Honors & Awards

  • NIH T32 Postdoctoral Fellow in Cardiovascular Imaging, Stanford University (2013)
  • Alumnus of the year finalist, Nova Southeastern University (2013)
  • Leadership Award, Nova Southeastern University College of Pharmacy (2004)
  • Mortar and Pestle Professionalism Award, Nova Southeastern University College of Pharmacy (2004)
  • Senior Recognition Award, American Pharmacists Association-Academy of Student Pharmacists (2004)
  • The Marcus Family Scholarship for Scholastic and Leadership Development, Florida Pharmacy Association (2004)
  • Phi Lambda Sigma National Pharmacy Leadership Society, Nova Southeastern University College of Pharmacy (2003)
  • Rho Chi Pharmaceutical Honor Society, Nova Southeastern University College of Pharmacy (2003)
  • Jean Lamberti Memorial Scholarship, Broward County Pharmacy Association (2002)

Professional Education

  • Doctor of Philosophy, University of Southern California (2012)
  • HIV Pharmacotherapy Fellowship, University of Southern California (2008)
  • Pharmacy Practice Residency, University of Southern California (2007)
  • Doctor of Pharmacy, Nova Southeastern University (2004)
  • Bachelor of Science, Nova Southeastern University (2002)

Stanford Advisors


  • Nicholas Mordwinkin, Paul Burridge, Jared Churko, Jordan Plews, Shijun Hu, Joseph Wu. "United States Patent S12-274 Methods and Compositions for the Generation of Endothelial Progenitor Cells and Endothelial Cells from Pluripotent Stem Cells", Leland Stanford Junior University, Nov 21, 2013
  • Nicholas Mordwinkin, Gere diZerega, Stan Louie, Kathleen Rodgers. "United States Patent USC12-496 Molecular markers of endothelial dysfunction in gestational diabetes", University of Southern California, Mar 1, 2013

Research & Scholarship

Current Research and Scholarly Interests

My research is focused on the biological mechanisms of adult stem cells and induced pluripotent stem cells. Our lab uses a combination of next generation sequencing, tissue engineering, physiological testing, and molecular imaging technologies to better understand stem cell biology in vitro and in vivo. For adult stem cells, we are interested in monitoring stem cell survival, proliferation, and differentiation. For induced pluripotent stem cells, we are interested in their tumorigenicity, immunogenicity, differentiation into cardiomyocytes and endothelial cells, cadiovascular disease modeling, drug screening, and cell therapy. We also develop novel vectors and therapeutic genes for cardiovascular gene therapy applications.

Lab Affiliations


Graduate and Fellowship Programs


Journal Articles

  • Stem cells and cardiovascular drug development--reply. JAMA : the journal of the American Medical Association Mordwinkin, N. M., Lee, A. S., Wu, J. C. 2014; 311 (10): 1070-1071

    View details for DOI 10.1001/jama.2014.634

    View details for PubMedID 24618976

  • Patient-specific stem cells and cardiovascular drug discovery. JAMA-the journal of the American Medical Association Mordwinkin, N. M., Lee, A. S., Wu, J. C. 2013; 310 (19): 2039-2040

    View details for DOI 10.1001/jama.2013.282409

    View details for PubMedID 24240927

  • The Role of SIRT6 Protein in Aging and Reprogramming of Human Induced Pluripotent Stem Cells. journal of biological chemistry Sharma, A., Diecke, S., Zhang, W. Y., Lan, F., He, C., Mordwinkin, N. M., Chua, K. F., Wu, J. C. 2013; 288 (25): 18439-18447


    Aging is known to be the single most important risk factor for multiple diseases. Sirtuin-6, or SIRT6, has recently been identified as a critical regulator of transcription, genome stability, telomere integrity, DNA repair, and metabolic homeostasis. A knockout mouse model of SIRT6 has displayed dramatic phenotypes of accelerated aging. In keeping with its role in aging, we demonstrated that human dermal fibroblasts (HDFs) from older subjects were more resistant to reprogramming by classic Yamanaka factors than those from young subjects, but the addition of SIRT6 during reprogramming substantially improved such efficiency in older HDFs. Despite the importance of SIRT6, little is known about the molecular mechanism of its regulation. We show for the first time post-transcriptional regulation of SIRT6 by miR-766 and inverse correlation in the expression of this microRNA in HDFs from different age groups. Our results suggest that SIRT6 regulates miR-766 transcription via a feedback regulatory loop, which has implications for the modulation of SIRT6 expression in reprogramming of aging cells.

