Jeffrey A Whitsett

Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States

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Publications (661)3377.21 Total impact

  • Michael A. McGuckin · David J. Thornton · Jeffrey A. Whitsett
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    ABSTRACT: Mucosal surfaces are exposed to the external environment and pathogens and are therefore protected by a secreted layer of mucus rich in mucin glycoproteins, which are the main components of mucus. Mucus provides physical protection and hydration, excludes pathogens, and is a reservoir for antimicrobial molecules. Underlying mucus further protection is provided by epithelial cell surface mucins, which limit microbial adherence and regulate growth and apoptosis. Differentiation of the cells that produce mucins, and expression of mucins and proteins involved in mucin biosynthesis, is regulated by innate and adaptive immunity. Experimental deficiencies in mucins lead to infectious and inflammatory diseases, and mucin gene polymorphisms are associated with disease. Many chronic mucosal inflammatory diseases are characterized by mucus hypersecretion driven by immune and microbial factors, which contributes to pathology and is a target for therapy. In this chapter we describe the nature of this mucosal barrier, its regulation and function, and its involvement in human disease, with particular emphasis on the mucin component of the barrier.
    No preview · Article · Dec 2015
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    Minzhe Guo · Hui Wang · S. Steven Potter · Jeffrey A. Whitsett · Yan Xu
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    ABSTRACT: A major challenge in developmental biology is to understand the genetic and cellular processes/programs driving organ formation and differentiation of the diverse cell types that comprise the embryo. While recent studies using single cell transcriptome analysis illustrate the power to measure and understand cellular heterogeneity in complex biological systems, processing large amounts of RNA-seq data from heterogeneous cell populations creates the need for readily accessible tools for the analysis of single-cell RNA-seq (scRNA-seq) profiles. The present study presents a generally applicable analytic pipeline (SINCERA: a computational pipeline for SINgle CEll RNA-seq profiling Analysis) for processing scRNA-seq data from a whole organ or sorted cells. The pipeline supports the analysis for: 1) the distinction and identification of major cell types; 2) the identification of cell type specific gene signatures; and 3) the determination of driving forces of given cell types. We applied this pipeline to the RNA-seq analysis of single cells isolated from embryonic mouse lung at E16.5. Through the pipeline analysis, we distinguished major cell types of fetal mouse lung, including epithelial, endothelial, smooth muscle, pericyte, and fibroblast-like cell types, and identified cell type specific gene signatures, bioprocesses, and key regulators. SINCERA is implemented in R, licensed under the GNU General Public License v3, and freely available from CCHMC PBGE website,
    Preview · Article · Nov 2015 · PLoS Computational Biology
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    ABSTRACT: Background: Amniotic fluid (AF) is a proximal fluid to the fetus containing higher amounts of cell-free fetal RNA/DNA than maternal serum, thereby making it a promising source for identifying novel biomarkers that predict fetal development and organ maturation. Our aim was to compare AF transcriptomic profiles at different time points in pregnancy to demonstrate unique genetic signatures that would serve as potential biomarkers indicative of fetal maturation. Methods: We isolated AF RNA from 16 women at different time points in pregnancy: 4 from 18 to 24 weeks, 6 from 34 to 36 weeks, and 6 from 39 to 40 weeks. RNA-sequencing was performed on cell-free RNA. Gene expression and splicing analyses were performed in conjunction with cell-type and pathway predictions. Results: Sample-level analysis at different time points in pregnancy demonstrated a strong correlation with cell types found in the intrauterine environment and fetal respiratory, digestive and external barrier tissues of the fetus, using high-confidence cellular molecular markers. While some RNAs and splice variants were present throughout pregnancy, many transcripts were uniquely expressed at different time points in pregnancy and associated with distinct neonatal co-morbidities (respiratory distress and gavage feeding), indicating fetal immaturity. Conclusion: The AF transcriptome exhibits unique cell/organ-selective expression patterns at different time points in pregnancy that can potentially identify fetal organ maturity and predict neonatal morbidity. Developing novel biomarkers indicative of the maturation of multiple organ systems can improve upon our current methods of fetal maturity testing which focus solely on the lung, and will better inform obstetrical decisions regarding delivery timing.
