Ge Tao, Ph.D.
Room 642, Basic Science Building
Office: (843) 792-5059
Lab: (843) 792-0626
Education:BS, Biological Sciences, China Agricultural University, Beijing, China (2007)
PhD, Molecular Cell & Developmental Biology, University of Miami, Miami FL (2012)
Postdoctoral Associate, Baylor College of Medicine, Houston TX (2017)
The Tao lab is dedicated to unveiling the cellular and molecular mechanisms underlying myocardial homeostasis, injury, and repair. We are interested in understanding how developmental pathways are connected to adult heart regeneration, and providing novel strategies for treating heart failure caused by numerous heart diseases.
Cardiovascular disease is the #1 killer worldwide, with heart failure as the most devastating consequence that accounts for the majority of the mortality. The hallmark of a failing heart is degenerative muscle that gradually loses healthy cardiomyocytes and contractility. Currently, there is no cure to reverse the pathological process. However, much effort has been made to reveal the biological principles of heart failure caused by severe heart diseases including myocardial infarction (MI) and arrhythmia (e.g. atrial fibrillation).
To repopulate an infarcted area caused by MI, one promising strategy is to reintroduce cardiomyocytes into cell cycle, inspired by the observance of regenerative capacity in mammalian hearts during early life. In mouse, neonatal hearts can fully regenerate after MI, however this ability is gradually lost and gone by Postnatal day 7 (Figure 1). Over the past 5 years, we and other groups have been focusing on identifying what the young hearts have and the adult hearts don’t. It turned out that certain molecular pathways are enriched in neonatal hearts, and grant them regenerative abilities. The same pathways, when genetically modified, can improve cardiac function and structure repair even in adult hearts. One such example is the Pitx2 signaling. The key component of the pathway is Pitx2, a homeodomain transcription factor that has been linked to human Rieger Syndrome and atrial fibrillation. The Pitx2 gene is activated by the upstream oxidative stress sensor, Nrf2, after MI. Nrf2 then facilitates the nuclei-shuttling of Pitx2 protein, which further couples with the Hippo signaling effector, Yap, to co-regulate downstream antioxidant scavengers, hence grants protection to myocardium (Tao et al., Nature 2016, Figure 2).
Project and Approach
The current projects in our lab include the expansion of Pitx2 studies to further dissect the pathway, as well as screening for other beneficial signaling. The technical strategies in Tao lab typically start with unbiased screening based on CRISPR technology and Next Generation Sequencing, which includes ChIP-Seq, RNA-Seq, ATAC-Seq and Drop-Seq (single cell transcriptome analysis). Once a target pathway has been identified, it will be validated in cell lines and tissue samples with molecular biology and biochemical experiments. Eventually, each hypothesis will be examined using an adult murine cardiac survival surgery model, where artificial myocardial infarction is induced by occluding the left anterior descending coronary artery (LAD-O, Figure 1). The effect of gene manipulation on the scarring and recovering of the myocardium will be assessed by non-invasive echocardiography, histology, immunofluorescence, and biochemistry. Trainees in Tao lab will have the opportunities to learn the key technologies and skills in each step mentioned above. We welcome enthusiastic students and postdocs to join our lab.
- Ai S, Yu X, Li Y, Peng Y, Li C, Yue Y, Tao G, Li C, Pu WT, He A. Divergent Requirements for EZH1 in Heart Development Versus Regeneration. Circulation research. 2017; 121(2):106-112. PMID: 28512107; PMCID: PMC5527745
- Tao G, Kahr PC, Morikawa Y, Zhang M, Rahmani M, Heallen TR, Li L, Sun Z, Olson EN, Amendt BA, Martin JF. Pitx2 promotes heart repair by activating the antioxidant response after cardiac injury. Nature. 2016; 534(7605):119-23. PMID:27251288; PMCID: PMC4999251
- Morikawa Y, Zhang M, Heallen T, Leach J, Tao G, Xiao Y, Bai Y, Li W, Willerson JT, Martin JF. Actin cytoskeletal remodeling with protrusion formation is essential for heart regeneration in Hippo-deficient mice. Science signaling. 2015; 8(375):ra41. PMID: 25943351; PMCID: PMC4442128
- Tao G, Wang J, Martin JF. Small RNA: from development to regeneration. Science translational medicine. 2015; 7(279):279fs12. PMID: 25787761
- Wang S, Lopez AL 3rd, Morikawa Y, Tao G, Li J, Larina IV, Martin JF, Larin KV. Noncontact quantitative biomechanical characterization of cardiac muscle using shear wave imaging optical coherence tomography. Biomedical optics express. 2014; 5(7):1980-92. PMID: 25071943; PMCID: PMC4102343
- Heallen T, Morikawa Y, Leach J, Tao G, Willerson JT, Johnson RL, Martin JF. Hippo signaling impedes adult heart regeneration. Development (Cambridge, England). 2013; 140(23):4683-90. PMID: 24255096; PMCID: PMC3833428
- Tao G, Martin JF. MicroRNAs get to the heart of development. eLife. 2013; 2:e01710. PMID: 24252874; PMCID: PMC3833033
- Bosse K, Hans CP, Zhao N, Koenig SN, Huang N, Guggilam A, LaHaye S, Tao G, Lucchesi PA, Lincoln J, Lilly B, Garg V. Endothelial nitric oxide signaling regulates Notch1 in aortic valve disease. Journal of molecular and cellular cardiology. 2013; 60:27-35. PMID: 23583836; PMCID: PMC4058883
- Tao G, Miller LJ, Lincoln J. Snai1 is important for avian epicardial cell transformation and motility. Developmental dynamics. 2013; 242(6):699-708. PMID: 23553854; PMCID: PMC3668562
- Tao G, Levay AK, Peacock JD, Huk DJ, Both SN, Purcell NH, Pinto JR, Galantowicz ML, Koch M, Lucchesi PA, Birk DE, Lincoln J. Collagen XIV is important for growth and structural integrity of the myocardium. Journal of molecular and cellular cardiology. 2012; 53(5):626-38. PMID: 22906538; PMCID: PMC3472103
- Tao G, Kotick JD, Lincoln J. Heart valve development, maintenance, and disease: the role of endothelial cells. Current topics in developmental biology. 2012; 100:203-32. PMID: 22449845
- Tao G, Levay AK, Gridley T, Lincoln J. Mmp15 is a direct target of Snai1 during endothelial to mesenchymal transformation and endocardial cushion development. Developmental biology. 2011; 359(2):209-21. PMID: 21920357; PMCID: PMC3202673
- Peacock JD, Levay AK, Gillaspie DB, Tao G, Lincoln J. Reduced sox9 function promotes heart valve calcification phenotypes in vivo. Circulation research. 2010; 106(4):712-9. PMID: 20056916; PMCID: PMC2863131