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4. VEGFA mRNA-LNP promotes biliary epithelial cell-to-hepatocyte conversion in acute and chronic liver diseases and reverses steatosis and fibrosis

Author

Rizvi, Fatima, Lee, Yu-Ri, Diaz-Aragon, Ricardo, Bawa, Pushpinder S., So, Juhoon, Florentino, Rodrigo M., Wu, Susan, Sarjoo, Arianna, Truong, Emily, Smith, Anna R., Wang, Feiya, Everton, Elissa, Ostrowska, Alina, Jung, Kyounghwa, Tam, Ying, Muramatsu, Hiromi, Pardi, Norbert, Weissman, Drew, Soto-Gutierrez, Alejandro, Shin, Donghun, and Gouon-Evans, Valerie

Published
2023
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5. De novo hematopoiesis from the fetal lung

Author

Yeung, Anthony K., Villacorta-Martin, Carlos, Lindstrom-Vautrin, Jonathan, Belkina, Anna C., Vanuytsel, Kim, Dowrey, Todd W., Ysasi, Alexandra B., Bawa, Pushpinder, Wang, Feiya, Vrbanac, Vladimir, Mostoslavsky, Gustavo, Balazs, Alejandro B., and Murphy, George J.

Published
2023
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10. Human iPSC-hepatocyte modeling of alpha-1 antitrypsin heterozygosity reveals metabolic dysregulation and cellular heterogeneity

Author

Kaserman, Joseph E., Werder, Rhiannon B., Wang, Feiya, Matte, Taylor, Higgins, Michelle I., Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S., Shi, Xu, Gerszten, Robert E., Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlos, Hollenberg, Anthony N., Kotton, Darrell N., and Wilson, Andrew A.

Published
2022
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11. Ebola virus infection induces a delayed type I IFN response in bystander cells and the shutdown of key liver genes in human iPSC-derived hepatocytes

Author

Scoon, Whitney A., Mancio-Silva, Liliana, Suder, Ellen L., Villacorta-Martin, Carlos, Lindstrom-Vautrin, Jonathan, Bernbaum, John G., Mazur, Steve, Johnson, Reed F., Olejnik, Judith, Flores, Elizabeth Y., Mithal, Aditya, Wang, Feiya, Hume, Adam J., Kaserman, Joseph E., March-Riera, Sandra, Wilson, Andrew A., Bhatia, Sangeeta N., Mühlberger, Elke, and Mostoslavsky, Gustavo

Published
2022
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12. Multi-modal profiling of human fetal liver hematopoietic stem cells reveals the molecular signature of engraftment

Author

Vanuytsel, Kim, Villacorta-Martin, Carlos, Lindstrom-Vautrin, Jonathan, Wang, Zhe, Garcia-Beltran, Wilfredo F., Vrbanac, Vladimir, Parsons, Dylan, Lam, Evan C., Matte, Taylor M., Dowrey, Todd W., Kumar, Sara S., Li, Mengze, Wang, Feiya, Yeung, Anthony K., Mostoslavsky, Gustavo, Dries, Ruben, Campbell, Joshua D., Belkina, Anna C., Balazs, Alejandro B., and Murphy, George J.

Published
2022
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15. Human iPSC-hepatocyte modeling of alpha-1 antitrypsin heterozygosity reveals metabolic dysregulation and cellular heterogeneity [Dataset]

Author

Kaserman, Joseph E., Werder, Rhiannon B., Wang, Feiya, Matte, Taylor, Higgins, Michelle I., Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S., Shi, Xu, Gerszten, Robert E., Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlos, Hollenberg, Anthony N., Kotton, Darrell N., Wilson, Andrew A., Kaserman, Joseph E., Werder, Rhiannon B., Wang, Feiya, Matte, Taylor, Higgins, Michelle I., Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S., Shi, Xu, Gerszten, Robert E., Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlos, Hollenberg, Anthony N., Kotton, Darrell N., and Wilson, Andrew A.