    Full-text · Article · Oct 2015 · BMC Medical Genomics
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    Dataset: JCI79422sd

    Full-text · Dataset · Jul 2015
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    ABSTRACT: To determine the use of the mucin proteins MUC5B and MUC5AC as prognosis markers for non-small cell lung cancer (NSCLC) carrying epidermal growth factor receptor (EGFR) mutations. Patients who underwent surgical resection at Nagasaki University Hospital and related facilities in Japan between June 1996 and March 2013. 159 Japanese patients (male: n=103; female: n=56) with NSCLC, who underwent surgical resection (EGFR-mutant type: n=78, EGFR wild type: n=81). Patients whose tumours expressed MUC5B had significantly longer overall survival and relapse-free survival compared to the MUC5B-negative patients with EGFR mutant NSCLC (p=0.0098 and p=0.0187, respectively). In patients with EGFR wild-type NSCLC, there was no association with MUC5B expression. MUC5AC expression was not different between EGFR mutant and wild-type NSCLC. Present findings indicate that MUC5B, but not MUC5AC, is a novel prognostic biomarker for patients with NSCLC carrying EGFR mutations but not for patients with NSCLC carrying wild-type EGFR. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
    Full-text · Article · Jul 2015 · BMJ Open
  • Yina Du · Minzhe Guo · Jeffrey A Whitsett · Yan Xu
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    ABSTRACT: We developed LungGENS (Lung Gene Expression iN Single-cell), a web-based bioinformatics resource for querying single-cell gene expression databases by entering a gene symbol or a list of genes or selecting a cell type of their interest. Gene query provides quantitative RNA expression of the gene of interest in each lung cell type. Cell type query returns associated selective gene signatures and genes encoding cell surface markers and transcription factors in interactive heatmap and tables. LungGENS will be broadly applicable in respiratory research, providing a cell-specific RNA expression resource at single-cell resolution. LungGENS is freely available for non-commercial use at Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to
    No preview · Article · Jun 2015 · Thorax
  • John Snowball · Manoj Ambalavanan · Jeffrey Whitsett · Debora Sinner
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    ABSTRACT: Tracheobronchomalacia is a common congenital defect in which the walls of the trachea and bronchi lack of adequate cartilage required for support of the airways. Deletion of Wls, a cargo receptor mediating Wnt ligand secretion, in the embryonic endoderm using ShhCre mice inhibited formation of tracheal-bronchial cartilaginous rings. The normal dorsal-ventral patterning of tracheal mesenchyme was lost. Smooth muscle cells, identified by Acta2 staining, were aberrantly located in ventral mesenchyme of the trachea, normally the region of Sox9 expression in cartilage progenitors. Wnt/β-catenin activity, indicated by Axin2 LacZ reporter, was decreased in tracheal mesenchyme of Wls(f/f);Shh(Cre/+) embryos. Proliferation of chondroblasts was decreased and reciprocally, proliferation of smooth muscle cells was increased in Wls(f/f);Shh(Cre/+) tracheal tissue. Expression of Tbx4, Tbx5, Msx1 and Msx2, known to mediate cartilage and muscle patterning, were decreased in tracheal mesenchyme of Wls(f/f);Shh(Cre/+) embryos. Ex vivo studies demonstrated that Wnt7b and Wnt5a, expressed by the epithelium of developing trachea, and active Wnt/β-catenin signaling are required for tracheal chondrogenesis before formation of mesenchymal condensations. In conclusion, Wnt ligands produced by the tracheal epithelium pattern the tracheal mesenchyme via modulation of gene expression and cell proliferation required for proper tracheal cartilage and smooth muscle differentiation. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Jun 2015 · Developmental Biology
  • Jeffrey A Whitsett · Timothy E Weaver