    View details for DOI 10.1074/jbc.M112.405928

    View details for PubMedID 23653361

  • Alteration of endothelial function markers in women with gestational diabetes and their fetuses JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE Mordwinkin, N. M., Ouzounian, J. G., Yedigarova, L., Montoro, M. N., Louie, S. G., Rodgers, K. E. 2013; 26 (5): 507-512


    We tested the hypothesis that women with gestational diabetes mellitus (GDM) and their fetuses would demonstrate alterations in markers of endothelial nitric oxide synthase (eNOS) uncoupling, oxidative stress, and endothelial dysfunction and these changes would correlate with the levels of hyperglycemia through a pilot observational case-control study of women with GDM and their fetuses.Levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), C-reactive protein (CRP), nitric oxide (NO), eNOS, p22-phox, and SOD gene expression, and endothelial progenitor cells (EPC) counts in both maternal and cord blood were measured at the time of delivery in women with and without GDM.We demonstrated the presence of decreased maternal circulating EPC counts, increased soluble adhesion molecules in maternal blood, decreased SOD expression in both maternal and cord blood and increased eNOS expression in both maternal and cord blood in women with GDM.These data suggest that the molecular mechanisms behind oxidative stress in women with GDM and their fetuses appear similar to those hypothesized for non-pregnant adults with type 2 diabetes mellitus (DM).

    View details for DOI 10.3109/14767058.2012.736564

    View details for Web of Science ID 000314974900014

    View details for PubMedID 23046386

  • A Review of Human Pluripotent Stem Cell-Derived Cardiomyocytes for High-Throughput Drug Discovery, Cardiotoxicity Screening, and Publication Standards JOURNAL OF CARDIOVASCULAR TRANSLATIONAL RESEARCH Mordwinkin, N. M., Burridge, P. W., Wu, J. C. 2013; 6 (1): 22-30


    Drug attrition rates have increased in past years, resulting in growing costs for the pharmaceutical industry and consumers. The reasons for this include the lack of in vitro models that correlate with clinical results and poor preclinical toxicity screening assays. The in vitro production of human cardiac progenitor cells and cardiomyocytes from human pluripotent stem cells provides an amenable source of cells for applications in drug discovery, disease modeling, regenerative medicine, and cardiotoxicity screening. In addition, the ability to derive human-induced pluripotent stem cells from somatic tissues, combined with current high-throughput screening and pharmacogenomics, may help realize the use of these cells to fulfill the potential of personalized medicine. In this review, we discuss the use of pluripotent stem cell-derived cardiomyocytes for drug discovery and cardiotoxicity screening, as well as current hurdles that must be overcome for wider clinical applications of this promising approach.

    View details for DOI 10.1007/s12265-012-9423-2

    View details for Web of Science ID 000313657700003

    View details for PubMedID 23229562

  • Second-generation codon optimized minicircle (CoMiC) for non-viral reprogramming of human adult fibroblasts Methods in Molecular Biology (in press) Diecke, S., Lisowski, L., Mordwinkin, N. M., Kooreman, N. G., Wu, J. C. 2013
  • Effects of combined radiation and burn injury on the renin-angiotensin system WOUND REPAIR AND REGENERATION Jadhav, S. S., Sharma, N., Meeks, C. J., Mordwinkin, N. M., Espinoza, T. B., Roda, N. R., diZerega, G. S., Hill, C. K., Louie, S. G., Rodgers, K. E. 2013; 21 (1): 131-140


    The renin-angiotensin system (RAS) plays an important role in wound repair; however, little is known pertaining to RAS expression in response to thermal injury and the combination of radiation plus burn injury (CRBI). The purpose of this study was to test the hypothesis that thermal injury modifies expression of RAS components and CRBI delayed this up-regulation of RAS. Skin from uninjured mice was compared with mice receiving local thermal injury or CRBI (injury site). Skin was analyzed for gene and protein expression of RAS components. There was an initial increase in the expression of various components of RAS following thermal injury. However, in the higher CRBI group there is an initial decrease in AT(1b) (vasoconstriction, pro-proliferative), AT(2) (vasodilation, differentiation), and Mas (vasodilation, anti-inflammatory) gene expression. This corresponded with a delay and decrease in AT(1) , AT(2) , and MAS protein expression in fibroblasts and keratinocytes. The reduction in RAS receptor positive fibroblasts and keratinocytes correlated with a reduction in collagen deposition and keratinocyte infiltration into the wounded area resulting in a delay of reepithelialization following CRBI. These data support the hypothesis that delayed wound healing observed in subjects following radiation exposure may be in part due to decreased expression of RAS.

