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Journal articles on the topic 'Lungs Differentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 January 2023

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1

Ito, T., N. Udaka, T. Yazawa, K. Okudela, H. Hayashi, T. Sudo, F. Guillemot, R. Kageyama, and H. Kitamura. "Basic helix-loop-helix transcription factors regulate the neuroendocrine differentiation of fetal mouse pulmonary epithelium." Development 127, no. 18 (September 15, 2000): 3913–21. http://dx.doi.org/10.1242/dev.127.18.3913.

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To clarify the mechanisms that regulate neuroendocrine differentiation of fetal lung epithelia, we have studied the expression of the mammalian homologs of achaete-scute complex (Mash1) (Ascl1 - Mouse Genome Informatics); hairy and enhancer of split1 (Hes1); and the expression of Notch/Notch-ligand system in the fetal and adult mouse lungs, and in the lungs of Mash1- or Hes1-deficient mice. Immunohistochemical studies revealed that Mash1-positive cells seemed to belong to pulmonary neuroendocrine cells (PNEC) and their precursors. In mice deficient for Mash1, no PNEC were detected. Hes1-positi

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2

Chytil, F. "The lungs and vitamin A." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 5 (May 1, 1992): L517—L527. http://dx.doi.org/10.1152/ajplung.1992.262.5.l517.

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Evidence is reviewed supporting the view that vitamin A (retinol) and its metabolite, retinoic acid, called natural retinoids, are major factors involved in differentiation and in maturation of the lungs. This conclusion is based on morphological observation that lack of this dietary micronutrient causes keratinizing squamous metaplasia of the bronchopulmonary tree that can be reversed by refeeding the animal with retinol. In addition to these observations suggesting an indirect participation of retinol and/or retinoic acid in the differentiation of this organ, more direct evidence is presente

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3

Besnard, V., S. E. Wert, K. H. Kaestner, and J. A. Whitsett. "Stage-specific regulation of respiratory epithelial cell differentiation by Foxa1." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 5 (November 2005): L750—L759. http://dx.doi.org/10.1152/ajplung.00151.2005.

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Foxa1 is a member of the winged helix family of transcription factors that is expressed in epithelial cells of the conducting airways and in alveolar type II cells of the lung. To determine the role of Foxa1 during lung morphogenesis, histology and gene expression were assessed in lungs from Foxa1−/− gene-targeted mice from embryonic day (E) 16.5 to postnatal day (PN) 13. Deletion of Foxa1 perturbed maturation of the respiratory epithelium at precise times during lung morphogenesis. While dilatation of peripheral lung saccules was delayed in Foxa1−/− mice at E16.5, sacculation was unperturbed

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4

BRODY, J. "Alveolar cell differentiation markers in human lungs." Journal of Molecular and Cellular Cardiology 21 (February 1989): 161–64. http://dx.doi.org/10.1016/0022-2828(89)90852-3.

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Meierovics, Anda I., and Siobhán C. Cowley. "MAIT cells promote inflammatory monocyte differentiation into dendritic cells during pulmonary intracellular infection." Journal of Experimental Medicine 213, no. 12 (October 31, 2016): 2793–809. http://dx.doi.org/10.1084/jem.20160637.

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Mucosa-associated invariant T (MAIT) cells are a unique innate T cell subset that is necessary for rapid recruitment of activated CD4+ T cells to the lungs after pulmonary F. tularensis LVS infection. Here, we investigated the mechanisms behind this effect. We provide evidence to show that MAIT cells promote early differentiation of CCR2-dependent monocytes into monocyte-derived DCs (Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection. Adoptive transfer of Mo-DCs to MAIT cell–deficient mice (MR1−/− mice) rescued their defect in the recruitment of activated CD4+ T cells to the lung

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6

Li, Changgong, Susan M. Smith, Neil Peinado, Feng Gao, Wei Li, Matt K. Lee, Beiyun Zhou, et al. "WNT5a-ROR Signaling Is Essential for Alveologenesis." Cells 9, no. 2 (February 7, 2020): 384. http://dx.doi.org/10.3390/cells9020384.

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WNT5a is a mainly “non-canonical” WNT ligand whose dysregulation is observed in lung diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and asthma. Germline deletion of Wnt5a disrupts embryonic lung development. However, the temporal-specific function of WNT5a remains unknown. In this study, we generated a conditional loss-of-function mouse model (Wnt5aCAG) and examined the specific role of Wnt5a during the saccular and alveolar phases of lung development. The lack of Wnt5a in the saccular phase blocked distal airway expansion and attenuated diff

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Raslan, Ahmed A., Youn Jeong Oh, Yong Ri Jin, and Jeong Kyo Yoon. "R-Spondin2, a Positive Canonical WNT Signaling Regulator, Controls the Expansion and Differentiation of Distal Lung Epithelial Stem/Progenitor Cells in Mice." International Journal of Molecular Sciences 23, no. 6 (March 13, 2022): 3089. http://dx.doi.org/10.3390/ijms23063089.