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    ABSTRACT: Gas exchange after birth is entirely dependent on the remarkable architecture of the alveoli, its formation and function being mediated by the interactions of numerous cell types whose precise positions and functions are controlled by a diversity of signaling and transcriptional networks. In the later stages of gestation, alveolar epithelial cells lining the peripheral lung saccules produce increasing amounts of surfactant lipids and proteins that are secreted into the airspaces at birth. The lack of lung maturation and associated lack of pulmonary surfactant in preterm infants causes respiratory distress syndrome (RDS), a common cause of morbidity and mortality associated with premature birth. At the time of birth, surfactant homeostasis begins to be established by balanced processes involved in surfactant production, storage, secretion, recycling, and catabolism that serve to maintain alveolar homeostasis. Insights from physiology and engineering made in the 20th century enabled survival of newborn infants requiring mechanical ventilation for the first time. Thereafter, advances in biochemistry, biophysics, and molecular biology led to an understanding of the pulmonary surfactant system that made possible exogenous surfactant replacement for treatment of preterm infants. Identification of surfactant proteins, cloning of the genes encoding them, and elucidation of their roles in the regulation of surfactant synthesis, structure, and function has provided increasing understanding of alveolar function and homeostasis in health and disease. This "perspective" seeks to consider developmental aspects of the pulmonary surfactant system and its importance in the pathogenesis of acute and chronic lung diseases related to alveolar homeostasis.
    No preview · Article · May 2015 · American Journal of Respiratory Cell and Molecular Biology
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    ABSTRACT: Epithelial cells that line the conducting airways provide the initial barrier and innate immune responses to the abundant particles, microbes, and allergens that are inhaled throughout life. The transcription factors SPDEF and FOXA3 are both selectively expressed in epithelial cells lining the conducting airways, where they regulate goblet cell differentiation and mucus production. Moreover, these transcription factors are upregulated in chronic lung disorders, including asthma. Here, we show that expression of SPDEF or FOXA3 in airway epithelial cells in neonatal mice caused goblet cell differentiation, spontaneous eosinophilic inflammation, and airway hyperresponsiveness to methacholine. SPDEF expression promoted DC recruitment and activation in association with induction of Il33, Csf2, thymic stromal lymphopoietin (Tslp), and Ccl20 transcripts. Increased Il4, Il13, Ccl17, and Il25 expression was accompanied by recruitment of Th2 lymphocytes, group 2 innate lymphoid cells, and eosinophils to the lung. SPDEF was required for goblet cell differentiation and pulmonary Th2 inflammation in response to house dust mite (HDM) extract, as both were decreased in neonatal and adult Spdef-/- mice compared with control animals. Together, our results indicate that SPDEF causes goblet cell differentiation and Th2 inflammation during postnatal development and is required for goblet cell metaplasia and normal Th2 inflammatory responses to HDM aeroallergen.
    Full-text · Article · Apr 2015 · The Journal of clinical investigation
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    Full-text · Dataset · Apr 2015
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    ABSTRACT: Midbrain dopamine neuronal progenitors develop into heterogeneous subgroups of neurons, such as substantia nigra pars compacta, ventral tegmental area and retrorubal field, that regulate motor control, motivated and addictive behaviours. The development of midbrain dopamine neurons has been extensively studied, and these studies indicate that complex cross-regulatory interactions between extrinsic and intrinsic molecules regulate a precise temporal and spatial programme of neurogenesis in midbrain dopamine progenitors. To elucidate direct molecular interactions between multiple regulatory factors during neuronal differentiation in mice, we characterised genome-wide binding sites of the forkhead/winged helix transcription factor Foxa1, which functions redundantly with Foxa2 to regulate the differentiation of mDA neurons. Interestingly, our studies identified a rostral brain floor plate Neurog2 enhancer that requires direct input from Otx2, Foxa1, Foxa2 and an E-box transcription factor for its transcriptional activity. Furthermore, the chromatin remodelling factor Smarca1 was shown to function downstream of Foxa1 and Foxa2 to regulate differentiation from immature to mature midbrain dopaminergic neurons. Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons. © 2015. Published by The Company of Biologists Ltd.