    View details for DOI 10.1111/j.1524-475X.2012.00867.x

    View details for Web of Science ID 000313348500052

    View details for PubMedID 23231670

  • Angiotensin-(1-7) Administration Reduces Oxidative Stress in Diabetic Bone Marrow ENDOCRINOLOGY Mordwinkin, N. M., Meeks, C. J., Jadhav, S. S., Espinoza, T., Roda, N., diZerega, G. S., Louie, S. G., Rodgers, K. E. 2012; 153 (5): 2189-2197


    Diabetics have an increased risk of developing cardiovascular disease, in part due to oxidative stress, resulting in endothelial nitric oxide synthase (eNOS) dysfunction. Studies have demonstrated that angiotensin-(1-7) [Ang-(1-7)] can activate eNOS activity. Because the bone marrow is a primary source of a number of progenitors important in physiological homeostasis and healing, the goal of this study was to evaluate the in vivo effects of Ang-(1-7) treatment on oxidative stress and the ensuing nitrative stress in diabetic bone marrow and its potential pathways. BKS.Cg-Dock7(m) +/+ Lepr(db)/J mice and their heterozygous controls were administered Ang-(1-7) alone or combined with A-779, losartan, PD123,319, nitro-l-arginine methyl ester, or icatibant sc for 14 d. The bone marrow was then collected to measure nitric oxide levels, eNOS phosphorylation, and expression of nitric oxide synthase, superoxide dismutase, and p22-phox. Nitric oxide levels in the bone marrow were significantly decreased in diabetic mice, and Ang-(1-7) treatment was able to significantly increase these measures (P < 0.01). This effect was blocked by the coadministration of PD123,319, A-779, nitro-l-arginine methyl ester, and icatibant. In addition, Ang-(1-7) treatment reversed the paradoxical increase in eNOS and neuronal nitric oxide synthase expression and decreased the phosphorylation of eNOS at Thr495 seen in diabetic mice. Ang-(1-7) also reversed diabetes-induced production of reactive oxygen species by decreasing p22-phox expression and increasing superoxide dismutase 3 expression, leading to a significant reduction in 3-nitrotyrosine formation in diabetic bone marrow (P < 0.05). Our findings demonstrate that Ang-(1-7) administration decreases diabetes-induced oxidative stress in the bone marrow and modifies pathways involved in eNOS dysfunction.

    View details for DOI 10.1210/en.2011-2031

    View details for Web of Science ID 000303860700018

    View details for PubMedID 22434085

  • Toxicological and toxicokinetic analysis of angiotensin (1-7) in two species JOURNAL OF PHARMACEUTICAL SCIENCES Mordwinkin, N. M., Russell, J. R., Burke, A. S., diZerega, G. S., Louie, S. G., Rodgers, K. E. 2012; 101 (1): 373-380


    The objectives of this study were to determine the potential systemic and local toxicity, as well as evaluate the toxicokinetic (TK) profile of angiotensin (1-7) [A(1-7)] when administered daily via subcutaneous injection for 28 days to Sprague-Dawley rats and Beagle dogs. A(1-7) is a member of the renin-angiotensin system and has undergone clinical evaluation for the treatment of chemotherapy-induced myelosuppression. In this present study, A(1-7) was given at 10 mg/(kg day) for 28 days to rats and canines. At day 27, blood was harvested to evaluate the TK parameters. On day 28, systemic toxicology was evaluated. Following A(1-7) administration for 27 days, no plasma A(1-7) accumulation was detected in canines; however, increased A(1-7) plasma concentrations were detected in rats. Despite the accumulation observed in rats, no detectable toxicity was found following A(1-7) administration for 28 days. The TK analysis of A(1-7) revealed a plasma half-life of 20-30 min in both rats and canines. The time to maximum plasma concentration was found to be 15 and 26.25 min in rats and canines, respectively. This study shows that subcutaneous administration of A(1-7) at 10 mg/(kg day) for 28 days did not lead to any detectable toxicities in either rats or canines.

    View details for DOI 10.1002/jps.22730

    View details for Web of Science ID 000298018000036

    View details for PubMedID 21858825

  • Interleukin-1 as an Injury Signal Mobilizes Retinyl Esters in Hepatic Stellate Cells through Down Regulation of Lecithin Retinol Acyltransferase PLOS ONE Kida, Y., Xia, Z., Zheng, S., Mordwinkin, N. M., Louie, S. G., Zheng, S. G., Feng, M., Shi, H., Duan, Z., Han, Y. 2011; 6 (11)