Published
2022

16. Human iPSC-hepatocyte modeling of alpha-1 antitrypsin heterozygosity reveals metabolic dysregulation and cellular heterogeneity

Author

National Health and Medical Research Council (Australia), National Institutes of Health (US), Alpha- Foundation, Kaserman, Joseph E., Werder, Rhiannon B., Wang, Feiya, Matte, Taylor, Higgins, Michelle I., Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S., Shi, Xu, Gerszten, Robert E., Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlos, Hollenberg, Anthony N., Kotton, Darrell N., Wilson, Andrew A., National Health and Medical Research Council (Australia), National Institutes of Health (US), Alpha- Foundation, Kaserman, Joseph E., Werder, Rhiannon B., Wang, Feiya, Matte, Taylor, Higgins, Michelle I., Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S., Shi, Xu, Gerszten, Robert E., Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlos, Hollenberg, Anthony N., Kotton, Darrell N., and Wilson, Andrew A.

Abstract

Individuals homozygous for the “Z” mutation in alpha-1 antitrypsin deficiency are known to be at increased risk for liver disease. It has also become clear that some degree of risk is similarly conferred by the heterozygous state. A lack of model systems that recapitulate heterozygosity in human hepatocytes has limited the ability to study the impact of a single Z alpha-1 antitrypsin (ZAAT) allele on hepatocyte biology. Here, we describe the derivation of syngeneic induced pluripotent stem cells (iPSCs) engineered to determine the effects of ZAAT heterozygosity in iPSC-hepatocytes (iHeps). We find that heterozygous MZ iHeps exhibit an intermediate disease phenotype and share with ZZ iHeps alterations in AAT protein processing and downstream perturbations including altered endoplasmic reticulum (ER) and mitochondrial morphology, reduced mitochondrial respiration, and branch-specific activation of the unfolded protein response in cell subpopulations. Our model of MZ heterozygosity thus provides evidence that a single Z allele is sufficient to disrupt hepatocyte homeostatic function.

Published
2022

17. 3213 – MULTI-MODAL PROFILING OF HUMAN FETAL LIVER HEMATOPOIETIC STEM CELLS REVEALS THE MOLECULAR SIGNATURE OF ENGRAFTMENT

Author

Vanuytsel, Kim, primary, Villacorta-Martin, Carlos, additional, Lindstrom-Vautrin, Jonathan, additional, Wang, zhe, additional, Garcia-Beltran, Wilfredo, additional, Vrbanac, Vladimir, additional, Parsons, Dylan, additional, Lam, Evan, additional, Matte, Taylor, additional, Dowrey, Todd, additional, Kumar, sara, additional, Li, Mengze, additional, Wang, Feiya, additional, Yeung, Anthony, additional, Mostoslavsky, Gustavo, additional, Dries, Ruben, additional, Campbell, Joshua, additional, Belkina, Anna, additional, Balazs, Alejandro, additional, and Murphy, George, additional

Published
2022
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20. Liver-Specific GH Receptor Gene-Disrupted (LiGHRKO) Mice Have Decreased Endocrine IGF-I, Increased Local IGF-I, and Altered Body Size, Body Composition, and Adipokine Profiles

Author

List, Edward O., Berryman, Darlene E., Funk, Kevin, Jara, Adam, Kelder, Bruce, Wang, Feiya, Stout, Michael B., Zhi, Xu, Sun, Liou, White, Thomas A., LeBrasseur, Nathan K., Pirtskhalava, Tamara, Tchkonia, Tamara, Jensen, Elizabeth A., Zhang, Wenjuan, Masternak, Michal M., Kirkland, James L., Miller, Richard A., Bartke, Andrzej, and Kopchick, John J.