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The lungs have a remarkable ability to regenerate damaged tissues caused by acute injury. Many lung diseases, especially chronic lung diseases, are associated with a reduced or disrupted regeneration potential of the lungs. Therefore, understanding the underlying mechanisms of the regenerative capacity of the lungs offers the potential to identify novel therapeutic targets for these diseases. R-spondin2, a co-activator of WNT/β-catenin signaling, plays an important role in embryonic murine lung development. However, the role of Rspo2 in adult lung homeostasis and regeneration remains unknown.

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Lai, Jen-Feng, Lucas J. Thompson, and Steven F. Ziegler. "TSLP drives acute TH2-cell differentiation in lungs." Journal of Allergy and Clinical Immunology 146, no. 6 (December 2020): 1406–18. http://dx.doi.org/10.1016/j.jaci.2020.03.032.

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9

Alabed, Mashael, Asma Sultana Shaik, Narjes Saheb Sharif-Askari, Fatemeh Saheb Sharif-Askari, Shirin Hafezi, Bushra Mdkhana, Elaref Ratemi, Saleh Al-Muhsen, Qutayba Hamid, and Rabih Halwani. "Enhanced Infiltration of Central Memory T Cells to the Lung Tissue during Allergic Lung Inflammation." International Archives of Allergy and Immunology 183, no. 2 (October 20, 2021): 127–41. http://dx.doi.org/10.1159/000518835.

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Memory T cells play a central role in regulating inflammatory responses during asthma. However, tissue distribution of effector memory (T<sub>EM</sub>) and central memory (T<sub>CM</sub>) T-cell subtypes, their differentiation, and their contribution to the persistence of lung tissue inflammation during asthma are not well understood. Interestingly, an increase in survival and persistence of memory T cells was reported in asthmatic lungs, which may suggest a shift toward the more persistent T<sub>CM</sub> phenotype. In this report, we investigated the differ

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Bedoya, Felipe, Guang-Shing Cheng, Abigail Leibow, Nardine Zakhary, Katherine Weissler, Victoria Garcia, Elizabeth Kropf, et al. "Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice (P1043)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 139.11. http://dx.doi.org/10.4049/jimmunol.190.supp.139.11.

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Abstract We have examined the formation, participation and functional specialization of virus-reactive Foxp3+ regulatory T cells (Tregs) in a mouse model of influenza virus infection. “Natural” Tregs generated intra-thymically based on interactions with a self-peptide proliferated in response to a homologous viral antigen in the lungs, and to a lesser extent in the lung-draining mediastinal LN (medLN), of virus-infected mice. By contrast, conventional CD4+ T cells with identical TCR specificity underwent little or no conversion to become “adaptive” Tregs. The virus-reactive Tregs in the medLN

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Tulo, Sukanta Kumar, Satyavratan Govindarajan, Palaniappan Ramu, and Ramakrishnan Swaminathan. "SHAPE CHARACTERIZATION OF MEDIASTINUM IN TUBERCULOSIS CHEST RADIOGRAPHS USING LEVEL SET SEGMENTATION." Biomedical Sciences Instrumentation 57, no. 2 (April 1, 2021): 212–18. http://dx.doi.org/10.34107/yhpn9422.04212.

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Mediastinum is considered as one of the substantial anatomical regions for the gross diagnosis of several chest related pathologies. The geometric variations of the mediastinum in Chest Radiographs (CXRs) could be utilised as potential image markers in the early detection of Tuberculosis (TB). This study attempts to segment mediastinum in CXRs using level sets for the shape characterization of TB conditions. The CXR images for this study are considered from a public database. An edge-based distance regularized level set evolution is employed to segment the lungs followed by a region-based Chan

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Larson, Janet E., Joseph B. Delcarpio, Michelle M. Farberman, Susan L. Morrow, and J. Craig Cohen. "CFTR modulates lung secretory cell proliferation and differentiation." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 2 (August 1, 2000): L333—L341. http://dx.doi.org/10.1152/ajplung.2000.279.2.l333.

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We have permanently reversed the lethal phenotype in the cystic fibrosis (CF) transmembrane conductance regulator (CFTR)-deficient (knockout) mouse after in utero gene therapy with an adenovirus containing the cftr gene. The gene transfer targeted somatic stem cells in the developing lung and intestine, and these epithelial surfaces demonstrated permanent developmental changes after treatment. The survival statistics from the progeny of heterozygote-heterozygote matings after in utero cftr gene treatment demonstrated an increased mortality in the homozygous normal pups, indicating that overexp

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Hayu, Tri Pangesti, and Ayly Soekanto. "Pengaruh Pemaparan Uap Anti Nyamuk Elektrik yang Mengandung Allathrin terhadap Berat dan Warna Paru-ParuTikusi." Jurnal Ilmiah Kedokteran Wijaya Kusuma 5, no. 1 (February 13, 2018): 26. http://dx.doi.org/10.30742/jikw.v5i1.3.

