3500 N Broad St MERB/ Rm 981

Philadelphia, PA 19140 Tel (215)707-4855

Cell (609) 682-0690 jibin.zhou@yahoo.com

Jibin Zhou, Ph.D.

Staff Scientist, Translational Medicine at Temple Univ School of Medicine

SUMMARY Pioneering research investigator in biomedical science with expertise in cardiovascular disease area, solid background and hands-on experience in molecular cell biology as well as pharmacology in study of dilated cardiomyopathy, heart failure and diabetic vascular disease; developed and optimized various in vitro assays in assessing and investigating therapeutics; author of numerous peer-reviewed publications; strong command of high throughput techniques and bioinformatics; effective problem-solving and excellent interpersonal skills; ample experience in project management and mentoring students and associates Look for new opportunities in biotechnology or biopharmaceuticals EDUCATION PhD: Physiology, Xi’an Medical University, China MS: Anatomy, Wuhan University School of Medicine Bachelor (MD equivalent): Medicine, Wuhan University School of Medicine, China PROFESSIONAL EXPERIENCE Scientist: Translational Medicine, Temple Univ School of Medicine; 2/12 - current Primary contributor in multiple projects including: 1) Endothelial progenitor cell-based therapy for diabetic vascular disease via epigenetic reprogramming; 2) Identification of loss-of cardiac GSK-3 induced mitotic catastrophe in the heart; 3) Determination of roles played by GSK-3α in aging Research Associate Scientist: Center for Translational Medicine, Jefferson Univ 1/06 – 1/12 Key player in projects including: 1) Elucidated the role of GSK-3α in regulating β-adrenergic signaling and the response of heart to hemodynamic stress; 2) Identified a novel mechanism whereby oxidant stress signals cell death via a SOK1/14-3-3ζ/ASK-1 cascade Postdoc: Cardiovascular Research Inst., Univ of South Dakota Sch of Medicine 1/03 – 1/06 1) Characterized roles of β-catenin, FAK in heart hypertrophy and heart failure progression 2) Constructed multiple vectors expressing LRPs and sFRPs for making the virus or transgenic mice SKILLS and EXPERTISE DNA & RNA: DNA cloning, site directed mutagenesis, cloning, PCR, reverse transcription, quantitative real time PCR (qPCR), 5' RACE and 3' RACE, cDNA library construction and screening, Southern/Northern hybridization, microRNA study Proteins: SDS-PAGE, Western blot, ELISA, immunoprecipitation, ChIP, X-ChIP Cell Culture: Cell lines (NIH3T3, HeLa, HEK293, HUVEC, etc.); primary neonatal/adult cardiomyocyte and fibroblast isolation, and mouse embryonic fibroblasts (MEFs); autophagy flux assays; bone marrow derived endothelial progenitor cell isolation Pathology: Tissue processing and sectioning; H&E, Masson’s trichrome, PAS, and enzymatic-histological staining (SA-β-gal, SDH, ATPase); immunocytochemistry including immunofluorescence; in situ hybridization histochemistry; light, fluorescence and confocal microscopy, electron microscopy

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In vivo: Designed, developed, and performed and coordinated experiments in various animal models including heart hypertrophy, dilated cardiomyopathy (DCM) and heart failure; excellent skills in echocardiography, hemodynamics and electrocardiography analysis; small animal surgeries such as TAC Bioinformatics and computer: Compile figures for publication; high throughput analysis (microarray, RNA-seq, PCR array); statistical analysis and downstream bioinformatics mining (pathway, GO enrichment, network analysis); R language; Ingenuity Pathway Analysis (IPA); sequence analysis (Align, ClustalW2); Similarity & Homology (BLAST, Primer-BLAST; FASTA); Vector NTI; Chromas2; MS Office; Adobe Photoshop; GraphPad Prism; SigmaStat & SigmaPlot COLLABORATIONS 1. Scientist at Temple, collaborate with Dr. Jim Woodgett at Lunenfeld‑Tanenbaum Research Institute in

Canada for the GSK-3 projects 2. Scientist at Temple, collaborated with Dr. John Farber at Jefferson University Hospital in pathology 3. Scientist, Temple, collaborated with Dr. Emily Mangano in Brigham and Women’s Hospital and

Harvard Medical School for brain research 4. Research Associate Scientist at Jefferson University, collaborated with Drs. Xiongwen Chen and

Steven Houser at Temple for cardiac physiology TEACHING EXPERIENCE Sun Yat-sen University of Medical Sciences, China. Neuroscience: lecture to second and third-year

medical students and graduates; 9/99 - 9/01. Three Gorges University School of Medicine, China. Human Physiology and Gross Anatomy and

Neuroanatomy: lecture to second and third-year medical students; 9/90 - 9/96 PUBLICATIONS (selected from 26) 1. Zhou J, Garikipati VNS, Cheng Z, Benedict C, Nickoloff E, Gao E, Verma S, Khan M, Kishore R.

