William E Lawson

United States Department of Veterans Affairs, Бедфорд, Massachusetts, United States

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Publications (73)384.79 Total impact

  • Jonathan A. Kropski · William E. Lawson · Timothy S. Blackwell

    No preview · Article · Dec 2015 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: Pulmonary hypertension (PH) complicating chronic parenchymal lung disease, such as idiopathic pulmonary fibrosis, results in significant morbidity and mortality. Since the hypoxia-inducible factor (HIF) signaling pathway is important for development of pulmonary hypertension in chronic hypoxia, we investigated whether HIF signaling in vascular endothelium regulates development of PH related to pulmonary fibrosis. We generated a transgenic model in which HIF is deleted within vascular endothelial cells, and then exposed these mice to chronic intraperitoneal bleomycin to induce PH associated with lung fibrosis. Although no differences in the degree of fibrotic remodeling were observed, we found that endothelial HIF deficient mice were protected against development of PH, including right ventricle and pulmonary vessel remodeling. Similarly, endothelial HIF deficient mice were protected from PH after 4 week exposure to normobaric hypoxia. In vitro studies of pulmonary vascular endothelial cells (PMVECs) isolated from the HIF targeted mice and controls revealed that endothelial HIF signaling increases endothelial cell expression of connective tissue growth factor (CTGF), enhances vascular permeability, and promotes pulmonary artery smooth muscle cell proliferation and wound healing ability, all of which have the potential to impact the development of PH in vivo. Taken together, these studies demonstrate that vascular endothelial cell HIF signaling is necessary for development of hypoxia and pulmonary fibrosis associated PH. As such, HIF and HIF-regulated targets represent a therapeutic target in these conditions.
    No preview · Article · Dec 2015 · AJP Lung Cellular and Molecular Physiology
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    ABSTRACT: Pulmonary fibrosis is often complicated by pulmonary hypertension (PH), and previous studies have shown a potential link between bone morphogenetic protein receptor II (BMPR2) and PH secondary to pulmonary fibrosis. We exposed transgenic mice expressing mutant BMPR2 and control mice to repetitive intraperitoneal injections of bleomycin for 4 weeks. The duration of transgene activation was too short for mutant BMPR2 mice to develop spontaneous PH. Mutant BMPR2 mice had increased right ventricular systolic pressure compared to control mice, without differences in pulmonary fibrosis. We found increased hypoxia-inducible factor (HIF)1-α stabilization in lungs of mutant-BMPR2-expressing mice compared to controls following bleomycin treatment. In addition, expression of the hypoxia response element protein connective tissue growth factor was increased in transgenic mice as well as in a human pulmonary microvascular endothelial cell line expressing mutant BMPR2. In mouse pulmonary vascular endothelial cells, mutant BMPR2 expression resulted in increased HIF1-α and reactive oxygen species production following exposure to hypoxia, both of which were attenuated with the antioxidant TEMPOL. These data suggest that expression of mutant BMPR2 worsens secondary PH through increased HIF activity in vascular endothelium. This pathway could be therapeutically targeted in patients with PH secondary to pulmonary fibrosis.
    No preview · Article · Oct 2015
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    ABSTRACT: Secretory immunoglobulin A (SIgA) reaches the airway lumen by local transcytosis across airway epithelial cells or with tracheobronchial submucosal gland secretions. In chronic obstructive pulmonary disease (COPD), deficiency of SIgA on the airway surface has been reported. However, reduction of SIgA levels in sputum and bronchoalveolar lavage (BAL) fluid has not been consistently observed. To explain this discrepancy, we analyzed BAL fluid and lung tissue from patients with COPD and control subjects. Immunohistochemical analysis of large and small airways of COPD patients showed that MUC5AC is the predominant mucin expressed by airway epithelial cells, whereas MUC5B is expressed in submucosal glands of large airways. Dual immunostaining with anti-IgA and anti-MUC5B antibodies showed reduction of IgA on the airway surface as well as accumulation of IgA within MUC5B-positive luminal mucus plugs, suggesting that luminal SIgA originates from submucosal glands in COPD patients. We found that the concentration of SIgA in BAL is inversely correlated with forced expiratory volume in 1 s (FEV1) in COPD, but that the ratio of SIgA/MUC5B is a better predictor of FEV1, particularly in patients with moderate COPD. Together, these findings suggest that SIgA production by submucosal glands, which are expanded in COPD, is insufficient to compensate for reduced SIgA transcytosis by airway epithelial cells. Localized SIgA deficiency on the surface of small airways is associated with COPD progression and represents a potential new therapeutic target in COPD.
