Search

Your search keyword '"Guttentag, Susan"' showing total 299 results
Start Over Author "Guttentag, Susan"
299 results on '"Guttentag, Susan"'

2. Single-Cell Transcriptomic Profiling of Pluripotent Stem Cell-Derived SCGB3A2+ Airway Epithelium

Author

McCauley, Katherine B, Alysandratos, Konstantinos-Dionysios, Jacob, Anjali, Hawkins, Finn, Caballero, Ignacio S, Vedaie, Marall, Yang, Wenli, Slovik, Katherine J, Morley, Michael, Carraro, Gianni, Kook, Seunghyi, Guttentag, Susan H, Stripp, Barry R, Morrisey, Edward E, and Kotton, Darrell N

Subjects
Lung, Stem Cell Research - Induced Pluripotent Stem Cell, Regenerative Medicine, Stem Cell Research, Stem Cell Research - Embryonic - Human, Respiratory, Animals, Cell Differentiation, Cell Line, Cell Lineage, Cell Plasticity, Epithelium, Gene Expression Profiling, Genes, Reporter, Humans, Induced Pluripotent Stem Cells, Kinetics, Mice, Secretoglobins, Sequence Analysis, RNA, Single-Cell Analysis, Solubility, Spheroids, Cellular, Time Factors, Transcriptome, Wnt Signaling Pathway, airway, alveoli, directed differentiation, lung epithelium, pluripotent stem cells, single-cell RNA sequencing, Biochemistry and Cell Biology, Clinical Sciences
Abstract

Lung epithelial lineages have been difficult to maintain in pure form in vitro, and lineage-specific reporters have proven invaluable for monitoring their emergence from cultured pluripotent stem cells (PSCs). However, reporter constructs for tracking proximal airway lineages generated from PSCs have not been previously available, limiting the characterization of these cells. Here, we engineer mouse and human PSC lines carrying airway secretory lineage reporters that facilitate the tracking, purification, and profiling of this lung subtype. Through bulk and single-cell-based global transcriptomic profiling, we find PSC-derived airway secretory cells are susceptible to phenotypic plasticity exemplified by the tendency to co-express both a proximal airway secretory program as well as an alveolar type 2 cell program, which can be minimized by inhibiting endogenous Wnt signaling. Our results provide global profiles of engineered lung cell fates, a guide for improving their directed differentiation, and a human model of the developing airway.

Published
2018

3. Patient-specific iPSCs carrying an SFTPC mutation reveal the intrinsic alveolar epithelial dysfunction at the inception of interstitial lung disease

Author

Alysandratos, Konstantinos-Dionysios, Russo, Scott J., Petcherski, Anton, Taddeo, Evan P., Acín-Pérez, Rebeca, Villacorta-Martin, Carlos, Jean, J.C., Mulugeta, Surafel, Rodriguez, Luis R., Blum, Benjamin C., Hekman, Ryan M., Hix, Olivia T., Minakin, Kasey, Vedaie, Marall, Kook, Seunghyi, Tilston-Lunel, Andrew M., Varelas, Xaralabos, Wambach, Jennifer A., Cole, F. Sessions, Hamvas, Aaron, Young, Lisa R., Liesa, Marc, Emili, Andrew, Guttentag, Susan H., Shirihai, Orian S., Beers, Michael F., and Kotton, Darrell N.

Published
2021
Full Text
View/download PDF

4. Folliculin Controls Lung Alveolar Enlargement and Epithelial Cell Survival through E-Cadherin, LKB1, and AMPK

Author

Goncharova, Elena A, Goncharov, Dmitry A, James, Melane L, Atochina-Vasserman, Elena N, Stepanova, Victoria, Hong, Seung-Beom, Li, Hua, Gonzales, Linda, Baba, Masaya, Linehan, W Marston, Gow, Andrew J, Margulies, Susan, Guttentag, Susan, Schmidt, Laura S, and Krymskaya, Vera P

Subjects
Lung, 2.1 Biological and endogenous factors, Aetiology, Respiratory, AMP-Activated Protein Kinases, Animals, Apoptosis, Birt-Hogg-Dube Syndrome, Cadherins, Cell Line, Tumor, Cell Survival, Gene Deletion, Humans, Mice, Protein Serine-Threonine Kinases, Proto-Oncogene Proteins, Pulmonary Alveoli, Rats, Respiratory Mucosa, Tumor Suppressor Proteins, Biochemistry and Cell Biology, Medical Physiology
Abstract

Spontaneous pneumothoraces due to lung cyst rupture afflict patients with the rare disease Birt-Hogg-Dubé (BHD) syndrome, which is caused by mutations of the tumor suppressor gene folliculin (FLCN). The underlying mechanism of the lung manifestations in BHD is unclear. We show that BHD lungs exhibit increased alveolar epithelial cell apoptosis and that Flcn deletion in mouse lung epithelium leads to cell apoptosis, alveolar enlargement, and an impairment of both epithelial barrier and overall lung function. We find that Flcn-null epithelial cell apoptosis is the result of impaired AMPK activation and increased cleaved caspase-3. AMPK activator LKB1 and E-cadherin are downregulated by Flcn loss and restored by its expression. Correspondingly, Flcn-null cell survival is rescued by the AMPK activator AICAR or constitutively active AMPK. AICAR also improves lung condition of Flcn(f/f):SP-C-Cre mice. Our data suggest that lung cysts in BHD may result from an underlying defect in alveolar epithelial cell survival, attributable to FLCN regulation of the E-cadherin-LKB1-AMPK axis.