    No preview · Article · Apr 2015 · Development
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    ABSTRACT: The PI3K-AKT pathway is expected to be a therapeutic target for non-small cell lung cancer (NSCLC) treatment. We previously reported that a novel PI3K inhibitor iMDK suppressed NSCLC cells in vitro and in vivo without harming normal cells and mice. Unexpectedly, iMDK activated the MAPK pathway, including ERK, in the NSCLC cells. Since iMDK did not eradicate such NSCLC cells completely, it is possible that the activated MAPK pathway confers resistance to the NSCLC cells against cell death induced by iMDK. In the present study, we assessed whether suppressing of iMDK-mediated activation of the MAPK pathway would enhance anti-tumorigenic activity of iMDK. PD0325901, a MAPK inhibitor, suppressed the MAPK pathway induced by iMDK and cooperatively inhibited cell viability and colony formation of NSCLC cells by inducing apoptosis in vitro. HUVEC tube formation, representing angiogenic processes in vitro, was also cooperatively inhibited by the combinatorial treatment of iMDK and PD0325901. The combinatorial treatment of iMDK with PD0325901 cooperatively suppressed tumor growth and tumor-associated angiogenesis in a lung cancer xenograft model in vivo. Here, we demonstrate a novel treatment strategy using iMDK and PD0325901 to eradicate NSCLC. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Mar 2015 · Experimental Cell Research
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    Jeffrey A Whitsett · Susan E Wert · Timothy E Weaver
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    ABSTRACT: Advances in physiology and biochemistry have provided fundamental insights into the role of pulmonary surfactant in the pathogenesis and treatment of preterm infants with respiratory distress syndrome. Identification of the surfactant proteins, lipid transporters, and transcriptional networks regulating their expression has provided the tools and insights needed to discern the molecular and cellular processes regulating the production and function of pulmonary surfactant prior to and after birth. Mutations in genes regulating surfactant homeostasis have been associated with severe lung disease in neonates and older infants. Biophysical and transgenic mouse models have provided insight into the mechanisms underlying surfactant protein and alveolar homeostasis. These studies have provided the framework for understanding the structure and function of pulmonary surfactant, which has informed understanding of the pathogenesis of diverse pulmonary disorders previously considered idiopathic. This review considers the pulmonary surfactant system and the genetic causes of acute and chronic lung disease caused by disruption of alveolar homeostasis.
    Full-text · Article · Jan 2015 · Annual Review of Pathology Mechanisms of Disease
  • Jeffrey A Whitsett · Theresa Alenghat
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    ABSTRACT: The epithelial surfaces of the lungs are in direct contact with the environment and are subjected to dynamic physical forces as airway tubes and alveoli are stretched and compressed during ventilation. Mucociliary clearance in conducting airways, reduction of surface tension in the alveoli, and maintenance of near sterility have been accommodated by the evolution of a multi-tiered innate host-defense system. The biophysical nature of pulmonary host defenses are integrated with the ability of respiratory epithelial cells to respond to and 'instruct' the professional immune system to protect the lungs from infection and injury.
    No preview · Article · Dec 2014 · Nature Immunology
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    ABSTRACT: The Hippo/Yap pathway is a well-conserved signaling cascade that regulates cell proliferation and differentiation to control organ size and stem/progenitor cell behavior. Following airway injury, Yap was dynamically regulated in regenerating airway epithelial cells. To determine the role of Hippo signaling in the lung, the mammalian Hippo kinases, Mst1 and Mst2, were deleted in epithelial cells of the embryonic and mature mouse lung. Mst1/2 deletion in the fetal lung enhanced proliferation and inhibited sacculation and epithelial cell differentiation. The transcriptional inhibition of cell proliferation and activation of differentiation during normal perinatal lung maturation were inversely regulated following embryonic Mst1/2 deletion. Ablation of Mst1/2 from bronchiolar epithelial cells in the adult lung caused airway hyperplasia and altered differentiation. Inhibitory Yap phosphorylation was decreased and Yap nuclear localization and transcriptional targets were increased after Mst1/2 deletion, consistent with canonical Hippo/Yap signaling. YAP potentiated cell proliferation and inhibited differentiation of human bronchial epithelial cells in vitro. Loss of Mst1/2 and expression of YAP regulated transcriptional targets controlling cell proliferation and differentiation, including Ajuba LIM protein. Ajuba was required for the effects of YAP on cell proliferation in vitro. Hippo/Yap signaling regulates Ajuba and controls proliferation and differentiation of lung epithelial progenitor cells. © The Author (2014). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS. All rights reserved.