    No preview · Article · Oct 2015 · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin
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    ABSTRACT: Tissue factor (TF) initiates the extrinsic coagulation cascade in response to tissue injury leading to local fibrin deposition. Low levels of TF in mice are associated with increased severity of acute lung injury (ALI) following intra-tracheal (IT) lipopolysaccharide (LPS) administration. However, the cellular sources of the TF required for protection from LPS-induced ALI remain unknown. In the current study, transgenic mice with cell-specific deletions of TF in the lung epithelium or myeloid cells were treated with IT LPS to determine the cellular sources of TF important in direct ALI. Cell-specific deletion of TF in the lung epithelium reduced total lung TF expression to 39% of wild-type levels at baseline and to 29% of wild-type levels after IT LPS. In contrast, there was no reduction of TF with myeloid cell TF deletion. Mice lacking myeloid cell TF (TF(Δmye)) did not differ from wild-type mice in coagulation, inflammation, permeability, or hemorrhage. However, mice lacking lung epithelial TF (TF(ΔLEpi)) had increased tissue injury, impaired activation of coagulation in the airspace, disrupted alveolar permeability, and increased alveolar hemorrhage after IT LPS. Deletion of epithelial TF did not affect alveolar permeability in an indirect model of ALI caused by systemic LPS infusion. These studies demonstrate that the lung epithelium is the primary source of TF in the lung contributing 60-70% of total lung TF and that lung epithelial but not myeloid TF may be protective in direct ALI.
    No preview · Article · Apr 2015 · American Journal of Respiratory Cell and Molecular Biology
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    ABSTRACT: The aged population suffers increased morbidity and higher mortality in response to episodes of acute kidney injury (AKI). Aging is associated with telomere shortening, and both telomerase reverse transcriptase (TerT) and RNA (TerC) are essential to maintain telomere length. To define a role of telomerase deficiency in susceptibility to AKI, we used ischemia/reperfusion injury in wild-type mice or mice with either TerC or TerT deletion. Injury induced similar renal impairment at day 1 in each genotype, as assessed by azotemia, proteinuria, acute tubular injury score, and apoptotic tubular epithelial cell index. However, either TerC or TerT knockout significantly delayed recovery compared with wild-type mice. Electron microscopy showed increased autophagosome formation in renal tubular epithelial cells in wild-type mice but a significant delay of their development in TerC and TerT knockout mice. There were also impeded increases in the expression of the autophagosome marker LC3 II, prolonged accumulation of the autophagosome protein P62, an increase of the cell cycle regulator p16, and greater activation of the mammalian target of rapamycin (mTOR) pathway. The mTORC1 inhibitor, rapamycin, partially restored the ischemia/reperfusion-induced autophagy response, without a significant effect on either p16 induction or tubule epithelial cell proliferation. Thus, muting the maintenance of normal telomere length in mice impaired recovery from AKI, owing to an increase in tubule cell senescence and impairment of mTOR-mediated autophagy.Kidney International advance online publication, 11 March 2015; doi:10.1038/ki.2015.69.