Published
2014

5. Alveolar repair following lipopolysaccharide-induced injury requires cell-extracellular matrix interactions

Author

Sucre, Jennifer M.S., primary, Bock, Fabian, additional, Negretti, Nicholas M., additional, Benjamin, John T., additional, Gulleman, Peter M., additional, Dong, Xinyu, additional, Ferguson, Kimberly T., additional, Jetter, Christopher S., additional, Han, Wei, additional, Liu, Yang, additional, Kook, Seunghyi, additional, Gokey, Jason J., additional, Guttentag, Susan H., additional, Kropski, Jonathan A., additional, Blackwell, Timothy S., additional, Zent, Roy, additional, and Plosa, Erin J., additional

Published
2023
Full Text
View/download PDF

6. Age-determined expression of priming protease TMPRSS2 and localization of SARS-CoV-2 in lung epithelium

Author

Schuler, Bryce A., Habermann, A. Christian, Plosa, Erin J., Taylor, Chase J., Jetter, Christopher, Negretti, Nicholas M., Kapp, Meghan E., Benjamin, John T., Gulleman, Peter, Nichols, David S., Braunstein, Lior Z., Hackett, Alice, Kolval, Michael, Guttentag, Susan H., Blackwel, Timothy S., Webber, Steven A., Banovich, Nicholas E., Kropski, Jonathan A., and Sucre, Jennifer M.S.

Subjects
Epidemics -- Control -- United States, Gene expression -- Health aspects, Proteases -- Health aspects, Respiratory tract infections -- Genetic aspects -- Development and progression -- Care and treatment, Health care industry
Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) novel coronavirus 2019 (COVID-19) global pandemic has led to millions of cases and hundreds of thousands of deaths. While older adults appear at high risk for severe disease, hospitalizations and deaths due to SARS-CoV-2 among children have been relatively rare. Integrating single-cell RNA sequencing (scRNA-seq) of developing mouse lung with temporally resolved immunofluorescence in mouse and human lung tissue, we found that expression of SARS-CoV-2 Spike protein primer TMPRSS2 was highest in ciliated cells and type I alveolar epithelial cells (AT1), and TMPRSS2 expression increased with aging in mice and humans. Analysis of autopsy tissue from fatal COVID-19 cases detected SARS-CoV-2 RNA most frequently in ciliated and secretory cells in airway epithelium and AT1 cells in peripheral lung. SARS-CoV-2 RNA was highly colocalized in cells expressing TMPRSS2. Together, these data demonstrate the cellular spectrum infected by SARS-CoV-2 in lung epithelium and suggest that developmental regulation of TMPRSS2 may underlie the relative protection of infants and children from severe respiratory illness., Introduction The emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) novel coronavirus 2019 (COVID-19) has led to a global pandemic, with more than 35 million cases as of [...]

Published
2021
Full Text
View/download PDF

7. Neutrophilic inflammation during lung development disrupts elastin assembly and predisposes adult mice to COPD

Author

Benjamin, John T., Plosa, Erin J., Sucre, Jennifer M.S., van der Meer, Riet, Dave, Shivangi, Gutor, Sergey, Nichols, David S., Gulleman, Peter M., Jetter, Christopher S., Han, Wei, Xin, Matthew, Dinella, Peter C., Catanzarite, Ashley, Kook, Seunghyi, Dolma, Kalsang, Lal, Charitharth V., Gaggar, Amit, Blalock, J. Edwin, Newcomb, Dawn C., Richmond, Bradley W., Kropski, Jonathan A., Young, Lisa R., Guttentag, Susan H., and Blackwell, Timothy S.

Subjects
Elastin -- Health aspects, Immune response -- Genetic aspects, Lung diseases, Obstructive -- Genetic aspects -- Risk factors, Health care industry
Abstract

Emerging evidence indicates that early life events can increase the risk for developing chronic obstructive pulmonary disease (COPD). Using an inducible transgenic mouse model for NF-[kappa]B activation in the airway epithelium, we found that a brief period of inflammation during the saccular stage (P3-P5) but not alveolar stage (P10-P12) of lung development disrupted elastic fiber assembly, resulting in permanent reduction in lung function and development of a COPD-like lung phenotype that progressed through 24 months of age. Neutrophil depletion prevented disruption of elastic fiber assembly and restored normal lung development. Mechanistic studies uncovered a role for neutrophil elastase (NE) in downregulating expression of critical elastic fiber assembly components, particularly fibulin-5 and elastin. Further, purified human NE and NE-containing exosomes from tracheal aspirates of premature infants with lung inflammation downregulated elastin and fibulin-5 expression by saccular-stage mouse lung fibroblasts. Together, our studies define a critical developmental window for assembling the elastin scaffold in the distal lung, which is required to support lung structure and function throughout the lifespan. Although neutrophils play a well-recognized role in COPD development in adults, neutrophilic inflammation may also contribute to early-life predisposition to COPD., Introduction Although the traditional view has been that cigarette smoking causes chronic obstructive pulmonary disease (COPD) through accelerated age-related lung-function decline in susceptible smokers, over the last several years it [...]

