Director of the new  Biomedical Institute for Regenerative Research at Texas A&M University-Commerce. He also was recently  selected as a Texas A&M University System Regents Professor. Dr. Lemanski’s research interests throughout his career have involved embryonic heart development and cardiac cell differentiation using a variety of morphological, cellular, biochemical, and molecular biology approaches. Dr. Lemanski’s research holds tremendous promise for the repair of damaged heart tissues in patients who have suffered heart attacks or have related cardiovascular diseases. In fact, he  has recently established a new biotechnology company, NeoHeart, LLC, which is in the process of translating his research discoveries to the clinical level. More information about Dr. Lemanski and his research can be found at
http://faculty.tamuc.edu/llemanski/


Abstract:

We have discovered a ribonucleic acid (RNA) from human heart that has the ability to turn non-muscle cells into functional cardiac muscle. A form of this RNA was first found in an amphibian species, the Mexican axolotl (a salamander) and later in human heart as a "functional" homologue of the original salamander RNA. We have termed this human RNA, Cardiac Inducing RNA or CIR. In our initial research, we used cardiac mutant axolotl embryos in which the heart forms, but fails to beat, as "bioassays" to test the CIR rescuing activity. These non-contracting mutant hearts that ordinarily lack organized myofibrils (the machinery for normal contraction of the heart) were placed in organ cultures in the presence of the cardiac inducing RNA (CIR). After 24-72 hours, the mutant hearts begin contracting rhythmically, and immunofluorescent staining with cardiac specific protein antibodies showed well-organized myofibrils of normal morphology. The RNA had converted these non-muscle cells in the mutant hearts into normally-appearing and normally-contracting cardiac muscle tissue. We then expanded our studies to mouse embryonic stem cells (ESC), mouse induced pluripotent stem (IPS) cells derived from fibroblasts and human induced pluripotent steam cells (iPS) derived from skin.  Immunofluorescent staining of the mouse or human stem cells cultured with CIR and stained with cardiac-specific protein antibodies for troponin T (cTnT) and tropomyosin, clearly showed their differentiation into cardiomyocytes with cardiac-specific proteins, characteristic spindle-shaped cardiomyocyte structures, and nascent cardiac myofibrils. Without the CIR treatment, the cells did not express cardiac-specific proteins or show cardiac morphologies. We are now creating a mouse acute myocardial infarction (AMI)(heart attack) model to test whether an infarcted myocardium treated with the CIRs, or with CIRs in combination with stem cells, can regenerate/repair the damaged heart muscle tissue from the infarcted area of the heart and turn that damaged region into normally-functioning cardiac muscle again. Defining the mechanisms by which CIR transforms nonmuscle cells into vigorously and rhythmically contracting cardiac muscle will represent a major breakthrough in modern medicine and biology and repair of the damaged areas of the heart with CIR-treated iPS cells will represent a significant step forward in the translation to new clinical treatments for human heart disease. Of the 935,000 Americans who suffer heart attacks each year, many are treated by balloon angioplasty, with or without stents, or receive coronary by-pass surgery to reduce their symptoms. While these interventions improve heart function and quality of life for some, many do not significantly recover because connective scar tissue, rather than new muscle, replaces the heart muscle in the infarcted area. If the dead/damaged cardiac cells and/or scar tissues were to be replaced with living, contracting cardiomyocytes, patients with heart disease could have normal heart function restored and those 935,000 Americans, and incalculable others worldwide, who suffer heart attacks each year, could return to normal pre-heart-attack activities again.

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