    No preview · Article · Mar 2015 · Kidney International

  • No preview · Article · Feb 2015
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    ABSTRACT: Background: Up to 20% of cases of idiopathic interstitial pneumonia (IIP) cluster in families, comprising the syndrome of Familial Interstitial Pneumonia (FIP); however, the genetic basis of FIP remains uncertain in a majority of families. We hypothesized that new disease-causing rare genetic variants could be identified using whole-exome sequencing of affected members from FIP families, providing additional insights into disease pathogenesis. Methods: Affected subjects from 25 kindreds were selected from an ongoing FIP registry for whole-exome sequencing (WES) from genomic DNA. Candidate rare variants were confirmed by Sanger sequencing and co-segregation analysis was performed in families, followed by additional sequencing of affected individuals from another163 kindreds. Results: We identified a potentially damaging rare variant in the gene encoding for regulator of telomere elongation helicase 1 (RTEL1) that segregated with disease and was associated with very short telomeres in peripheral blood mononuclear cells in one of 25 families in our original WES cohort. Evaluation of affected individuals in 163 additional kindreds revealed another 8 families (5%) with heterozygous rare variants in RTEL1 that segregated with clinical FIP. Probands and unaffected carriers of these rare variants had short telomeres (<10% for age) in peripheral blood mononuclear cells and increased T-circle formation, suggesting impaired RTEL1 function. Conclusions: Rare loss-of-function variants in RTEL1 represent a newly defined genetic predisposition for FIP, supporting the importance of telomere-related pathways in pulmonary fibrosis.
    Full-text · Article · Feb 2015 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: Introduction: Asymptomatic relatives of patients with Familial Interstitial Pneumonia (FIP), the inherited form of Idiopathic Interstitial Pneumonia (IIP), carry increased risk for developing interstitial lung disease. Studying these at-risk individuals provides a unique opportunity to investigate early stages of FIP pathogenesis and develop predictive models of disease onset. Methods: Seventy-five asymptomatic first-degree relatives of FIP patients (mean age 50.8 years) underwent blood sampling and high-resolution chest CT (HRCT) scan in an ongoing cohort study; 72 consented to bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsies. Twenty-seven healthy individuals were used as controls. Results: Eleven of 75 at-risk subjects (14%) had evidence of interstitial changes by HRCT while 35.2% had abnormalities on transbronchial biopsies. No differences were noted in inflammatory cells in BAL between at-risk individuals and controls. At-risk subjects had increased herpesvirus DNA in cell-free BAL and evidence of herpesvirus antigen expression in alveolar epithelial cells (AECs), which correlated with expression of endoplasmic reticulum stress markers in AECs. Peripheral blood mononuclear cell and AEC telomere length were shorter in at-risk individuals than healthy controls. The minor allele frequency of the Muc5B rs35705950 promoter polymorphism was increased in at-risk subjects. Levels of several plasma biomarkers differed between at-risk subjects and controls, and correlated with abnormal HRCT scans. Conclusions: Evidence of lung parenchymal remodeling and epithelial dysfunction were identified in asymptomatic individuals at-risk for FIP. Together, these findings offer new insights into the early pathogenesis of IIP and provide an ongoing opportunity to characterize presymptomatic abnormalities that predict progression to clinical disease.
    Full-text · Article · Nov 2014 · American Journal of Respiratory and Critical Care Medicine
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    Full-text · Article · Nov 2014 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: Short telomeres are frequently identified in patients with idiopathic pulmonary fibrosis (IPF) and its inherited form, familial interstitial pneumonia (FIP). We identified an FIP kindred with short telomeres who did not carry a mutation in known FIP genes TERT or hTR. We performed targeted sequencing of other telomere-related genes to identify the genetic basis of FIP in this kindred. DNA was isolated from peripheral blood mononuclear cells or paraffin-embedded lung block and PCR-based sequencing of DKC1, NOP10, TINF2 and NHP2 was performed. Peripheral blood mononuclear cell telomere length was measured by southern blot. Alveolar epithelial cell (AEC) telomere length was measured by fluorescence-in-situ-hydridization. Dyskerin and hTR expression in lymphoblastoid cell lines were measured by qPCR. The proband was a 69 year-old man with dyspnea, restrictive pulmonary function tests and reticular changes on high-resolution CT. An older male sibling had died from IPF. The proband had markedly shortened telomeres in peripheral blood and undetectably short telomeres in alveolar epithelial cells. Sequencing of dyskerin (DKC1) revealed that both affected siblings shared a novel A to G 1213 transition near the hTR binding domain that is predicted to encode a Thr405Ala amino acid substitution. hTR levels were decreased out of proportion to DKC1 expression in the T405A DKC1 proband, suggesting this mutation destabilizes hTR and impairs telomerase function. This DKC1 variant represents the third telomere-related gene identified as a genetic cause of FIP. Further investigation into mechanism by which dyskerin contributes to the development of lung fibrosis is warranted.