Published
2021
Full Text
View/download PDF

8. Contributors

Author

Abman, Steven H., primary, Allegaert, Karel, additional, Arya, Bhawna, additional, Askenazi, David, additional, Azhibekov, Timur, additional, Back, Stephen A., additional, Baldwin, H. Scott, additional, Ballard, Roberta A., additional, Bancalari, Eduardo, additional, Bates, Carlton M., additional, Batra, Maneesh, additional, Bayart, Cheryl B., additional, Bellus, Gary A., additional, Benedetti, Thomas J., additional, Benjamin, John T., additional, Bennett, James T., additional, Berry, Gerard T., additional, Binenbaum, Gil, additional, Boos, Markus D., additional, Bouchard, Maryse, additional, Brandling-Bennett, Heather A., additional, Broughton, Darcy E., additional, Brown, Zane, additional, Campbell, Katherine H., additional, Carmichael, Suzan L., additional, Carter, Brian S., additional, Cederbaum, Stephen, additional, Chabra, Shilpi, additional, Chang, Justine, additional, Cheng, Edith Y., additional, Chisholm, Karen M., additional, Christensen, Robert D., additional, Chun, Terrence, additional, Claure, Nelson, additional, Clyman, Ronald I., additional, Colaizy, Tarah T., additional, Cortezzo, DonnaMaria E., additional, Cotten, C. Michael, additional, Cunningham, Michael L., additional, de Alba Campomanes, Alejandra G., additional, Dees, Ellen, additional, DeMauro, Sara B., additional, Denne, Scott C., additional, Deschmann, Emöke, additional, Cecilia, Carolina, additional, DiBlasi, Robert M., additional, Dimmitt, Reed A., additional, DiVall, Sara A., additional, Djahangirian, Orchid, additional, Doherty, Dan, additional, Eichenwald, Eric C., additional, Engen, Rachel, additional, Engmann, Cyril, additional, Evans, Jacquelyn R., additional, Evans, Kelly N., additional, Farmer, Diana L., additional, Fechner, Patricia Y., additional, Ferrieri, Patricia, additional, Finer, Neil N., additional, Fleishman, Rachel A., additional, Fleiss, Bobbi, additional, Flynn, Joseph T., additional, Flynn-O'Brien, Katherine T., additional, Frey, Mark R., additional, Furman, Lydia, additional, Gallagher, Renata C., additional, Gauda, Estelle B., additional, Gleason, Christine A., additional, Goldberg, Michael J., additional, Goldin, Adam B., additional, Gospe, Sidney M., additional, Gressens, Pierre, additional, Gupta, Deepti, additional, Guttentag, Susan H., additional, Haldeman-Englert, Chad R., additional, Hansen, Thomas N., additional, Hing, Anne V., additional, Hingorani, Sangeeta, additional, Hintz, Susan R., additional, Hirose, Shinjiro, additional, Hodson, W. Alan, additional, Hoppe, Kara K., additional, Hostetter, Margaret K., additional, Huang, Benjamin, additional, Huang, Sarah Bauer, additional, Inder, Terrie E., additional, Inoita, Cristian, additional, Jackson, J. Craig, additional, Jain, Deepak, additional, Jain, Lucky, additional, Javid, Patrick J., additional, Josephson, Cassandra D., additional, Jungheim, Emily S., additional, Juul, Sandra E., additional, Katheria, Anup, additional, Keller, Benjamin A., additional, Keller, Roberta L., additional, Kelly, Thomas F., additional, Khorsand, Kate, additional, Kim, Grace, additional, Kinsella, John P., additional, Koves, Ildiko H., additional, Lam, Christina, additional, Lane, Erin R., additional, Lantos, John D., additional, Ledbetter, Daniel J., additional, Lee, Ben, additional, Levy, Harvey L., additional, Levy, Ofer, additional, Lewin, Mark B., additional, Lewis, David B., additional, Lin, P. Ling, additional, Lin, Tiffany Fangtse, additional, Lorch, Scott A., additional, Maheshwari, Akhil, additional, Maltepe, Emin, additional, Marsh, Ketzela J., additional, Martin, Richard J., additional, Mayock, Dennis E., additional, McAdams, Ryan Michael, additional, McAleer, Irene, additional, McElroy, Steven J., additional, McNelis, Kera M., additional, McQuillen, Patrick, additional, Meadow, William L., additional, Merguerian, Paul A., additional, Merjaneh, Lina, additional, Merritt, J. Lawrence, additional, Mezger, Valerie, additional, Michaels, Marian G., additional, Miller, Steven P., additional, Mohan, Sowmya S., additional, Mollen, Thomas J., additional, Moore, Thomas R., additional, Murray, Jeffrey C., additional, Murray, Karen F., additional, Nandi-Munshi, Debika, additional, Natarajan, Niranjana, additional, Neil, Jeffrey J., additional, Ness, Kathryn D., additional, Neu, Josef, additional, Siu-Ying, Angel, additional, Noori, Shahab, additional, O'Mahony, Lila, additional, Palma, Jonathan P., additional, Paneth, Nigel, additional, Parker, Thomas A., additional, Patel, Ravi Mangal, additional, Penn, Anna A., additional, Pettker, Christian M., additional, Peyvandi, Shabnam, additional, Pihoker, Cate, additional, Plosa, Erin, additional, Poindexter, Brenda B., additional, Posencheg, Michael A., additional, Reinking, Benjamin E., additional, Rice-Townsend, Samuel, additional, Richards, Morgan K., additional, Richardson, C. Peter, additional, Richardson, Kelsey, additional, Riggle, Kevin M., additional, Robbins, Elizabeth, additional, Rollins, Mark D., additional, Rosen, Mark A., additional, Rowe, Courtney K., additional, Sahai, Inderneel, additional, Saitta, Sulagna C., additional, Salehi, Parisa, additional, Sanchez, Pablo, additional, Saxonhouse, Matthew A., additional, Schanler, Richard J., additional, Schleiss, Mark R., additional, Scholz, Thomas, additional, Schwaderer, Andrew L., additional, Selewski, David, additional, Sellers, Zachary M., additional, Seri, Istvan, additional, Shnorhavorian, Margarett, additional, Sibley, Eric, additional, Sidbury, Robert, additional, Simmons, Rebecca, additional, Smith, Caitlin, additional, Sola-Visner, Martha C., additional, Srinivasan, Lakshmi, additional, Steinhorn, Robin H., additional, Stevenson, David K., additional, Stolp, Helen, additional, Taplin, Craig, additional, Tarczy-Hornoch, Peter, additional, Taylor, James A., additional, Thomas, Janet A., additional, Thompson, Tracy, additional, Tiller, George E., additional, Torres, Benjamin A., additional, Traudt, Christopher Michael, additional, van den Anker, John N., additional, Vernon, Margaret M., additional, Vohr, Betty, additional, Walker, Valencia P., additional, Wallen, Linda D., additional, Wallenstein, Matthew B., additional, Wang, Peter (Zhan Tao), additional, Warady, Bradley A., additional, Ward, Robert M., additional, Watchko, Jon F., additional, Wehbi, Elias, additional, Weitkamp, Joern-Hendrik, additional, Werny, David, additional, White, Klane K., additional, Willig, Laurel, additional, Woodrum, David, additional, Woodward, George A., additional, Wright, Clyde J., additional, Wright, Jeffrey A., additional, Yonekawa, Karyn, additional, and Zackai, Elaine H., additional

Published
2018
Full Text
View/download PDF

10. Prospective isolation of NKX2-1-expressing human lung progenitors derived from pluripotent stem cells

Author

Hawkins, Finn, Kramer, Philipp, Jacob, Anjali, Driver, Ian, Thomas, Dylan C., McCauley, Katherine B., Skvir, Nicholas, Crane, Ana M., Kurmann, Anita A., Hollenberg, Anthony N., Nguyen, Sinead, Wong, Brandon G., Khalil, Ahmad S., Huang, Sarah X.L., Guttentag, Susan, Rock, Jason R., Shannon, John M., Davis, Brian R., and Kotton, Darrell N.