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Lungs as place where the gases exchange inside the body is related to enviroment sorrounding. Usage of electric mosquito repellent that contained allethrin on certain period can inflict lung’s abnormalities.The aim to this research is to find the effect of fumes exposure from the electric mosquito repellent that contained allethrin to weight and colour of rat’s lungs. The research was experimental laboratory. 24 male rats strain Wistar that devided into 4 groups, which were group 1 control (P0) without exposure, group 2 (P1) exposed 4 hours a day, group 3 (P2) exposed 6 hours a day and group 4

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Yao, Jiayi, Pierre J. Guihard, Xiuju Wu, Ana M. Blazquez-Medela, Melissa J. Spencer, Medet Jumabay, Peter Tontonoz, Alan M. Fogelman, Kristina I. Boström, and Yucheng Yao. "Vascular endothelium plays a key role in directing pulmonary epithelial cell differentiation." Journal of Cell Biology 216, no. 10 (August 24, 2017): 3369–85. http://dx.doi.org/10.1083/jcb.201612122.

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The vascular endothelium is critical for induction of appropriate lineage differentiation in organogenesis. In this study, we report that dysfunctional pulmonary endothelium, resulting from the loss of matrix Gla protein (MGP), causes ectopic hepatic differentiation in the pulmonary epithelium. We demonstrate uncontrolled induction of the hepatic growth factor (HGF) caused by dysregulated cross talk between pulmonary endothelium and epithelium in Mgp-null lungs. Elevated HGF induced hepatocyte nuclear factor 4 α (Hnf4a), which competed with NK2 homeobox 1 (Nkx2.1) for binding to forkhead box A

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Xie, Ke, Yu-sen Chai, Shi-hui Lin, Fang Xu, and Chuan-jiang Wang. "Luteolin Regulates the Differentiation of Regulatory T Cells and Activates IL-10-Dependent Macrophage Polarization against Acute Lung Injury." Journal of Immunology Research 2021 (January 18, 2021): 1–12. http://dx.doi.org/10.1155/2021/8883962.

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Objectives. Inflammatory disease characterized by clinical destructive respiratory disorder is called acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Studies have shown that luteolin exerts anti-inflammatory effects by increasing regulatory T cells (Tregs). In this study, we aimed to determine the effects of luteolin on ALI/ARDS and Treg differentiation. Methods. In this paper, we used cecal ligation puncture (CLP) to generate an ALI mouse model to determine the effects of luteolin on ALI/ARDS. Lung tissues were stained for interleukin- (IL-) 17A and myeloperoxidase (MPO) by

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Biswas, Deblina, Anshu Kumari, George C. K. Chen, Srivathsan Vasudevan, Sharad Gupta, Supriya Shukla, and Umesh K. Garg. "Quantitative Differentiation of Pneumonia from Normal Lungs: Diagnostic Assessment Using Photoacoustic Spectral Response." Applied Spectroscopy 71, no. 11 (September 8, 2017): 2532–37. http://dx.doi.org/10.1177/0003702817708320.

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Pneumonia is an acute lung infection that takes life of many young children in developing countries. Early stage (red hepatization) detection of pneumonia would be pragmatic to control mortality rate. Detection of this disease at early stages demands the knowledge of pathology, making it difficult to screen noninvasively. We propose photoacoustic spectral response (PASR), a noninvasive elasticity-dependent technique for early stage pneumonia detection. We report the quantitative red hepatization detection of pneumonia through median frequency, spectral energy, and variance. Significant contras

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Cornez, Isabelle, Sowmya Parampalli Yajnanarayana, Natascha Hermann-Kleiter, Stefan Ulrich Schmidt, Peter Brossart, Natalio Garbi, Gottfried Baier, and Dominik Wolf. "The E3 Ubiquitin Ligase Cbl-b Limits Nascent Th9 Differentiation." Blood 126, no. 23 (December 3, 2015): 2222. http://dx.doi.org/10.1182/blood.v126.23.2222.2222.

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Abstract Introduction: Th9 cells are critical mediators of allergy and anti-cancer immunity. The E3 ubiquitin ligase Cbl-b modulates T cell activation via regulation of the T cell receptor (TCR) activation threshold as well as by inducing TGF-β sensitivity, which is a critical differentiation factor for Th9 differentiation. Even though some evidence shows that Cbl-b impairs Th9 differentiation by targeting IL-4 dependent STAT6 activation, a complete suppression of Th9 differentiation in the absence of both STAT6 and Cbl-b is not achieved, implying the involvement of additional mechanisms. In t

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Molinar-Rode, R., R. J. Smeyne, T. Curran, and J. I. Morgan. "Regulation of proto-oncogene expression in adult and developing lungs." Molecular and Cellular Biology 13, no. 6 (June 1993): 3213–20. http://dx.doi.org/10.1128/mcb.13.6.3213-3220.1993.

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Activation of immediate-early gene expression has been associated with mitogenesis, differentiation, nerve cell depolarization, and recently, terminal differentiation processes and programmed cell death. Previous evidence also suggested that immediate-early genes play a role in the physiology of the lungs (J. I. Morgan, D. R. Cohen, J. L. Hempstead, and T. Curran, Science 237:192-197, 1987). Therefore, we analyzed c-fos expression in adult and developing lung tissues. Seizures elicited by chemoconvulsants induced expression of mRNA for c-fos, c-jun, and junB and Fos-like immunoreactivity in lu

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Molinar-Rode, R., R. J. Smeyne, T. Curran, and J. I. Morgan. "Regulation of proto-oncogene expression in adult and developing lungs." Molecular and Cellular Biology 13, no. 6 (June 1993): 3213–20. http://dx.doi.org/10.1128/mcb.13.6.3213.