    Full-text · Article · Feb 2014 · Chest
  • William E. Lawson · James E. Loyd
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    ABSTRACT: The interstitial lung diseases (ILDs) comprise a heterogeneous group of lung disorders in which inflammation and/or fibrosis in the interstitial space between alveoli, the gas exchanging area of the lung, leads to restrictive pulmonary physiology, hypoxemia, and respiratory failure. ILD may be due to systemic disorders or environmental exposures or may be a manifestation of an underlying genetic syndrome. However, a significant percentage of cases of ILD do not have a readily identifiable cause, with this group of disorders referred to as the idiopathic interstitial pneumonias (IIPs). Familial interstitial pneumonia (FIP) is defined when two or more individuals in a given family have an IIP. Analysis of FIP kindreds has led to the identification of genetic causes of IIP in adults, with mutations in the genes encoding surfactant protein C, surfactant protein A2, telomerase reverse transcriptase, and telomerase RNA component found. Furthermore, pediatric cases of ILD have been linked to mutations in the genes encoding surfactant protein C and ATP-binding cassette transporter A3. In addition to the IIPs, systemic diseases such as systemic sclerosis and sarcoidosis likely have strong genetic associations. Finally, multiple genetic syndromes have been described that can have prominent ILD manifestations, including dyskeratosis congenita and Hermansky-Pudlak syndrome.
    No preview · Article · Dec 2013
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    ABSTRACT: Although in some cases clinical and radiographic features may be sufficient to establish a diagnosis of diffuse parenchymal lung disease (DPLD), surgical lung biopsy is frequently required. Recently a new technique for bronchoscopic lung biopsy has been developed using flexible cryo-probes. In this study we describe our clinical experience using bronchoscopic cryobiopsy for diagnosis of diffuse lung disease. A retrospective study of subjects who had undergone bronchoscopic cryobiopsy for evaluation of DPLD at an academic tertiary care center from January 1, 2012 through January 15, 2013 was performed. The procedure was performed using a flexible bronchoscope to acquire biopsies of lung parenchyma. H&E stained biopsies were reviewed by an expert lung pathologist. Twenty-five eligible subjects were identified. With a mean area of 64.2 mm(2), cryobiopsies were larger than that typically encountered with traditional transbronchial forceps biopsy. In 19 of the 25 subjects, a specific diagnosis was obtained. In one additional subject, biopsies demonstrating normal parenchyma were felt sufficient to exclude diffuse lung disease as a cause of dyspnea. The overall diagnostic yield of bronchoscopic cryobiopsy was 80% (20/25). The most frequent diagnosis was usual interstitial pneumonia (UIP) (n = 7). Three of the 25 subjects ultimately required surgical lung biopsy. There were no significant complications. In patients with suspected diffuse parenchymal lung disease, bronchoscopic cryobiopsy is a promising and minimally invasive approach to obtain lung tissue with high diagnostic yield.
    Full-text · Article · Nov 2013 · PLoS ONE
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    ABSTRACT: The median survival of patients with idiopathic pulmonary fibrosis continues to be approximately 3 years from the time of diagnosis, underscoring the lack of effective medical therapies for this disease. In the United States alone, approximately 40,000 patients die of this disease annually. In November 2012, the National Heart, Lung and Blood Institute held a workshop aimed at coordinating research efforts and accelerating the development of idiopathic pulmonary fibrosis therapies. Basic, translational and clinical researchers gathered with representatives from the National Heart Lung and Blood Institute, patient advocacy groups, pharmaceutical companies and the Food and Drug Administration to review the current state of idiopathic pulmonary fibrosis research and identify priority areas, opportunities for collaborations and directions for future research. The workshop was organized into groups that were tasked with assessing and making recommendations to promote progress in one of the following six critical areas of research: 1) biology of alveolar epithelial injury and aberrant repair, 2) role of extracellular matrix, 3) preclinical modeling, 4) the role of inflammation and immunity, 5) genetic, epigenetic and environmental determinants, 6) translation of discoveries into diagnostics and therapeutics. The workshop recommendations provide a basis for directing future research and strategic planning by scientific, professional and patient communities and the National Heart Lung and Blood Institute.