Subjects
Lung -- Genetic aspects -- Health aspects, Stem cells -- Genetic aspects -- Health aspects, Gene expression -- Health aspects, Health care industry
Abstract

It has been postulated that during human fetal development, all cells of the lung epithelium derive from embryonic, endodermal, NK2 homeobox 1-expressing ([NKX2-1.sup.+]) precursor cells. However, this hypothesis has not been formally tested owing to an inability to purify or track these progenitors for detailed characterization. Here we have engineered and developmentally differentiated [NKX2-1.sup.GFP] reporter pluripotent stem cells (PSCs) in vitro to generate and isolate human primordial lung progenitors that express NKX2-1 but are initially devoid of differentiated lung lineage markers. After sorting to purity, these primordial lung progenitors exhibited lung epithelial maturation. In the absence of mesenchymal coculture support, this [NKX2-1.sup.+] population was able to generate epithelial-only spheroids in defined 3D cultures. Alternatively, when recombined with fetal mouse lung mesenchyme, the cells recapitulated epithelial-mesenchymal developing lung interactions. We imaged these progenitors in real time and performed time-series global transcriptomic profiling and single-cell RNA sequencing as they moved through the earliest moments of lung lineage specification. The profiles indicated that evolutionarily conserved, stage-dependent gene signatures of early lung development are expressed in primordial human lung progenitors and revealed a [CD47.sup.hi][CD26.sup.lo] cell surface phenotype that allows their prospective isolation from untargeted, patient-specific PSCs for further in vitro differentiation and future applications in regenerative medicine., Introduction Little is known about the early stages of human lung development, preventing an understanding of whether successful healing from adult lung injury involves recapitulation of embryonic mechanisms and limiting [...]

Published
2017
Full Text
View/download PDF

11. Epithelial Outgrowth Through Mesenchymal Rings Drives Alveologenesis

Author

Negretti, Nicholas M., primary, Son, Yeongseo, additional, Crooke, Philip, additional, Plosa, Erin J., additional, Benjamin, John T., additional, Jetter, Christopher S., additional, Bunn, Claire, additional, Mignemi, Nicholas, additional, Marini, John, additional, Hackett, Alice N., additional, Ransom, Meaghan, additional, Nichols, David, additional, Guttentag, Susan H., additional, Pua, Heather H., additional, Blackwell, Timothy S., additional, Zacharias, William, additional, Frank, David B., additional, Kozub, John A., additional, Mahadevan-Jansen, Anita, additional, Kropski, Jonathan A., additional, Wright, Christopher V.E., additional, Millis, Bryan, additional, and Sucre, Jennifer M. S., additional

Published
2022
Full Text
View/download PDF

12. Alveolar Epithelial Cell Differentiation During Lung Repair Requires Cell-Extracellular Matrix Interactions

Author

Sucre, Jennifer M.S., primary, Bock, Fabian, additional, Negretti, Nicholas M., additional, Benjamin, John T., additional, Gulleman, Peter M., additional, Dong, Xinyu, additional, Ferguson, Kimberly T., additional, Jetter, Christopher S., additional, Han, Wei, additional, Liu, Yang, additional, Kook, Seunghyi, additional, Gokey, Jason, additional, Guttentag, Susan H., additional, Kropski, Jonathan A., additional, Blackwell, Timothy S., additional, Zent, Roy, additional, and Plosa, Erin J., additional

Published
2022
Full Text
View/download PDF

13. A single-cell atlas of mouse lung development

Author

Negretti, Nicholas M., primary, Plosa, Erin J., additional, Benjamin, John T., additional, Schuler, Bryce A., additional, Habermann, A. Christian, additional, Jetter, Christopher S., additional, Gulleman, Peter, additional, Bunn, Claire, additional, Hackett, Alice N., additional, Ransom, Meaghan, additional, Taylor, Chase J., additional, Nichols, David, additional, Matlock, Brittany K., additional, Guttentag, Susan H., additional, Blackwell, Timothy S., additional, Banovich, Nicholas E., additional, Kropski, Jonathan A., additional, and Sucre, Jennifer M. S., additional

Published
2021
Full Text
View/download PDF

15. Cxcr2 and Cxcl5 regulate the IL-17/G-CSF axis and neutrophil homeostasis in mice

Author

Mei, Junjie, Liu, Yuhong, Dai, Ning, Hoffmann, Christian, Hudock, Kristin M., Zhang, Peggy, Guttentag, Susan H., Kolls, Jay K., Oliver, Paula M., Bushman, Frederic D., and Worthen, G. Scott

Subjects
Granulocyte colony-stimulating factor -- Physiological aspects -- Research -- Genetic aspects, Genes -- Physiological aspects -- Research, Neutrophils -- Physiological aspects -- Research, Interleukins -- Physiological aspects -- Research -- Genetic aspects, Health care industry
Abstract

Neutrophils are essential for maintaining innate immune surveillance under normal conditions, but also represent a major contributor to tissue damage during inflammation. Neutrophil homeostasis is therefore tightly regulated. Cxcr2 plays a critical role in neutrophil homeostasis, as [Cxcr2.sup.-/-] mice demonstrate mild neutrophilia and severe neutrophil hyperplasia in the bone marrow. The mechanisms underlying these phenotypes, however, are unclear. We report here that Cxcr2 on murine neutrophils inhibits the IL-17A/G-CSF axis that regulates neutrophil homeostasis. Furthermore, enterocyte-derived Cxcl5 in the gut regulates IL-17/G-CSF levels and contributes to Cxcr2-dependent neutrophil homeostasis. Conversely, G-CSF was required for Cxcl5-dependent regulation of neutrophil homeostasis, and inhibition of IL-17A reduced plasma G-CSF concentrations and marrow neutrophil numbers in both [Cxcl5.sup.-/-] and [Cxcr2.sup.-/-] mice. [Cxcr2.sup.-/-] mice constitutively expressed IL-17A and showed increased numbers of IL-17A-producing cells in the lung, terminal ileum, and spleen. Most IL-17- producing splenocytes were responsive to IL-1 β plus IL-23 in vitro. Depletion of commensal microbes by antibiotic treatment in [Cxcr2.sup.-/-] mice markedly decreased IL-17A and G-CSF expression, neutrophilia, and marrow myeloid hyperplasia. These data suggest a critical role for Cxcr2, Cxcl5, and commensal bacteria in regulation of the IL-17/G-CSF axis and neutrophil homeostasis at mucosal sites and have implications for the development of treatments for pathologies resulting from either excessive or ineffective neutrophil responses., Introduction Neutrophils are an essential component of innate immunity and host defense against bacterial and fungal infections by virtue of their rapid response to potential pathogens. In addition to this [...]