    Full-text · Article · Dec 2014 · Journal of Molecular Cell Biology
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    ABSTRACT: The ocular surface epithelia, including the stratified but non-keratinized corneal, limbal and conjunctival epithelium, in concert with the epidermal keratinized eyelid epithelium, function together to maintain eye health and vision. Abnormalities in cellular proliferation or differentiation in any of these surface epithelia are central in the pathogenesis of many ocular surface disorders. Goblet cells are important secretory cell components of various epithelia, including the conjunctiva; however, mechanisms that regulate goblet cell differentiation in the conjunctiva are not well understood. Herein, we report that conditional deletion of transforming growth factor β receptor II (Tgfbr2) in keratin 14-positive stratified epithelia causes ocular surface epithelial hyperplasia and conjunctival goblet cell expansion that invaginates into the subconjunctival stroma in the mouse eye. We found that, in the absence of an external phenotype, the ocular surface epithelium develops properly, but young mice displayed conjunctival goblet cell expansion, demonstrating that TGFβ signaling is required for normal restriction of goblet cells within the conjunctiva. We observed increased expression of SAM-pointed domain containing ETS transcription factor (SPDEF) in stratified conjunctival epithelial cells in Tgfbr2 cKO mice, suggesting that TGFβ restricted goblet cell differentiation directly by repressing Spdef transcription. Gain of function of Spdef in keratin 14-positive epithelia resulted in the ectopic formation of goblet cells in the eyelid and peripheral cornea in adult mice. We found that Smad3 bound two distinct sites on the Spdef promoter and that treatment of keratin 14-positive cells with TGFβ inhibited SPDEF activation, thereby identifying a novel mechanistic role for TGFβ in regulating goblet cell differentiation.
    Full-text · Article · Nov 2014 · Development
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    ABSTRACT: Current treatments for inflammation associated with bronchopulmonary dysplasia fail to show clinical efficacy. Foxm1, a transcription factor of the Forkhead box family, is a critical mediator of lung development and carcinogenesis, but its role in bronchopulmonary dysplasia-associated pulmonary inflammation is unknown. Immunohistochemistry and RNA analysis were used to assess Foxm1 in lung tissue from hyperoxia-treated mice and patients with bronchopulmonary dysplasia. LysM-Cre/Foxm1-/- mice, in which Foxm1 was deleted from myeloid-derived inflammatory cells, including macrophages, monocytes and neutrophils, were exposed to neonatal hyperoxia causing lung injury and remodeling. Measurements of lung function and flow cytometry were used to evaluate effects of Foxm1 deletion on pulmonary inflammation and repair. Increased Foxm1 expression was observed in pulmonary macrophages of hyperoxia-exposed mice and lung tissue from patients with bronchopulmonary dysplasia. After hyperoxia, deletion of Foxm1 from the myeloid cell lineage decreased numbers of interstitial macrophages (CD45+CD11b+Ly6C-Ly6G-F4/80+CD68-) and impaired alveologenesis and lung function. The exaggerated bronchopulmonary dysplasia-like phenotype observed in hyperoxia-exposed LysM-Cre/Foxm1-/- mice was associated with increased expression of neutrophil-derived myeloperoxidase, proteinase 3 and cathepsin-g, all of which are critical for lung remodeling and inflammation. Our data demonstrate that Foxm1 influences pulmonary inflammatory responses to hyperoxia, inhibiting neutrophil-derived enzymes and enhancing monocytic responses that limit alveolar injury and remodeling in neonatal lungs.