Published
2014

25. Metabolic effects of intra-abdominal fat in GHRKO mice

Author

Masternak, Michal M., Bartke, Andrzej, Wang, Feiya, Spong, Adam, Gesing, Adam, Fang, Yimin, Salmon, Adam B., Hughes, Larry F., Liberati, Teresa, Boparai, Ravneet, Kopchick, John J., and Westbrook, Reyhan

Subjects
Male, Mice, Knockout, Longevity, Receptors, Somatotropin, Glucose Tolerance Test, Intra-Abdominal Fat, Lipid Metabolism, Article, Body Temperature, Mice, Glucose, Growth Hormone, Animals, Insulin, Adiponectin, Insulin Resistance, Phosphorylation, Biomarkers, Gene Deletion, Caloric Restriction, Signal Transduction
Abstract

Mice with targeted deletion of the growth hormone receptor (GHRKO mice) are growth hormone (GH) resistant, small, obese, hypoinsulinemic, highly insulin sensitive and remarkably long-lived. To elucidate the unexpected coexistence of adiposity with improved insulin sensitivity and extended longevity, we examined effects of surgical removal of visceral (epididymal and perinephric) fat on metabolic traits related to insulin signaling and longevity. Comparison of results obtained in GHRKO mice and in normal animals from the same strain revealed disparate effects of visceral fat removal (VFR) on insulin and glucose tolerance, adiponectin levels, accumulation of ectopic fat, phosphorylation of insulin signaling intermediates, body temperature, and respiratory quotient (RQ). Overall, VFR produced the expected improvements in insulin sensitivity and reduced body temperature and RQ in normal mice and had opposite effects in GHRKO mice. Some of the examined parameters were altered by VFR in opposite directions in GHRKO and normal mice, and others were affected in only one genotype or exhibited significant genotype × treatment interactions. Functional differences between visceral fat of GHRKO and normal mice were confirmed by measurements of adipokine secretion, lipolysis, and expression of genes related to fat metabolism. We conclude that in the absence of GH signaling, the secretory activity of visceral fat is profoundly altered and unexpectedly promotes enhanced insulin sensitivity. The apparent beneficial effects of visceral fat in GHRKO mice may also explain why reducing adiposity by calorie restriction fails to improve insulin signaling or further extend longevity in these animals.

Published
2011

26. Key Regulators of Mitochondrial Biogenesis are Increased in Kidneys of Growth Hormone Receptor Knockout (GHRKO) Mice

Author

Gesing, Adam, Bartke, Andrzej, Wang, Feiya, Karbownik-Lewinska, Malgorzata, and Masternak, Michal M.

Subjects
Mice, Knockout, Nitric Oxide Synthase Type III, Receptors, Somatotropin, AMP-Activated Protein Kinases, Intra-Abdominal Fat, Kidney, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Article, GTP Phosphohydrolases, Mitochondria, Mice, Sirtuin 3, Trans-Activators, Animals, Female, Phosphorylation, Muscle, Skeletal, Caloric Restriction, Transcription Factors
Abstract

The growth hormone (GH) receptor knockout mice (GHRKO) are remarkably long-lived and highly insulin sensitive. Alterations in mitochondrial biogenesis are associated with aging and various metabolic derangements. We have previously demonstrated increased gene expression of key regulators of mitochondriogenesis in kidneys, hearts and skeletal muscles of GHRKO mice. The aim of the present study was to quantify the protein levels of the following regulators of mitochondriogenesis: peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), AMP-activated protein kinase α (AMPKα), phospho-AMPKα (p-AMPKα), sirtuin-3 (SIRT-3), endothelial nitric oxide synthase (eNOS), phospho-eNOS (p-eNOS), nuclear respiratory factor-1 (NRF-1) and mitofusin-2 (MFN-2) in skeletal muscles and kidneys of GHRKOs in comparison to normal mice. We were also interested in the effects of calorie restriction (CR) and visceral fat removal (VFR) on these parameters. Both CR and VFR improve insulin sensitivity and can extend lifespan. Results: The renal levels of PGC-1α, AMPKα, p-AMPKα, SIRT-3, eNOS, p-eNOS and MFN-2 were increased in GHRKOs. In the GHRKO skeletal muscles, only MFN-2 was increased. Levels of the examined proteins were not affected by CR (except for PGC-1α and p-eNOS in skeletal muscles) or VFR. Conclusion: GHRKO mice have increased renal protein levels of key regulators of mitochondriogenesis and this may contribute to increased longevity of these knockouts.