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Activation of immediate-early gene expression has been associated with mitogenesis, differentiation, nerve cell depolarization, and recently, terminal differentiation processes and programmed cell death. Previous evidence also suggested that immediate-early genes play a role in the physiology of the lungs (J. I. Morgan, D. R. Cohen, J. L. Hempstead, and T. Curran, Science 237:192-197, 1987). Therefore, we analyzed c-fos expression in adult and developing lung tissues. Seizures elicited by chemoconvulsants induced expression of mRNA for c-fos, c-jun, and junB and Fos-like immunoreactivity in lu

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Dovat, Sinisa, Kirk A. Gilbert, Lidija Petrovic-Dovat, and D. Eugene Rannels. "Targeted identification of zinc finger genes expressed in rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 1 (July 1, 1998): L30—L37. http://dx.doi.org/10.1152/ajplung.1998.275.1.l30.

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Control of alveolar cell growth and differentiation after pneumonectomy likely involves changes in expression of regulatory genes, including those encoding zinc finger (ZF) proteins. To explore this premise, total RNA from the lungs of control and pneumonectomized rats was reverse transcribed; PCRs were performed with degenerate primers corresponding to amino acid sequences HTGEKP and CPECGK(N), which are evolutionarily conserved among ZF genes. Reaction products corresponding to three and four ZF units were isolated and cloned. Sixteen clones were sequenced and found to represent rat lung ZF

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Archavachotikul, Kwanchai, Teriggi J. Ciccone, Mala R. Chinoy, Heber C. Nielsen, and Maryann V. Volpe. "Thyroid hormone affects embryonic mouse lung branching morphogenesis and cellular differentiation." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 3 (March 1, 2002): L359—L369. http://dx.doi.org/10.1152/ajplung.00400.2000.

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Although thyroid hormone (T3) influences epithelial cell differentiation during late fetal lung development, its effects on early lung morphogenesis are unknown. We hypothesized that T3 would alter embryonic lung airway branching and temporal-spatial differentiation of the lung epithelium and mesenchyme. Gestational day 11.5 embryonic mouse lungs were cultured for 72 h in BGJb serum-free medium without or with added T3 (0.2, 2.0, 10.0, or 100 nM). Evaluation of terminal bud counts showed a dose- and time-dependent decrease in branching morphogenesis. Cell proliferation was also significantly d

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Lanzke, Nadine, Mario Menk, Clarissa von Haefen, Lilit Sargsyan, Bianca Scharf, Klaus-Dieter Wernecke, and Claudia D. Spies. "Ethanol-Induced Alterations of T Cells and Cytokines after Surgery in a Murine Infection Model." International Journal of Inflammation 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/1067598.

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Background. Interactions between alcohol, infection, and surgery and their effect on differentiation and functionality of T helper cells are not yet completely understood. We hypothesized that alcohol and surgery disturb differentiation of T helper cells and contribute to an impaired immune response.Methods. Mice were treated with alcohol for two weeks. Saline treatment served as control. Clinical performance and weight were assessed. On day 14, a median laparotomy was performed and animals were challenged withKlebsiella pneumoniaeintranasally. Bacterial load was determined in lungs and blood.

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Beal, Allison, Hilda Ramon, George Worthen, and Paula Oliver. "The E3 ubiquitin ligase adaptor Ndfip1 regulates TH17 differentiation by limiting the production of pro-inflammatory cytokines (175.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 175.11. http://dx.doi.org/10.4049/jimmunol.188.supp.175.11.

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Abstract Ndfip1 is an adaptor that promotes polyubiquitylation by the E3 ubiquitin ligase Itch. Mice that lack either Ndfip1 or Itch develop a severe TH2-mediated inflammatory disease at sites of environmental antigen exposure, including the lung. Here we demonstrate that lungs from Ndfip1-/- mice showed increased numbers of neutrophils and TH17 cells. This was not because Ndfip1-/- T cells are intrinsically biased towards TH17 differentiation. In fact, fewer Ndfip1-/- T cells differentiated into TH17 cells in vitro due to the overproduction of IL-4 production. Rather, TH17 differentiation in

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Bellusci, S., R. Henderson, G. Winnier, T. Oikawa, and B. L. Hogan. "Evidence from normal expression and targeted misexpression that bone morphogenetic protein (Bmp-4) plays a role in mouse embryonic lung morphogenesis." Development 122, no. 6 (June 1, 1996): 1693–702. http://dx.doi.org/10.1242/dev.122.6.1693.

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Epithelial-mesenchymal interactions are critical for the branching and differentiation of the lung, but the mechanisms involved are still unclear. To investigate this problem in mouse embryonic lung, we have studied the temporal and spatial expression of genes implicated in the morphogenesis of other organs. At 11.5 days p.c., hepatocyte nuclear factor-3beta (Hnf-3beta) is expressed uniformly throughout the epithelium, while Wnt-2 expression is confined to the distal mesenchyme. Sonic hedgehog (Shh) transcripts are found throughout the epithelium, with high levels in the distal tips of the ter

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Chang, Liming, Meihua Zhang, Qiheng Chen, Jiongyu Liu, Wei Zhu, and Jianping Jiang. "From Water to Land: The Structural Construction and Molecular Switches in Lungs during Metamorphosis of Microhyla fissipes." Biology 11, no. 4 (March 30, 2022): 528. http://dx.doi.org/10.3390/biology11040528.