Published
2012
Full Text
View/download PDF

18. Increasing Volume-Targeted Ventilation Use in the NICU

Author

Hatch, L. Dupree, primary, Sala, Christa, additional, Araya, Wendy, additional, Rivard, Matthew, additional, Bolton, Joyce, additional, Rivard, Amanda, additional, Morris, Emily A., additional, McNeer, Elizabeth, additional, Guttentag, Susan H., additional, Grubb, Peter H., additional, Stark, Ann R., additional, and Markham, Melinda H., additional

Published
2021
Full Text
View/download PDF

19. A Single Cell Atlas of Lung Development

Author

Negretti, Nicholas M., primary, Plosa, Erin J., additional, Benjamin, John T., additional, Schuler, Bryce A., additional, Habermann, A. Christian, additional, Jetter, Christopher, additional, Gulleman, Peter, additional, Taylor, Chase J., additional, Nichols, David, additional, Matlock, Brittany K., additional, Guttentag, Susan H., additional, Blackwell, Timothy S., additional, Banovich, Nicholas E., additional, Kropski, Jonathan A., additional, and Sucre, Jennifer M. S., additional

Published
2021
Full Text
View/download PDF

20. Wnt/[beta]-catenin signaling acts upstream of N-myc, BMP4, and FGF signaling to regulate proximal distal patterning in the lung

Author

Shu, Weiguo, Guttentag, Susan, Wang, Zhishan, Andl, Thomas, Ballard, Philip, Lu, Min Min, Piccolo, Stefano, Birchmeier, Walter, Whitsett, Jeffrey A., Millar, Sarah E., and Morrisey, Edward E.

Subjects
Developmental biology -- Research, Morphogenesis -- Research, Biological sciences
Abstract

Branching morphogenesis in the lung serves as a model for the complex patterning that is reiterated in multiple organs throughout development. [beta]-catenin and Wnt signaling mediate critical functions in cell fate specification and differentiation, but specific functions during branching morphogenesis have remained unclear. Here, we show that Wnt/[beta]-catenin signaling regulates proximal distal differentiation of airway epithelium. Inhibition of Wnt/[beta]-catenin signaling, either by expression of Dkk1 or by tissue-specific deletion of [beta]-catenin, results in disruption of distal airway development and expansion of proximal airways. Wnt/[beta]-catenin functions upstream of BMP4, FGF signaling, and Nmyc. Moreover, we show that [beta]-catenin and LEF/TCF activate the promoters of BMP4 and N-myc. Thus, Wnt/[beta]-catenin signaling is a critical upstream regulator of proximal--distal patterning in the lung, in part, through regulation of N-myc, BMP4, and FGF signaling. Keywords: Wnt; [beta]-catenin; Dickkopf-1; BMP; FGF; Lung development