    No preview · Article · Oct 2014 · American Journal of Respiratory Cell and Molecular Biology
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    ABSTRACT: SAM-pointed domain-containing ETS transcription factor (SPDEF) is expressed in normal prostate epithelium. While its expression changes during prostate carcinogenesis (PCa), the role of SPDEF in prostate cancer remains controversial due to the lack of genetic mouse models. In present study, we generated transgenic mice with the loss- or gain-of-function of SPDEF in prostate epithelium to demonstrate that SPDEF functions as tumor suppressor in prostate cancer. Loss of SPDEF increased cancer progression and tumor cell proliferation, whereas over-expression of SPDEF in prostate epithelium inhibited carcinogenesis and reduced tumor cell proliferation in vivo and in vitro. Transgenic over-expression of SPDEF inhibited mRNA and protein levels of Foxm1, a transcription factor critical for tumor cell proliferation, and reduced expression of Foxm1 target genes, including Cdc25b, Cyclin B1, Cyclin A2, Plk-1, AuroraB, CKS1 and Topo2alpha. Deletion of SPDEF in transgenic mice and cultures prostate tumor cells increased expression of Foxm1 and its target genes. Furthermore, an inverse correlation between SPDEF and Foxm1 levels was found in human prostate cancers. The two-gene signature of low SPDEF and high FoxM1 predicted poor survival in prostate cancer patients. Mechanistically, SPDEF bound to, and inhibited transcriptional activity of Foxm1 promoter by interfering with the ability of Foxm1 to activate its own promoter through auto-regulatory site located in the -745/-660 bp Foxm1 promoter region. Re-expression of Foxm1 restored cellular proliferation in the SPDEF-positive cancer cells and rescued progression of SPDEF-positive tumors in mouse prostates. Altogether, SPDEF inhibits prostate carcinogenesis by preventing Foxm1-regulated proliferation of prostate tumor cells. The present study identified novel crosstalk between SPDEF tumor suppressor and Foxm1 oncogene and demonstrated that this crosstalk is required for tumor cell proliferation during progression of prostate cancer in vivo.
    Preview · Article · Sep 2014 · PLoS Genetics
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    ABSTRACT: Respiratory disease is the third leading cause of death in the industrialized world. Consequently, the trachea, lungs, and cardiopulmonary vasculature have been the focus of extensive investigations. Recent studies have provided new information about the mechanisms driving lung development and differentiation. However, there is still much to learn about the ability of the adult respiratory system to undergo repair and to replace cells lost in response to injury and disease. This Review highlights the multiple stem/progenitor populations in different regions of the adult lung, the plasticity of their behavior in injury models, and molecular pathways that support homeostasis and repair.
    No preview · Article · Aug 2014 · Cell Stem Cell
  • Jeffrey A Whitsett
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    ABSTRACT: Advances in the physiology, biochemistry, molecular and cell biology of the pulmonary surfactant system transformed the clinical care and outcome of preterm infants with respiratory distress syndrome. The molecular era of surfactant biology provided genetic insights into the pathogenesis of pulmonary disorders, previously termed 'idiopathic', that affect newborn infants, children and adults. Knowledge related to the structure and function of the surfactant proteins and their roles in alveolar homeostasis has provided new diagnostic, prognostic and therapeutic tools to advance our understanding of the causes and treatments of acute and chronic lung diseases. Severe lung disease in newborn infants and older patients is caused by mutations in genes regulating alveolar epithelial cells and surfactant homeostasis. Mutations in genes encoding the surfactant proteins, transcription factors critical for alveolar morphogenesis and surfactant clearance, are now known to play important roles in the pathogenesis of chronic lung diseases. Identification of the genes underlying the diseases of alveolar homeostasis is useful for the diagnosis of lung disease before and after birth. © 2014 S. Karger AG, Basel.