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Most anurans must undergo metamorphosis to adapt to terrestrial life. This process enhances the air-breathing ability of the lungs to cope with the change in oxygen medium from water to air. Revealing the structural construction and molecular switches of lung organogenesis is essential to understanding the realization of the air-breathing function. In this study, histology and transcriptomics were conducted in combination to explore these issues in Microhyla fissipes’ lungs during metamorphosis. During the pro-metamorphic phase, histological structural improvement of the alveolar wall is accom

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Anis, Mursalin M., Scott A. Fulton, Scott M. Reba, Clifford V. Harding, and W. Henry Boom. "Modulation of Naive CD4+ T-Cell Responses to an Airway Antigen during Pulmonary Mycobacterial Infection." Infection and Immunity 75, no. 5 (February 12, 2007): 2260–68. http://dx.doi.org/10.1128/iai.01709-06.

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ABSTRACT During pulmonary mycobacterial infection, there is increased trafficking of dendritic cells from the lungs to the draining lymph nodes. We hypothesized that ongoing mycobacterial infection would modulate recruitment and activation of antigen-specific naive CD4+ T cells after airway antigen challenge. BALB/c mice were infected by aerosol with Mycobacterium bovis BCG. At peak bacterial burden in the lungs (4 to 6 weeks postinfection), carboxy-fluorescein diacetate succinimidyl ester-labeled naive ovalbumin-specific DO11.10 T cells were adoptively transferred into infected and uninfected

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Vuckovic, Aline, Susanne Herber-Jonat, Andreas W. Flemmer, Ina M. Ruehl, Carmela Votino, Valérie Segers, Alexandra Benachi та ін. "Increased TGF-β: a drawback of tracheal occlusion in human and experimental congenital diaphragmatic hernia?" American Journal of Physiology-Lung Cellular and Molecular Physiology 310, № 4 (15 лютого 2016): L311—L327. http://dx.doi.org/10.1152/ajplung.00122.2015.

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Survivors of severe congenital diaphragmatic hernia (CDH) present significant respiratory morbidity despite lung growth induced by fetal tracheal occlusion (TO). We hypothesized that the underlying mechanisms would involve changes in lung extracellular matrix and dysregulated transforming growth factor (TGF)-β pathway, a key player in lung development and repair. Pulmonary expression of TGF-β signaling components, downstream effectors, and extracellular matrix targets were evaluated in CDH neonates who died between birth and the first few weeks of life after prenatal conservative management or

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Enomoto, Yasunori, Sayomi Matsushima, Kiyoshi Shibata, Yoichiro Aoshima, Haruna Yagi, Shiori Meguro, Hideya Kawasaki, et al. "LTBP2 is secreted from lung myofibroblasts and is a potential biomarker for idiopathic pulmonary fibrosis." Clinical Science 132, no. 14 (July 31, 2018): 1565–80. http://dx.doi.org/10.1042/cs20180435.

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Although differentiation of lung fibroblasts into α-smooth muscle actin (αSMA)-positive myofibroblasts is important in the progression of idiopathic pulmonary fibrosis (IPF), few biomarkers reflecting the fibrotic process have been discovered. We performed microarray analyses between FACS-sorted steady-state fibroblasts (lineage (CD45, TER-119, CD324, CD31, LYVE-1, and CD146)-negative and PDGFRα-positive cells) from untreated mouse lungs and myofibroblasts (lineage-negative, Sca-1-negative, and CD49e-positive cells) from bleomycin-treated mouse lungs. Amongst several genes up-regulated in the

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Piairo, Paulina, Rute S. Moura, Maria João Baptista, Jorge Correia-Pinto, and Cristina Nogueira-Silva. "STATs in Lung Development: Distinct Early and Late Expression, Growth Modulation and Signaling Dysregulation in Congenital Diaphragmatic Hernia." Cellular Physiology and Biochemistry 45, no. 1 (December 22, 2017): 1–14. http://dx.doi.org/10.1159/000486218.

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Background: Congenital diaphragmatic hernia (CDH) is a life-threatening developmental anomaly, intrinsically combining severe pulmonary hypoplasia and hypertension. During development, signal transducers and activators of transcription (STAT) are utilized to elicit cell growth, differentiation, and survival. Methods: We used the nitrofen-induced CDH rat model. At selected gestational time points, lungs were divided into two experimental groups, i.e., control or CDH. We performed immunohistochemistry and western blotting analysis to investigate the developmental expression profile of the comple

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Meneghetti, A., W. V. Cardoso, J. S. Brody, and M. C. Williams. "Epithelial marker genes are expressed in cultured embryonic rat lung and in vivo with similar spatial and temporal patterns." Journal of Histochemistry & Cytochemistry 44, no. 10 (October 1996): 1173–82. http://dx.doi.org/10.1177/44.10.8813083.