Published
2005

21. Contributors

Author

Abman, Steven H., primary, Ahmed, Amina, additional, Allen, Marilee C., additional, Askenazi, David, additional, Back, Stephen A., additional, Baldwin, H. Scott, additional, Ballard, Roberta A., additional, Bancalari, Eduardo, additional, Bates, Carlton M., additional, Batisky, Donald L., additional, Baumgart, Stephen, additional, Benedetti, Thomas J., additional, Berry, Gerard T., additional, Bianchi, Diana W., additional, Binenbaum, Gil, additional, Bollepalli, Sureka, additional, Bonifacio, Sonia L., additional, Cairo, Mitchell S., additional, Campbell, Katherine H., additional, Caplan, Michael, additional, Cederbaum, Stephen, additional, Chandra, Sudhish, additional, Chen, Ming, additional, Claure, Nelson, additional, Clyman, Ronald I., additional, Cohen, Bernard A., additional, Cole, F. Sessions, additional, Copelovitch, Lawrence, additional, Cunningham, Michael, additional, de Alba Campomanes, Alejandra G., additional, Dees, Ellen, additional, Denne, Scott C., additional, Devaskar, Sherin U., additional, DiBlasi, Robert M., additional, Dimmitt, Reed A., additional, Eichenwald, Eric C., additional, Eisenstein, Eli M., additional, Evans, Jacquelyn R., additional, Evans, Kelly, additional, Farmer, Diana L., additional, Ferrieri, Patricia, additional, Ferriero, Donna M., additional, Finer, Neil N., additional, Fraga, Maria Victoria, additional, Furman, Lydia, additional, Furth, Susan, additional, Gauda, Estelle B., additional, Glader, Bertil, additional, Gleason, Christine A., additional, Goldberg, Michael J., additional, Gonzalez, Fernando, additional, Gopalani, Sameer, additional, Grant, P. Ellen, additional, Greene, Carol L., additional, Guevara-Gallardo, Salvador, additional, Guignard, Jean-Pierre, additional, Guttentag, Susan, additional, Haldeman-Englert, Chad R., additional, Hansen, Thomas, additional, Hing, Anne V., additional, Hohimer, A. Roger, additional, Hostetter, Margaret K., additional, Hull, Andrew D., additional, Jackson, J. Craig, additional, Jain, Lucky, additional, Jain, Vandana, additional, Janjua, Halima Saadia, additional, Juul, Sandra E., additional, Kalkunte, Satyan, additional, Kaplan, Bernard S., additional, Keller, Roberta L., additional, Kelly, Thomas F., additional, Kern, Steven E., additional, Kerkar, Nanda, additional, Kinsella, John P., additional, Kirsch, Roxanne, additional, Kleinman, Monica E., additional, Klitzner, Thomas S., additional, Lambert, Sarah M., additional, Lantos, John D., additional, Leone, Tina A., additional, Leppert, Mary, additional, Levy, Harvey L., additional, Lewin, Mark, additional, Lin-Su, Karen, additional, L. Loh, Mignon, additional, Lorch, Scott A., additional, Lugo, Ralph A., additional, Mai, Volker, additional, Marino, Bradley S., additional, Markovitz, Barry, additional, Marquard, Kerri, additional, Martin, Camilia R., additional, Martin, Richard J., additional, Matthay, Katherine K., additional, Matthews, Dana C., additional, Mayock, Dennis E., additional, Meadow, William L., additional, Menon, Ram K., additional, Mercuri, Eugenio, additional, Mohan, Sowmya S., additional, Moley, Kelle, additional, Mollen, Thomas J., additional, Moore, Jeremy P., additional, Moore, Thomas R., additional, Munson, David A., additional, Murray, Jeffrey C., additional, Neu, Josef, additional, New, Maria I., additional, Nguyen-Vermillion, Annie, additional, Niklas, Victoria, additional, Nimkarn, Saroj, additional, Padbury, James F., additional, Pane, Marika, additional, Paneth, Nigel, additional, Parker, Thomas A., additional, Patterson, Janna C., additional, Pettker, Christian M., additional, Plawner, Lauren L., additional, Poenaru, Dan, additional, Poindexter, Brenda B., additional, Posencheg, Michael A., additional, Prabhu, Sanjay P., additional, Püttgen, Katherine B., additional, Quinn, Graham E., additional, Raju, Tonse N.K., additional, Ramos, Gladys A., additional, Reinking, Benjamin E., additional, Richardson, C. Peter, additional, Rimoin, David L., additional, Robbins, Elizabeth, additional, Robertson, Richard L., additional, Rollins, Mark D., additional, Rose, Susan R., additional, Rosen, Mark A., additional, Rubin, Lewis P., additional, Sahai, Inderneel, additional, Saitta, Sulagna C., additional, Sánchez, Pablo J., additional, Satou, Gary M., additional, Schanler, Richard J., additional, Scher, Mark S., additional, Schleiss, Mark R., additional, Scholz, Thomas D., additional, Schwaderer, Andrew L., additional, Seri, Istvan, additional, Sharma, Surendra, additional, Shereck, Evan B., additional, Sibley, Eric, additional, Signore, Caroline, additional, Simmons, Rebecca, additional, Smith, Jeffrey B., additional, Smith, Lorie B., additional, Song, Clara, additional, Steinhorn, Robin H., additional, Suchy, Frederick J., additional, Sulyok, Endre, additional, Tarczy-Hornoch, Peter, additional, Taylor, George A., additional, Taylor, James A., additional, Thomas, Janet A., additional, Tiller, George E., additional, Tran, Mark M., additional, Trautman, Michael Stone, additional, Upperman, Jeffrey S., additional, van de Ven, Carmella, additional, Vernon, Margaret M., additional, Allan Walker, W., additional, Wallen, Linda D., additional, Waller, Sarah A., additional, Warady, Bradley A., additional, Ward, Robert M., additional, Watchko, Jon F., additional, Wernovsky, Gil, additional, White, Klane K., additional, Williams, Calvin B., additional, Woodrum, David, additional, Woodward, George A., additional, Wright, Dakara Rucker, additional, Wright, Jeffrey A., additional, Wright, Linda L., additional, Young, Christopher M., additional, Young, Guy, additional, Zackai, Elaine H., additional, and Zderic, Stephen A., additional

Published
2012
Full Text
View/download PDF

23. Developmental regulation of claudin localization by fetal alveolar epithelial cells

Author

Daugherty, Brandy L., Mateescu, Madalina, Patel, Anand S., Wade, Kelly, Kimura, Shioko, Gonzales, Linda W., Guttentag, Susan, Ballard, Philip L., and Koval, Michael

Subjects
Lungs -- Research, Endocytosis -- Research, Biological sciences
Abstract

Tight junction proteins in the claudin family regulate epithelial barrier function. We examined claudin expression by human fetal lung (HFL) alveolar epithelial cells cultured in medium containing dexamethasone, 8-bromo-cAMP, and isobutylmethylxanthanine (DCI), which promotes alveolar epithelial cell differentiation to a type II phenotype. At the protein level, HFL cells expressed claudin-1, claudin-3, claudin-4, claudin-5, claudin-7, and claudin-18, where levels of expression varied with culture conditions. DCI-treated differentiated HFL cells cultured on permeable supports formed tight transepithelial barriers, with transepithelial resistance (TER) >1,700 ohm/[cm.sup.2]. In contrast, HFL cells cultured in control medium without DCI did not form tight barriers (TER tight junction; endocytosis; lung development; epithelial barrier function; pneumocytes

Published
2004

24. Pepsinogen C: a type 2 cell-specific protease

Author

Foster, Cherie, Aktar, Amana, Kopf, Denel, Zhang, Peggy, and Guttentag, Susan

Subjects
Pepsinogen -- Research, Biological sciences
Abstract

Pepsinogen C, also known as progastricsin or pepsinogen II, is an aspartic protease expressed primarily in gastric chief cells. Prior microarray studies of an in vitro model of type 2 cell differentiation indicated that pepsinogen C RNA was highly induced, comparable to surfactant protein RNA induction. Using second-trimester human fetal lung, third-trimester postnatal and adult lung, and a model of type 2 cell differentiation, we examined the specificity of pepsinogen C expression in lung. Pepsinogen C RNA and protein were only detected in >22 wk gestation samples of neonatal lung or in adult lung tissue. By immunohistochemistry and in situ hybridization, pepsinogen C expression was restricted to type 2 cells. Pepsinogen C expression was rapidly induced during type 2 cell differentiation and rapidly quenched with dedifferentiation of type 2 cells after withdrawal of hormones. In all samples, pepsinogen C expression occurred concomitantly with or in advance of processing of surfactant protein-B to its mature 8-kDa form. Our results indicate that pepsinogen C is a type 2 cell-specific marker that exhibits tight developmental regulation in vivo during human lung development, as well as during in vitro differentiation and dedifferentiation of type 2 cells. pepsinogen C; alveolar type 2 cell; cell differentiation

Published
2004

26. Differentiation of human pulmonary type II cells in vitro by glucocorticoid plus cAMP

Author

Gonzales, Linda W., Guttentag, Susan H., Wade, Kelly C., Postle, Anthony D., and Ballard, Philip L.