    No preview · Article · Jun 2014 · Neonatology

Publication Stats

34k Citations
3,377.21 Total Impact Points


  • 1985-2015
    • Cincinnati Children's Hospital Medical Center
      • • Division of Pulmonary Biology
      • • Department of Pediatrics
      Cincinnati, Ohio, United States
  • 1977-2015
    • University of Cincinnati
      • • College of Medicine
      • • Department of Pediatrics
      • • Division of Pulmonary, Critical Care & Sleep Medicine
      • • Department of Obstetrics and Gynecology
      Cincinnati, Ohio, United States
  • 1992-2011
    • University of Pittsburgh
      • Department of Ophthalmology
      Pittsburgh, Pennsylvania, United States
    • National Cancer Institute (USA)
      베서스다, Maryland, United States
  • 2010
    • University of California, San Diego
      San Diego, California, United States
  • 2008
    • The University of Manchester
      • Faculty of Life Sciences
      Manchester, England, United Kingdom
    • University of Chicago
      • Department of Medicine
      Chicago, Illinois, United States
  • 2007
    • RIKEN
      Вако, Saitama, Japan
  • 2006
    • Stanford University
      Stanford, California, United States
    • Boston University
      Boston, Massachusetts, United States
  • 1995-2006
    • Vanderbilt University
      • Department of Pediatrics
      Нашвилл, Michigan, United States
    • VU University Amsterdam
      • Department of Molecular Cell Biology and Immunology
      Amsterdamo, North Holland, Netherlands
  • 1983-2006
    • University of Cincinnati Medical Center
      Cincinnati, Ohio, United States
  • 2005
    • University of Texas Health Science Center at Tyler
      Tyler, Texas, United States
  • 2001-2005
    • Johns Hopkins University
      • Department of Pediatrics
      Baltimore, Maryland, United States
    • Johns Hopkins Medicine
      Baltimore, Maryland, United States
  • 1999-2004
    • University of Illinois at Chicago
      • Department of Biochemistry and Molecular Genetics (Chicago)
      Chicago, IL, United States
    • University of South Florida
      Tampa, Florida, United States
    • Armed Forces Institute of Pathology
      Ralalpindi, Punjab, Pakistan
  • 1994-2004
    • Washington University in St. Louis
      • Department of Pediatrics
      San Luis, Missouri, United States
    • University of California, San Francisco
      San Francisco, California, United States
    • Valley Children's Hospital
      Мадера, California, United States
    • Children's National Medical Center
      Washington, Washington, D.C., United States
  • 2003
    • Max-Delbrück-Centrum für Molekulare Medizin
      Berlín, Berlin, Germany
    • University of Western Australia
      • Centre for Health Services Research
      Perth City, Western Australia, Australia
    • University of North Carolina at Chapel Hill
      • Department of Pediatrics
      Chapel Hill, NC, United States
  • 2002
    • William Penn University
      Filadelfia, Pennsylvania, United States
    • University of Pennsylvania
      • Department of Medicine
      Philadelphia, PA, United States
    • National Institutes of Health
      • Laboratory of Metabolism
      Maryland, United States
  • 2000
    • Royal Melbourne Hospital
      Melbourne, Victoria, Australia
    • University of Colorado
      • Division of Pulmonary Sciences and Critical Care Medicine
      Denver, CO, United States
  • 1998
    • University of Iowa
      • Department of Pediatrics
      Iowa City, IA, United States
  • 1997
    • Mayo Clinic - Rochester
      Рочестер, Minnesota, United States
  • 1996
    • Massachusetts Institute of Technology
      • Department of Biology
      Cambridge, Massachusetts, United States
    • Cook Children's Health Care System
      Fort Worth, Texas, United States
  • 1992-1995
    • University of California, Davis
      • School of Veterinary Medicine
      Davis, California, United States
  • 1993
    • Harbor-UCLA Medical Center
      • Department of Pediatrics
      Torrance, California, United States
    • The University of Western Ontario
      • Department of Obstetrics and Gynaecology
      London, Ontario, Canada