Published
2011

30. Metabolic effects of intra‐abdominal fat in GHRKO mice

Author

Masternak, Michal M., primary, Bartke, Andrzej, additional, Wang, Feiya, additional, Spong, Adam, additional, Gesing, Adam, additional, Fang, Yimin, additional, Salmon, Adam B., additional, Hughes, Larry F., additional, Liberati, Teresa, additional, Boparai, Ravneet, additional, Kopchick, John J., additional, and Westbrook, Reyhan, additional

Published
2011
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31. Human iPSC-hepatocyte modeling of alpha-1 antitrypsin heterozygosity reveals metabolic dysregulation and cellular heterogeneity

Author

Joseph E. Kaserman, Rhiannon B. Werder, Feiya Wang, Taylor Matte, Michelle I. Higgins, Mark Dodge, Jonathan Lindstrom-Vautrin, Pushpinder Bawa, Anne Hinds, Esther Bullitt, Ignacio S. Caballero, Xu Shi, Robert E. Gerszten, Nicola Brunetti-Pierri, Marc Liesa, Carlos Villacorta-Martin, Anthony N. Hollenberg, Darrell N. Kotton, Andrew A. Wilson, Kaserman, Joseph E, Werder, Rhiannon B, Wang, Feiya, Matte, Taylor, Higgins, Michelle I, Dodge, Mark, Lindstrom-Vautrin, Jonathan, Bawa, Pushpinder, Hinds, Anne, Bullitt, Esther, Caballero, Ignacio S, Shi, Xu, Gerszten, Robert E, Brunetti-Pierri, Nicola, Liesa, Marc, Villacorta-Martin, Carlo, Hollenberg, Anthony N, Kotton, Darrell N, Wilson, Andrew A, National Health and Medical Research Council (Australia), National Institutes of Health (US), and Alpha- Foundation

Subjects
alpha-1 antitrypsin deficiency, metabolic dysregulation, induced pluripotent stem cell, Liver fibrosis, Induced Pluripotent Stem Cells, liver fibrosi, unfolded protein response, proteostasi, General Biochemistry, Genetics and Molecular Biology, CP: Metabolism, CP: Stem cell research, iPSC-derived hepatocytes, cellular heterogeneity, mitochondrial dysfunction, Proteostasis, Hepatocytes, Humans, ER stre, ER stress, iPSC-derived hepatocyte
Abstract

Individuals homozygous for the “Z” mutation in alpha-1 antitrypsin deficiency are known to be at increased risk for liver disease. It has also become clear that some degree of risk is similarly conferred by the heterozygous state. A lack of model systems that recapitulate heterozygosity in human hepatocytes has limited the ability to study the impact of a single Z alpha-1 antitrypsin (ZAAT) allele on hepatocyte biology. Here, we describe the derivation of syngeneic induced pluripotent stem cells (iPSCs) engineered to determine the effects of ZAAT heterozygosity in iPSC-hepatocytes (iHeps). We find that heterozygous MZ iHeps exhibit an intermediate disease phenotype and share with ZZ iHeps alterations in AAT protein processing and downstream perturbations including altered endoplasmic reticulum (ER) and mitochondrial morphology, reduced mitochondrial respiration, and branch-specific activation of the unfolded protein response in cell subpopulations. Our model of MZ heterozygosity thus provides evidence that a single Z allele is sufficient to disrupt hepatocyte homeostatic function., This work was supported by an Alpha-1 Foundation John W. Walsh Translational Research Award (to J.E.K.); a CJ Martin Early Career Fellowship from the Australian National Health and Medical Research Council (to R.B.W.); NIH grant R01HL095993 (to D.N.K.); and NIH grants R01DK101501 (to A.A.W.) and R01DK117940 (to A.N.H. and A.A.W.). iPSC distribution and disease modeling is supported by NIH grants U01TR001810 (to D.N.K. and A.A.W.) and N0175N92020C00005 (to D.N.K.); and by The Alpha-1 Project (TAP), a wholly owned subsidiary of the Alpha-1 Foundation (to D.N.K. and A.A.W.).