Subjects
Immunization of infants -- Health aspects, Infants, Respiratory distress syndrome -- Prevention, Biological sciences
Abstract

Mature alveolar type II cells that produce pulmonary surfactant are essential for adaptation to extrauterine life and prevention of infant respiratory distress syndrome. We have developed a new in vitro model to further investigate regulation of type II cell differentiation. Epithelial cells isolated from human fetal lung were cultured in serum-free medium on plastic. Cells treated with dexamethasone + cAMP analog and isobutylmethylxanthine for 4 days exhibited increased phosphatidylcholine synthesis and content of disaturated phosphatidylcholine species, manyfold increases in all surfactant proteins with processing to mature forms, and abundant lamellar bodies. DNA microarray analysis identified ~3,100 expressed genes, including subsets of genes induced 2- to >100-fold (~2.5%) or repressed 2- to 18-fold (~1.2%) by hormone treatment. Of the highly regulated genes, most were coregulated in an additive or synergistic manner by dexamethasone and cAMP agents. Approximately 90% of the regulated genes identified by this initial microarray analysis have not been previously recognized as hormone responsive. One newly identified hormone-induced gene is Nkx2.1 (thyroid transcription factor-1), which has a critical role in surfactant protein gene expression. Our findings indicate that glucocorticoid + cAMP is sufficient and necessary for precocious induction of functional type II cells in this in vitro system and that these hormones act primarily in combination to regulate expression of a subset of specific genes. surfactant development; human fetal lung; thyroid transcription factor-1; cDNA microarray

Published
2002

31. Patient-specific iPSCs carrying anSFTPCmutation reveal the intrinsic alveolar epithelial dysfunction at the inception of interstitial lung disease

Author

Alysandratos, Konstantinos-Dionysios, primary, Russo, Scott J., additional, Petcherski, Anton, additional, Taddeo, Evan P., additional, Acín-Pérez, Rebeca, additional, Villacorta-Martin, Carlos, additional, Jean, J. C., additional, Mulugeta, Surafel, additional, Blum, Benjamin C., additional, Hekman, Ryan M., additional, Vedaie, Marall, additional, Kook, Seunghyi, additional, Wambach, Jennifer A., additional, Cole, F. Sessions, additional, Hamvas, Aaron, additional, Emili, Andrew, additional, Guttentag, Susan H., additional, Shirihai, Orian S., additional, Beers, Michael F., additional, and Kotton, Darrell N., additional

Published
2020
Full Text
View/download PDF

32. Hyperoxia Injury in the Developing Lung Is Mediated by Mesenchymal Expression of Wnt5A

Author

Sucre, Jennifer M. S., primary, Vickers, Kasey C., additional, Benjamin, John T., additional, Plosa, Erin J., additional, Jetter, Christopher S., additional, Cutrone, Alissa, additional, Ransom, Meaghan, additional, Anderson, Zachary, additional, Sheng, Quanhu, additional, Fensterheim, Benjamin A., additional, Ambalavanan, Namasivayam, additional, Millis, Bryan, additional, Lee, Ethan, additional, Zijlstra, Andries, additional, Königshoff, Melanie, additional, Blackwell, Timothy S., additional, and Guttentag, Susan H., additional

Published
2020
Full Text
View/download PDF

33. Reconstructed Single-Cell Fate Trajectories Define Lineage Plasticity Windows during Differentiation of Human PSC-Derived Distal Lung Progenitors

Author

Hurley, Killian, primary, Ding, Jun, additional, Villacorta-Martin, Carlos, additional, Herriges, Michael J., additional, Jacob, Anjali, additional, Vedaie, Marall, additional, Alysandratos, Konstantinos D., additional, Sun, Yuliang L., additional, Lin, Chieh, additional, Werder, Rhiannon B., additional, Huang, Jessie, additional, Wilson, Andrew A., additional, Mithal, Aditya, additional, Mostoslavsky, Gustavo, additional, Oglesby, Irene, additional, Caballero, Ignacio S., additional, Guttentag, Susan H., additional, Ahangari, Farida, additional, Kaminski, Naftali, additional, Rodriguez-Fraticelli, Alejo, additional, Camargo, Fernando, additional, Bar-Joseph, Ziv, additional, and Kotton, Darrell N., additional

Published
2020
Full Text
View/download PDF

36. β1 Integrin regulates adult lung alveolar epithelial cell inflammation

Author

Plosa, Erin J., primary, Benjamin, John T., additional, Sucre, Jennifer M., additional, Gulleman, Peter M., additional, Gleaves, Linda A., additional, Han, Wei, additional, Kook, Seunghyi, additional, Polosukhin, Vasiliy V., additional, Haake, Scott M., additional, Guttentag, Susan H., additional, Young, Lisa R., additional, Pozzi, Ambra, additional, Blackwell, Timothy S., additional, and Zent, Roy, additional

Published
2020
Full Text
View/download PDF

37. Patient-Specific iPSCs Carrying an SFTPC Mutation Reveal the Intrinsic Alveolar Epithelial Dysfunction at the Inception of Interstitial Lung Disease

Author

Alysandratos, Konstantinos-Dionysios, primary, Russo, Scott J., additional, Petcherski, Anton, additional, Taddeo, Evan P., additional, Acín-Pérez, Rebeca, additional, Villacorta-Martin, Carlos, additional, Jean, J. C., additional, Mulugeta, Surafel, additional, Blum, Benjamin C., additional, Hekman, Ryan M., additional, Minakin, Kasey, additional, Vedaie, Marall, additional, Kook, Seunghyi, additional, Wambach, Jennifer A., additional, Cole, F. Sessions, additional, Hamvas, Aaron, additional, Young, Lisa R., additional, Liesa, Marc, additional, Emili, Andrew, additional, Guttentag, Susan H., additional, Shirihai, Orian S., additional, Beers, Michael F., additional, and Kotton, Darrell N., additional