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Explants of embryonic lung are often used to characterize lung growth, bronchial tree pattern, and cell differentiation. Most investigators culture lungs for 3-7 days in defined media lacking, e.g., added growth factors or hormones. If growth and differentiation are comparable to that in vivo, these cultures show considerable promise for identifying developmental regulatory molecules and target genes, and for elucidating molecular responses. We used in situ hybridization and RT-PCR to compare times and sites of expression of mRNAs of six epithelial genes in cultured and uncultured fetal rat lu

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Coleman, C., J. Zhao, M. Gupta, S. Buckley, J. D. Tefft, C. W. Wuenschell, P. Minoo, K. D. Anderson, and D. Warburton. "Inhibition of vascular and epithelial differentiation in murine nitrofen-induced diaphragmatic hernia." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (April 1, 1998): L636—L646. http://dx.doi.org/10.1152/ajplung.1998.274.4.l636.

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Neonates with congenital diaphragmatic hernia (DH) die of pulmonary hypoplasia and persistent pulmonary hypertension. We used immunohistochemical localization of α-smooth muscle actin (α-SMA), platelet endothelial cell adhesion molecule (PECAM)-1, thyroid transcription factor (TTF)-1, surfactant protein (SP) A, SP-C, and competitive RT-PCR quantitation of TTF-1, SP-A, SP-C, and α-SMA mRNA expression to characterize the epithelial and vascular phenotype of lungs from ICR fetal mice with a nitrofen-induced DH. Nitrofen (25 mg) was gavage fed to pregnant mice on day 8 of gestation. Fetal mice wer

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Song, MeiJuan, Qi Lv, XiuWei Zhang, Juan Cao, ShuLi Sun, PeiXin Xiao, ShiKe Hou, et al. "Dynamic Tracking Human Mesenchymal Stem Cells Tropism following Smoke Inhalation Injury in NOD/SCID Mice." Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/1691856.

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Multiple preclinical evidences have supported the potential value of mesenchymal stem cells (MSCs) for treatment of acute lung injury (ALI). However, few studies focus on the dynamic tropism of MSCs in animals with acute lung injury. In this study, we track systemically transplanted human bone marrow-derived mesenchymal stem cells (hBMSCs) in NOD/SCID mice with smoke inhalation injury (SII) through bioluminescence imaging (BLI). The results showed that hBMSCs systemically delivered into healthy NOD/SCID mouse initially reside in the lungs and then partially translocate to the abdomen after 24

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Chapoval, Svetlana P., Ann E. Kelly-Welch, Elizabeth Smith, and Achsah D. Keegan. "Complex role of STAT6 in allergic airway inflammation (39.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S27. http://dx.doi.org/10.4049/jimmunol.178.supp.39.11.

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Abstract STAT6 plays a critical role in Th2 cell differentiation and in allergic lung inflammation. Using a chimeric mouse model, we observed alternative lung pathology in STAT6 KO mice even when WT bone marrow or Th2 cells were provided. Thus, we hypothesized that STAT6 contributes to inflammation in a complex manner. To detail STAT6 function, WT and STAT6 KO mice were subjected to OVA priming and challenges. Broncho-alveolar lavage (BAL) cell composition, lung histology, and FACS analysis of digested lungs were assessed 48h after the last challenge. As expected, eosinophils composed a majori

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Das, Sushant Kumar, Dong Jun Yang, Jin Liang Wang, Chuan Zhang, and Han Feng Yang. "Non-Gaussian diffusion imaging for malignant and benign pulmonary nodule differentiation: a preliminary study." Acta Radiologica 58, no. 1 (July 19, 2016): 19–26. http://dx.doi.org/10.1177/0284185116639763.

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Background Diffusion-weighted imaging (DWI) derived apparent diffusion coefficient (ADC) has demonstrated inconsistent results in pulmonary nodule differentiation. Diffusion kurtosis imaging (DKI), which quantifies non-Gaussian diffusion, is believed to better characterize tissue micro-structure than conventional DWI. Purpose To assess the feasibility of DKI in human lungs and to compare its diagnostic value with standard DWI in differentiating malignancies from benign pulmonary nodules. Material and Methods Thirty-five pulmonary nodules in 32 consecutive patients were evaluated by DKI by usin

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Shan, Lin, Jon C. Aster, Jeffrey Sklar, and Mary E. Sunday. "Notch-1 regulates pulmonary neuroendocrine cell differentiation in cell lines and in transgenic mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (February 2007): L500—L509. http://dx.doi.org/10.1152/ajplung.00052.2006.

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The notch gene family encodes transmembrane receptors that regulate cell differentiation by interacting with surface ligands on adjacent cells. Previously, we demonstrated that tumor necrosis factor-α (TNF) induces neuroendocrine (NE) cell differentiation in H82, but not H526, undifferentiated small cell lung carcinoma lines. We now test the hypothesis that TNF mediates NE cell differentiation in part by altering Notch gene expression. First, using RT-PCR, we determined that TNF treatment of H82, but not H526, transiently decreases notch-1 mRNA in parallel with induction of gene expression for

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Shan, Ming, Han-Fang Cheng, David Corry, and Farrah Kheradmand. "Lung antigen presenting cells in human emphysema (93.21)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 93.21. http://dx.doi.org/10.4049/jimmunol.184.supp.93.21.