    Full-text · Article · Oct 2013 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: PGI2 signaling through IP inhibits allergen-induced inflammatory responses in mice. We reported previously that PGI2 analogs decreased proinflammatory cytokine and chemokine production by mature BMDCs. However, whether PGI2 modulates the function of immature DCs has not been investigated. We hypothesized that PGI2 negatively regulates immature DC function and investigated the effect of PGI2 analogs on immature BMDC antigen uptake and migration in vitro and in vivo. Immature BMDCs were obtained from WT and IPKO mice, both on a C57BL/6 background. The PGI2 analog cicaprost decreased FITC-OVA uptake by immature BMDCs. In addition, cicaprost increased immature BMDC podosome dissolution, pro-MMP-9 production, cell surface CCR7 expression, and chemotactic migration toward CCL19 and CCL21, as well as chemokinesis, in an IP-specific fashion. These in vitro results suggested that cicaprost promotes migration of immature DCs from mucosal surface to draining LNs. This concept was supported by the finding that migration of immature GFP(+) BMDCs to draining LNs was enhanced by pretreatment with cicaprost. Further, migration of immature lung DCs labeled with PKH26 was enhanced by intranasal cicaprost administration. Our results suggest PGI2-IP signaling increases immature DC migration to the draining LNs and may represent a novel mechanism by which this eicosanoid inhibits immune responses.
    Preview · Article · Apr 2013 · Journal of leukocyte biology
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    William E Lawson · Timothy S Blackwell
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    ABSTRACT: Not needed.
    Preview · Article · Mar 2013 · AJP Lung Cellular and Molecular Physiology
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    ABSTRACT: Interstitial lung fibrosis can develop as a consequence of occupational or medical exposures, as a result of genetic defects, following trauma or acute lung injury leading to fibroproliferative acute respiratory distress syndrome (ARDS) or can develop in an idiopathic manner. The pathogenesis of each of these forms of lung fibrosis is poorly understood. They each result in progressive loss of lung function with increasing dyspnea and ultimately, most forms result in mortality. To better understand the pathogenesis of lung fibrotic disorders, multiple animal models have been developed. This review summarizes common and emerging models of lung fibrosis to highlight their usefulness for understanding cell-cell and soluble mediator interactions which drive fibrotic responses. Recent advances have allowed for development of models to study targeted injury of type II alveolar epithelial cells, fibroblast autonomous effects and targeted genetic defects. Repetitive dosing in some models has more closely mimicked the pathology of human fibrotic lung disease. We also have a much better understanding of the fact that the aged lung increases susceptibility to fibrosis. Each of these models reviewed in this report offer a powerful tool to study some aspect of fibrotic lung disease.
    Full-text · Article · Mar 2013 · American Journal of Respiratory Cell and Molecular Biology
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    ABSTRACT: Aquaporin 11 (Aqp11) is a newly described member of the protein family of transport channels. Aqp11 associates with the endoplasmic reticulum (ER) and is highly expressed in proximal tubular epithelial cells in the kidney. Previously, we identified and characterized a recessive mutation of the highly conserved Cys227 to Ser227 in mouse Aqp11 that caused proximal tubule (PT) injury and kidney failure in mutant mice. The current study revealed induction of ER stress, unfolded protein response, and apoptosis as molecular mechanisms of this PT injury. Cys227Ser mutation interfered with maintenance of Aqp11oligomeric structure. Aqp11 is abundantly expressed in the S1 PT segment, a site of major renal glucose flux, and Aqp11 mutant mice developed PT-specific mitochondrial injury. Glucose increased Aqp11 protein expression in wild type kidney and up-regulation of Aqp11 expression by glucose in vitro was prevented by phlorizin, an inhibitor of sodium-dependent glucose transport across PT. Total Aqp11 levels in heterozygotes were higher than in wild type mice but were not further increased in response to glucose. In Aqp11 insufficient PT cells, glucose potentiated increases in reactive oxygen species (ROS) production. ROS production was also elevated in Aqp11 mutation carriers. Phenotypically normal mice heterozygous for the Aqp11 mutation repeatedly treated with glucose showed increased blood urea nitrogen levels that was prevented by the antioxidant sulforaphane or by phlorizin. Our results indicate an important role for Aqp11 to prevent glucose-induced oxidative stress in proximal tubules.