    Retinoids are mostly stored as retinyl esters in hepatic stellate cells (HSCs) through esterification of retinol and fatty acid, catalyzed by lecithin-retinol acyltransferase (LRAT). This study is designated to address how retinyl esters are mobilized in liver injury for tissue repair and wound healing. Initially, we speculated that acute inflammatory cytokines may act as injury signal to mobilize retinyl esters by down-regulation of LRAT in HSCs. By examining a panel of cytokines we found interleukin-1 (IL-1) can potently down-regulate mRNA and protein levels of LRAT, resulting in mobilization of retinyl esters in primary rat HSCs. To simulate the microenvironment in the space of Disse, HSCs were embedded in three-dimensional extracellular matrix, by which HSCs retaine quiescent phenotypes, indicated by up-regulation of LRAT and accumulation of lipid droplets. Upon IL-1 stimulation, LRAT expression went down together with mobilization of lipid droplets. Secreted factors from Kupffer cells were able to suppress LRAT expression in HSCs, which was neutralized by IL-1 receptor antagonist. To explore the underlying mechanism we noted that the stability of LRAT protein is not significantly regulated by IL-1, indicating the regulation is likely at transcriptional level. Indeed, we found that IL-1 failed to down-regulate recombinant LRAT protein expressed in HSCs by adenovirus, while transcription of endogenous LRAT was promptly decreased. Following liver damage, IL-1 was promptly elevated in a close pace with down-regulation of LRAT transcription, implying their causative relationship. After administration of IL-1, retinyl ester levels in the liver, as measured by LC/MS/MS, decreased in association with down-regulation of LRAT. Likewise, IL-1 receptor knockout mice were protected from injury-induced down-regulation of LRAT. In summary, we identified IL-1 as an injury signal to mobilize retinyl ester in HSCs through down-regulation of LRAT, implying a mechanism governing transition from hepatic injury to wound healing.

    View details for DOI 10.1371/journal.pone.0026644

    View details for Web of Science ID 000297198200015

    View details for PubMedID 22073179

  • Discovery and Preclinical Evaluation of a Novel Class of Cytotoxic Propynoic Acid Carbamoyl Methyl Amides (PACMAs) JOURNAL OF MEDICINAL CHEMISTRY Yamada, R., Cao, X., Butkevich, A. N., Millard, M., Odde, S., Mordwinkin, N., Gundla, R., Zandi, E., Louie, S. G., Petasis, N. A., Neamati, N. 2011; 54 (8): 2902-2914


    Herein, we discovered a series of propynoic acid carbamoyl methyl-amides (PACMAs) with potent cytotoxicity against a panel of cancer cell lines. These compounds interrupted cell cycle progression at low micromolar concentrations and induced early and late stage apoptosis. A representative compound suppressed tumor growth without apparent toxicity in an MDA-MB-435 mouse xenograft model. We used a Kinexus 628-antibody microarray and the Ingenuity Pathway Analysis (IPA) bioinformatics tools to better understand their mechanisms. The IPA analysis revealed the initiation of Nrf2-mediated oxidative stress through modulating the expression of SOD1 and STIP1 by compound 1. The involvement of the oxidative stress pathway was further validated by measuring the levels of the PACMA-induced mitochondrial superoxide species. To our knowledge, this is the first report on the discovery and biological evaluations of PACMAs as anticancer agents. Their broad-spectrum in vitro cytotoxicity, possibly through an oxidative stress-mediated pathway, and in vivo efficacy warrant further preclinical investigations.

    View details for DOI 10.1021/jm101655d

    View details for Web of Science ID 000289697800025

    View details for PubMedID 21443194

  • Estimation of Glomerular Filtration Rate by Using Serum Cystatin C and Serum Creatinine Concentrations in Patients with Human Immunodeficiency Virus PHARMACOTHERAPY Beringer, P. M., Owens, H., Nguyen, A., Mordwinkin, N., Louie, S., Mak, M., Sattler, F. 2010; 30 (10): 1004-1010