Published
2022

32. Abnormal global longitudinal strain and reduced serum inflammatory markers in cardiac AL amyloidosis patients without significant amyloid fibril deposition.

Author

Edwards CV, Ferri GM, Villegas-Galaviz J, Ghosh S, Bawa PS, Wang F, Klimtchuk E, Ajayi TB, Morgan GJ, Prokaeva T, Staron A, Ruberg FL, Sanchorawala V, Giadone RM, and Murphy GJ

Abstract

Background: Cardiac dysfunction in AL amyloidosis is thought to be partly related to the direct impact of AL LCs on cardiomyocyte function, with the degree of dysfunction at diagnosis as a major determinant of clinical outcomes. Nonetheless, mechanisms underlying LC-induced myocardial toxicity are not well understood., Methods: We identified gene expression changes correlating with human cardiac cells exposed to a cardiomyopathy-associated κAL LC. We then sought to confirm these findings in a clinical dataset by focusing on clinical parameters associated with the pathways dysregulated at the gene expression level., Results: Upon exposure to a cardiomyopathy-associated κAL LC, cardiac cells exhibited gene expression changes related to myocardial contractile function and inflammation, leading us to hypothesize that there could be clinically detectable changes in GLS on echocardiogram and serum inflammatory markers in patients. Thus, we identified 29 patients with normal IVSd but abnormal cardiac biomarkers suggestive of LC-induced cardiac dysfunction. These patients display early cardiac biomarker staging, abnormal GLS, and significantly reduced serum inflammatory markers compared to patients with clinically evident amyloid fibril deposition., Conclusion: Collectively, our findings highlight early molecular and functional signatures of cardiac AL amyloidosis, with potential impact for developing improved patient biomarkers and novel therapeutics.

Published
2024
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33. Generation of human alveolar epithelial type I cells from pluripotent stem cells.

Author

Burgess CL, Huang J, Bawa P, Alysandratos KD, Minakin K, Morley MP, Babu A, Villacorta-Martin C, Hinds A, Thapa BR, Wang F, Matschulat AM, Morrisey EE, Varelas X, and Kotton DN

Abstract

In the distal lung, alveolar epithelial type I cells (AT1s) comprise the vast majority of alveolar surface area and are uniquely flattened to allow the diffusion of oxygen into the capillaries. This structure along with a quiescent, terminally differentiated phenotype has made AT1s particularly challenging to isolate or maintain in cell culture. As a result, there is a lack of established models for the study of human AT1 biology, and in contrast to alveolar epithelial type II cells (AT2s), little is known about the mechanisms regulating their differentiation. Here we engineer a human in vitro AT1 model system through the directed differentiation of induced pluripotent stem cells (iPSC). We first define the global transcriptomes of primary adult human AT1s, suggesting gene-set benchmarks and pathways, such as Hippo-LATS-YAP/TAZ signaling, that are enriched in these cells. Next, we generate iPSC-derived AT2s (iAT2s) and find that activating nuclear YAP signaling is sufficient to promote a broad transcriptomic shift from AT2 to AT1 gene programs. The resulting cells express a molecular, morphologic, and functional phenotype reminiscent of human AT1 cells, including the capacity to form a flat epithelial barrier which produces characteristic extracellular matrix molecules and secreted ligands. Our results indicate a role for Hippo-LATS-YAP signaling in the differentiation of human AT1s and demonstrate the generation of viable AT1-like cells from iAT2s, providing an in vitro model of human alveolar epithelial differentiation and a potential source of human AT1s that until now have been challenging to viably obtain from patients.

Published
2023
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