Epigenetic Reprogramming Rescues Diabetic Endothelial Progenitor Cell Dysfunctions and Enhances their Reparative Activities in Ischemic Tissue Repair. (Entire manuscript ready for submission)

2. Zhou J, Ahmad F, Parikh S, Hoffman NE, Rajan S, Song J, Yuan A, Shanmughapriya S, Guo Y, Kishore R, Koch W, Woodgett JR, Gao E, Madesh M, Lal H, Force T. Loss of adult cardiomyocyte GSK-3 leads to mitotic catastrophe resulting in fatal dilated cardiomyopathy. Circ Res, 2016 Apr 15;118(8):1208-22

3. Ahmad F, Lal H, Zhou J, Vagnozzi RJ, Yu JE, Shang X, Woodgett JR, Gao E, Force T. Cardiomyocyte-specific deletion of Gsk3α mitigates post–myocardial infarction remodeling, contractile dysfunction, and heart failure. JACC, 2014, 64(7):696-706

4. Lal H, Ahmad F, Zhou J, Yu JE. Yu, Vagnozzi RJ, Guo Y, Yu D, Tsai EJ, Woodgett JR, Gao E, Force T. Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart. Circulation, 2014, 130(5):419-30

5. Zhou J and Force T. Focusing the spotlight on GSK-3 in aging. Aging (Albany NY). 2013; 5(6):388-9

6. Zhou J, Freeman TA, Ahmad F, Shang X, Mangano E, Gao E, Farber J, Wang Y, Ma XL, Woodgett J, Vagnozzi RJ, Lal H, Force T. GSK-3α is a central regulator of age-related pathologies in mice. J Clin Invest. 2013; 123(4):1821-32

7. Lal H, Zhou J, Ahmad F, Zaka R, Vagnozzi RJ, Decaul M, Woodgett J, Gao E, Force T. Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death. Circulation. 2012; 125(1): 65-75

8. Zhou J, Lal H, Chen X, Shang X, Song J, Li Y, Kerkela R, Doble BW, MacAulay K, DeCaul M, Koch WJ, Farber J, Woodgett J, Gao E, Force T. GSK-3α directly regulates β-adrenergic signaling and the response of the heart to hemodynamic stress in mice. J Clin Invest. 2010; 120(7): 2280-91

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9. Woulfe KC, Gao E, Lal H, Harris D, Fan Q, Vagnozzi R, DeCaul M, Shang X, Patel S, Woodgett JR, Force T, Zhou J. Glycogen synthase kinase-3β regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo. Circ Res. 2010; 106(10): 1635-45

10. Zhou J, Shao Z, Kerkela R, Ichijo H, Muslin A, Pombo C, Force T. Serine 58 of 14-3-3ζ is a molecular switch regulating ASK1 and oxidant stress-induced cell death. Mol Cell Biol. 2009; 29(15): 4167-76

11. Kerkela R, Kockeritz L, MacAulay K, Zhou J, Doble BW, Beahm C, Greytak S, Woulfe K, Trivedi CM, Woodgett JR, Epstein JA, Force T, Huggins GS. Deletion of GSK-3β in mice leads to hypertrophic cardiomyopathy secondary to cardiomyoblast hyperproliferation. J Clin Invest. 2008, 118(11): 3609–3618

PRESENTATION & COMMUNICATION (selected) 1. Cardiac-specific deletion of GSK-3α and GSK-3β leads to fatal dilated cardiomyopathy with mitotic

catastrophe. AHA Scientific Sessions 2014; November 15-19, Chicago, Illinois (Poster) 2. Deletion of GSK-3α, but not GSK-3β, defines an essential role in β-adrenergic responsiveness and

identifies a novel strategy for β-blockage. Late-Breaking Basic Science-AHA Scientific Sessions 2009; Orlando, Florida; November 13-18 (Oral)

3. Deletion of GSK-3α causes a glycogen storage cardiomyopathy. AHA Scientific Sessions 2008; New Orleans, Louisiana; November 8-12 (Poster)

4. Phosphorylation status of Ser58 of 14-3-3 proteins is a novel molecular switch oxidant stress-induced death via ASK-1. AHA Scientific Sessions 2007; Orlando, Florida; November 4-7 (Poster)

5. Targeted Deletion of Glycogen Synthase Kinase-3 (GSK-3α) vs. GSK-3ß identifies unique isoform-specific effects on development and hypertrophy. AHA Scientific Sessions 2007; Orlando, Florida; November 4-7 (Poster)

REFEREES References available through email or post.