    Full-text · Article · Mar 2013 · AJP Renal Physiology
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    ABSTRACT: RATIONALE: Alveolar epithelial cells (AECs) play central roles in the response to lung injury and the pathogenesis of pulmonary fibrosis. OBJECTIVES: We aimed to determine the role of β-catenin in alveolar epithelium during bleomycin induced lung fibrosis. METHODS: Genetically modified mice were developed to selectively delete β-catenin in AECs and were crossed to cell fate reporter mice that express β-galactosidase (βgal) in cells of AEC lineage. Mice were given intratracheal bleomycin (0.04 units) and assessed for AEC death, inflammation, lung injury, and fibrotic remodeling. Mouse lung epithelial cells (MLE12) with siRNA knockdown of β-catenin underwent evaluation for wound closure, proliferation, and bleomycin induced cytotoxicity. MEASUREMENTS AND MAIN RESULTS: Increased β-catenin expression was noted in lung parenchyma following bleomycin. Mice with selective deletion of β-catenin in AECS had greater AEC death at 1 week following bleomycin, followed by increased numbers of fibroblasts and enhanced lung fibrosis as determined by semiquantitative histological scoring and total collagen content. However, no differences in lung inflammation or protein levels in bronchoalveolar lavage were noted. In vitro, β-catenin deficient AECs showed increased bleomycin induced cytotoxicity, as well as reduced proliferation and impaired wound closure. Consistent with these findings, mice with AEC β-catenin deficiency showed delayed recovery after bleomycin. CONCLUSIONS: β-catenin in the alveolar epithelium protects against bleomycin induced fibrosis. Our studies suggest that AEC survival and wound healing are enhanced through β-catenin dependent mechanisms. Activation of the developmentally important β-catenin pathway in AECs appears to contribute to epithelial repair following epithelial injury.
    No preview · Article · Jan 2013 · American Journal of Respiratory and Critical Care Medicine
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    ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a progressive and often fatal lung disease for which there is no known treatment. Although the traditional paradigm of IPF pathogenesis emphasized chronic inflammation as the primary driver of fibrotic remodeling, more recent insights have challenged this view. Linkage analysis and candidate gene approaches have identified four genes that cause the inherited form of IPF, familial interstitial pneumonia (FIP). These four genes encode two surfactant proteins, surfactant protein C (encoded by SFTPC) and surfactant protein A2 (SFTPA2), and two components of the telomerase complex, telomerase reverse transcriptase (TERT) and the RNA component of telomerase (TERC). In this review, we discuss how investigating these mutations, as well as genetic variants identified in other inherited disorders associated with pulmonary fibrosis, are providing new insights into the pathogenesis of common idiopathic interstitial lung diseases, particularly IPF. Studies in this area have highlighted key roles for epithelial cell injury and dysfunction in the development of lung fibrosis. In addition, genetic approaches have uncovered the importance of several processes - including endoplasmic reticulum stress and the unfolded protein response, DNA-damage and -repair pathways, and cellular senescence - that might provide new therapeutic targets in fibrotic lung diseases.
    No preview · Article · Jan 2013 · Disease Models and Mechanisms

Publication Stats

2k Citations
384.79 Total Impact Points

Institutions

  • 2007-2015
    • United States Department of Veterans Affairs
      Бедфорд, Massachusetts, United States
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 2004-2015
    • Vanderbilt University
      • • Department of Medicine
      • • Division of Allergy, Pulmonary and Critical Care
      Нашвилл, Michigan, United States
  • 2009-2011
    • U.S. Department of Veterans Affairs
      Washington, Washington, D.C., United States