Published
2020
Full Text
View/download PDF

39. Contributors

Author

Adams-Chapman, Ira, primary, Ades, Anne M., additional, Ahmed, Amina, additional, Albers, Simone, additional, Allen, Marilee C., additional, Andrew, Maureen, additional, Back, Stephen A., additional, Baldwin, H. Scott, additional, Ballard, Philip L., additional, Ballard, Roberta A., additional, Banks-Randall, Beverly A., additional, Baumgart, Stephen, additional, Beckerman, Karen P., additional, Benedetti, Thomas J., additional, Berry, Gerard T., additional, Berseth, Carol Lynn, additional, Bethin, Kathleen E., additional, Bianchi, Diana W., additional, Cairo, Mitchell S., additional, Caldamone, Anthony, additional, Chandra, Sudhish, additional, Chmait, Ramen, additional, Clyman, Ronald I., additional, Cohen, Bernard A., additional, Cohen, Meryl S., additional, Cohen, Mitchell I., additional, Cohn, Robert M., additional, Cole, F. Sessions, additional, Corbet, Anthony, additional, Denne, Scott C., additional, Di Maggio, Theresa J., additional, Eichenwald, Eric C., additional, Evans, Jacquelyn R., additional, Evans, Nick, additional, Fanaroff, Avroy A., additional, Ferriero, Donna M., additional, Fisher, Delbert A., additional, Flores-Sarnat, Laura, additional, Friedlich, Philippe S., additional, Gaynor, J. William, additional, Gest, Alfred L., additional, Geva, Tal, additional, Gibbons, Mary Ann E., additional, Gilbert, William M., additional, Glader, Bertil E., additional, Gleason, Christine A., additional, Goldberg, Michael J., additional, Good, William V., additional, Goodwin, Gregory, additional, Gopalani, Sameer, additional, Greene, Carol L., additional, Grottkau, Brian E., additional, Gruber, Peter J., additional, Guignard, Jean-Pierre, additional, Guttentag, Susan, additional, Hamrick, Shannon E.G., additional, Hansen, Thomas N., additional, Hostetter, Margaret K., additional, Hughes, Samuel C., additional, Hull, Andrew D., additional, Jedeikin, Roy, additional, Juul, Sandra E., additional, Kaplan, Bernard S., additional, Kaplan, Paige, additional, Kazin, Rebecca A., additional, Kelly, Thomas F., additional, Kuhle, Stefan, additional, Laing, Ian A., additional, Levy, Harvey L., additional, Loh, Mignon L., additional, Lorch, Scott A., additional, Lugo, Ralph A., additional, Machin, Geoffrey A., additional, MacMahon, James R., additional, Macones, George A., additional, Madan, Ashima, additional, Marino, Bradley S., additional, Martinez, Alma, additional, Maschoff, Kathryn L., additional, Massicotte, Patricia, additional, Matthay, Katherine K., additional, Mentzer, William C., additional, Merrill, Jeffrey D., additional, Miller, Carol A., additional, Mitchell, Lesley, additional, Moise, Alicia A., additional, Mollen, Thomas J., additional, Monahan, Timothy P., additional, Moore, Thomas R., additional, Muglia, Louis J., additional, Nelson, Robert M., additional, Newman, Thomas B., additional, Pallotto, Eugenia K., additional, Pan, Erica S., additional, Parravicini, Elvira, additional, Partridge, J. Colin, additional, Poenaru, Dan, additional, Poindexter, Brenda B., additional, Polin, Richard A., additional, Polk, Daniel H., additional, Pursley, DeWayne M., additional, Ramanathan, Rangasamy, additional, Ramierez-Schrempp, Daniela, additional, Regan, Joan A., additional, Richard, Elisabeth G., additional, Robertson, Richard L., additional, Rosen, Mark A., additional, Rubin, Lewis P., additional, Rychik, Jack, additional, Saitta, Sulagna C., additional, Sánchez, Pablo J., additional, Sarnat, Harvey B., additional, Schanler, Richard J., additional, Scher, Mark S., additional, Seri, Istvan, additional, Siegfried, Elaine C., additional, Silverman, Gary A., additional, Simmons, Rebecca, additional, Sniderman, Susan, additional, Spray, Thomas L., additional, Stanley, Charles A., additional, Stevenson, David K., additional, Stoll, Barbara J., additional, Taeusch, H. William, additional, Tarczy-Hornoch, Peter, additional, Taylor, George A., additional, Thomas, Janet A., additional, Tulassay, Tivadar, additional, van de Ven, Carmella, additional, Vohr, Betty R., additional, Ward, Robert M., additional, Weintrub, Peggy Sue, additional, Welty, Stephen, additional, Wernovsky, Gil, additional, Williams, Calvin B., additional, Wright, Linda L., additional, Young, Alison Z., additional, Zackai, Elaine H., additional, and Zderic, Stephen A., additional

Published
2005
Full Text
View/download PDF

40. Surfactant protein B processing in human fetal lung

Author

Guttentag, Susan H., Beers, Michael F., Bieler, Bert M., and Ballard, Philip L.

Subjects
Pulmonary surfactant -- Research, Proteins -- Research, Antigenic determinants -- Research, Peptides -- Research, Lungs -- Cytology, Biological sciences
Abstract

Human fetal lung in explant culture and polyclonal antibodies to human surfactant protein B (SP-B8) and to epitopes within propeptides of human proSP-B were used to characterize SP-B processing in human type 2 cells. Results showed that NH2-terminal protopeptide processing of proSP-B includes the preservation of a small peptide N-flanking the mature SP-B sequence, resulting in a novel 9-kDa intermediate of SP-B processing. In addition, type 2 cell-specific distal processing events were both shown to be developmentally and hormonally regulated.

Published
1998

Catalog

Books, media, physical & digital resources
See catalog results