    To compare the predictive performance of four equations for estimating glomerular filtration rate (GFR) relative to the gold standard measurement, iothalamate clearance, in patients with human immunodeficiency virus (HIV) who have various degrees of kidney function.Prospective, cross-sectional analysis.General clinical research center.Twenty-two adult (mean age 51 yrs) HIV-positive patients with various degrees of stable kidney function and with lean body mass considered normal for a well-nourished person.Patients were administered a single dose of intravenous iothalamate 456 mg as a rapid infusion over 3 minutes, 1 hour after an oral fluid load of 600 ml of caffeine-free, sugar-free liquids.Serial blood and urine samples were obtained for determination of measured GFR. Estimated GFR values were calculated by using four equations: the Cockcroft-Gault equation, the simplified Modification of Diet in Renal Disease Study (MDRD) equation, an equation that incorporates serum creatinine and cystatin C concentrations, and an equation incorporating only serum cystatin C concentration. The predictive performance of the equations was determined by comparing the bias, accuracy, and precision of the estimates with the measured values. Body composition was determined by dual-energy x-ray absorptiometry. The four predictive equations underestimated the measured GFR obtained by the iothalamate method, but the differences were not statistically significant. The MDRD equation and the equation that included both serum cystatin C and creatinine concentrations, as well as age, sex, and race, provided the least bias, most precision, and best accuracy in estimating the measured GFR.The MDRD equation and the equation that included both serum cystatin C and creatinine concentrations appear to provide accurate, precise, and relatively unbiased estimates of GFR in patients with HIV. Larger studies are needed that include patients with muscle wasting and lipodystrophy in order to validate these preliminary observations and the effects of body composition on the predictability of GFR with use of these equations.

    View details for Web of Science ID 000282831700005

    View details for PubMedID 20874037

  • Can Therapeutic Drug Monitoring Improve Pharmacotherapy of HIV Infection in Adolescents? THERAPEUTIC DRUG MONITORING Rakhmanina, N. Y., van den Anker, J. N., Soldin, S. J., van Schaik, R. H., Mordwinkin, N., Neely, M. N. 2010; 32 (3): 273-281


    Currently, therapeutic drug monitoring (TDM) of antiretroviral therapy (ART) is not performed in the United States as part of routine clinical care of an HIV-infected adolescent patient. TDM is recommended to rule out subtherapeutic drug concentrations and to differentiate among malabsorption, drug interactions, poor adherence, or increased drug metabolism or clearance as possible causes of decreased drug exposure. The use of TDM is also considered to assist in finding the optimal dose of a drug in patients whose virus has shown reduced susceptibility to that drug. The dosing of antiretroviral (ARV) drugs in adolescent patients with HIV infection depends on the chronologic age, weight, height, and the stage of sexual maturation. As a result of the limited data on the pharmacokinetics of ART during puberty, the transition of a dosing regimen from higher pediatric (weight and surface-based) to adult (fixed) range is not well defined. Developmental pharmacokinetic differences contribute to high variability in pediatric and adolescent patients and an increased frequency of suboptimal ARV exposure as compared to in adults. Individualized, concentration-targeted optimal dosing of ARV medications can be beneficial to patients for whom only limited dosing guidelines are available. This article describes three cases of the application of TDM in treatment-experienced adolescent patients whose ART was optimized using ARV TDM. TDM of ARV drugs is useful in managing the pharmacotherapy of HIV in adolescent patients and is well received by the adolescent patients with HIV and their families. Among others, the benefits of TDM provide evidence for adherence interventions and create grounds for enhanced education of the adolescent patient and involved adult caregivers about ART. Finally, TDM in adolescents provides valuable information about the clinical pharmacology of ART during puberty.

    View details for DOI 10.1097/FTD.0b013e3181dca14b

    View details for Web of Science ID 000278379400009

    View details for PubMedID 20445485

  • Aralast: An alpha(1)-protease inhibitor for the treatment of alpha-antitrypsin deficiency EXPERT OPINION ON PHARMACOTHERAPY Mordwinkin, N. M., Louie, S. G. 2007; 8 (15): 2609-2614


    Alpha-antitrypsin (AAT) is a serine protease inhibitor, which inhibits the proteolytic enzyme elastase. Individuals with a deficiency of AAT may develop clinical manifestations that include a decline in lung function. Deficiency of AAT can lead to many clinical manifestations, most commonly chronic obstructive pulmonary disease in the form of emphysema. However, patients with this genetic disorder may also develop dysfunctions of other organs such as the liver and/or skin. There are approximately 100 alleles associated with the gene encoding for AAT, where the estimated prevalence of this disorder is approximately as common as cystic fibrosis; however, misdiagnosis continues to be a problem. Augmentation therapy using intravenous AAT has been shown to reduce the forced expiratory volume in one second decline, associated with AAT deficiency. Restoration of serum AAT concentrations above 11 microM have correlated with a reduced level of disease progression. The normal dosing regimen of intravenous AAT is 60 mg/kg given every week. Although a dosage consolidation of 250 mg/kg given every 28 days has been explored, long-term efficacy has not been determined. Aralast is one of three approved human plasma-derived treatment options used to prevent the progression of emphysema associated with AAT deficiency disorder.

    View details for DOI 10.1517/14656566.8.15.2609

    View details for Web of Science ID 000250426000013

    View details for PubMedID 17931094

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