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Abstract Exposure to tobacco smoke activates innate and adaptive immune responses that in long-term smokers have been linked to diseases of the lungs, cardiovascular system, joints, and other organs. The destruction of lung tissue that underlies smoking-induced emphysema has been associated with T helper 1 cells that recognize the matrix protein elastin. Factors that result in the development of such autoreactive T cells in smokers remain unknown but are crucial for further understanding the pathogenesis of systemic inflammatory diseases in smokers. Here, we show that lung myeloid dendritic ce

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Yoo, Jae-Kwang, Eleanor Fish, and Thomas Braciale. "A novel mechanism regulating anti-viral humoral response: interplay between IL-21, LAPC and TFH in anti-IAV humoral response. (P6174)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 189.2. http://dx.doi.org/10.4049/jimmunol.190.supp.189.2.

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Abstract The humoral immune response to most respiratory virus infections plays a prominent role in virus clearance and is essential for resistance to reinfection. T follicular helper (TFH) cells are believed to support the development both of a potent primary antibody response and of the germinal center response critical for memory B cell development. Using a model of primary murine influenza A virus (IAV) infection, we demonstrate that a novel APC, the LAPC (Late-activator APC), promotes the TFH response in the draining LNs (dLNs) of the IAV-infected lungs. LAPCs migrate from the infected lu

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Yang, Guang, Maurice D. Hinson, Jessica E. Bordner, Qing S. Lin, Amal P. Fernando, Ping La, Clyde J. Wright та Phyllis A. Dennery. "Silencing hyperoxia-induced C/EBPα in neonatal mice improves lung architecture via enhanced proliferation of alveolar epithelial cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 301, № 2 (серпень 2011): L187—L196. http://dx.doi.org/10.1152/ajplung.00082.2011.

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Postnatal lung development requires proliferation and differentiation of specific cell types at precise times to promote proper alveolar formation. Hyperoxic exposure can disrupt alveolarization by inhibiting cell growth; however, it is not fully understood how this is mediated. The transcription factor CCAAT/enhancer binding protein-α (C/EBPα) is highly expressed in the lung and plays a role in cell proliferation and differentiation in many tissues. After 72 h of hyperoxia, C/EBPα expression was significantly enhanced in the lungs of newborn mice. The increased C/EBPα protein was predominantl

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Rotin, D., B. J. Goldstein, and C. A. Fladd. "Expression of the tyrosine phosphatase LAR-PTP2 is developmentally regulated in lung epithelia." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 3 (September 1, 1994): L263—L270. http://dx.doi.org/10.1152/ajplung.1994.267.3.l263.

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The role of tyrosine kinases in regulating cell proliferation, differentiation, and development has been well documented. In contrast, little is known about the role of protein tyrosine phosphatases (PTPs) in mammalian development. To identify PTPs that may be involved in lung development, we have isolated (by polymerase chain reaction) from rat fetal alveolar epithelial cells a cDNA fragment which was identified as the recently cloned tyrosine phosphatase LAR-PTP2. Analysis of tissue expression of LAR-PTP2 identified a approximately 7.5-kb message in the lung, which is also expressed weakly i

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Liu, Yuru, Ruxana T. Sadikot, Guy R. Adami, Vladimir V. Kalinichenko, Srikanth Pendyala, Viswanathan Natarajan, You-yang Zhao, and Asrar B. Malik. "FoxM1 mediates the progenitor function of type II epithelial cells in repairing alveolar injury induced by Pseudomonas aeruginosa." Journal of Experimental Medicine 208, no. 7 (June 27, 2011): 1473–84. http://dx.doi.org/10.1084/jem.20102041.

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The alveolar epithelium is composed of the flat type I cells comprising 95% of the gas-exchange surface area and cuboidal type II cells comprising the rest. Type II cells are described as facultative progenitor cells based on their ability to proliferate and trans-differentiate into type I cells. In this study, we observed that pneumonia induced by intratracheal instillation of Pseudomonas aeruginosa (PA) in mice increased the expression of the forkhead transcription factor FoxM1 in type II cells coincidentally with the induction of alveolar epithelial barrier repair. FoxM1 was preferentially

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Shrestha, Amrit Kumar, Matthew L. Bettini, Renuka T. Menon, Vashisht Y. N. Gopal, Shixia Huang, Dean P. Edwards, Mohan Pammi, Roberto Barrios, and Binoy Shivanna. "Consequences of early postnatal lipopolysaccharide exposure on developing lungs in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 316, no. 1 (January 1, 2019): L229—L244. http://dx.doi.org/10.1152/ajplung.00560.2017.

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease of infants that is characterized by interrupted lung development. Postnatal sepsis causes BPD, yet the contributory mechanisms are unclear. To address this gap, studies have used lipopolysaccharide (LPS) during the alveolar phase of lung development. However, the lungs of infants who develop BPD are still in the saccular phase of development, and the effects of LPS during this phase are poorly characterized. We hypothesized that chronic LPS exposure during the saccular phase disrupts lung development by mechanisms that promote inflamma

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Zhao, Lihua, Meishuang Li, Zhibao Yin, Limin Lv, Meng Zhou, Yixi Wang, Manling Zhang, et al. "Development of a Lung Vacancy Mouse Model through CRISPR/Cas9-Mediated Deletion of Thyroid Transcription Factor 1 Exon 2." Cells 11, no. 23 (December 1, 2022): 3874. http://dx.doi.org/10.3390/cells11233874.

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A developmental niche vacancy in host embryos is necessary for stem cell complementation-based organ regeneration (SCOG). Thyroid transcription factor 1 (TTF-1) is a tissue-specific transcription factor that regulates the embryonic development and differentiation of the thyroid and, more importantly, lungs; thus, it has been considered as a master gene to knockout in order to develop a lung vacancy host. TTF-1 knockout mice were originally produced by inserting a stop codon in Exon 3 of the gene (E3stop) through embryonic stem cell-based homologous recombination. The main problems of utilizing

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Cohen, Pazit Y., Raphael Breuer, Philip Zisman, and Shulamit B. Wallach-Dayan. "Bleomycin-Treated Chimeric Thy1-Deficient Mice with Thy1-Deficient Myofibroblasts and Thy-Positive Lymphocytes Resolve Inflammation without Affecting the Fibrotic Response." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/942179.

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Lung fibrosis is characterized by abnormal accumulation of fibroblasts in the interstitium of the alveolar space. Two populations of myofibroblasts, distinguished by Thy1 expression, are detected in human and murine lungs. Accumulation of Thy1-negative (Thy1−) myofibroblasts was shown in the lungs of humans with idiopathic pulmonary fibrosis (IPF) and of bleomycin-treated mice. We aimed to identify genetic changes in lung myofibroblasts following Thy1 crosslinking and assess the impact of specific lung myofibroblast Thy1-deficiency, in vivo, in bleomycin-injured mouse lungs. Thy1 increased in

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Clark, Jean C., Jay W. Tichelaar, Susan E. Wert, Nobuyuki Itoh, Anne-Karina T. Perl, Mildred T. Stahlman, and Jeffrey A. Whitsett. "FGF-10 disrupts lung morphogenesis and causes pulmonary adenomas in vivo." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L705—L715. http://dx.doi.org/10.1152/ajplung.2001.280.4.l705.

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Transgenic mice in which fibroblast growth factor (FGF)-10 was expressed in the lungs of fetal and postnatal mice were generated with a doxycycline-inducible system controlled by surfactant protein (SP) C or Clara cell secretory protein (CCSP) promoter elements. Expression of FGF-10 mRNA in the fetal lung caused adenomatous malformations, perturbed branching morphogenesis, and caused respiratory failure at birth. When expressed after birth, FGF-10 caused multifocal pulmonary tumors. FGF-10-induced tumors were highly differentiated papillary and lepidic pulmonary adenomas. Epithelial cells lini

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Colvin, Jennifer S., Andrew C. White, Stephen J. Pratt, and David M. Ornitz. "Lung hypoplasia and neonatal death inFgf9-null mice identify this gene as an essential regulator of lung mesenchyme." Development 128, no. 11 (June 1, 2001): 2095–106. http://dx.doi.org/10.1242/dev.128.11.2095.

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Mammalian lung develops as an evagination of ventral gut endoderm into the underlying mesenchyme. Iterative epithelial branching, regulated by the surrounding mesenchyme, generates an elaborate network of airways from the initial lung bud. Fibroblast growth factors (FGFs) often mediate epithelial-mesenchymal interactions and mesenchymal Fgf10 is essential for epithelial branching in the developing lung. However, no FGF has been shown to regulate lung mesenchyme. In embryonic lung, Fgf9 is detected in airway epithelium and visceral pleura at E10.5, but is restricted to the pleura by E12.5. We r

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Wang, J., B. Campos, M. A. Kaetzel, and J. R. Dedman. "Expression of a calmodulin inhibitor peptide in progenitor alveolar type II cells disrupts lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (August 1, 1996): L245—L250. http://dx.doi.org/10.1152/ajplung.1996.271.2.l245.

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Calmodulin (CaM) is a major intracellular Ca2+ mediator protein involved in cell growth and differentiation. To evaluate calmodulin function in lung, it was necessary to construct a gene that encodes a high-affinity calmodulin binding peptide, since chemically synthesized calmodulin inhibitors lack binding and targeting specificity. This calmodulin inhibitor peptide gene was targeted to type II epithelial cells in transgenic mice using the human surfactant protein C promoter. Neutralization of calmodulin function in progenitor type II epithelial pneumocytes alters epithelial cell growth and di

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Vasilescu, Dragoş M., Christine Klinge, Lars Knudsen, Leilei Yin, Ge Wang, Ewald R. Weibel, Matthias Ochs, and Eric A. Hoffman. "Stereological assessment of mouse lung parenchyma via nondestructive, multiscale micro-CT imaging validated by light microscopic histology." Journal of Applied Physiology 114, no. 6 (March 15, 2013): 716–24. http://dx.doi.org/10.1152/japplphysiol.00855.2012.

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Quantitative assessment of the lung microstructure using standard stereological methods such as volume fractions of tissue, alveolar surface area, or number of alveoli, are essential for understanding the state of normal and diseased lung. These measures are traditionally obtained from histological sections of the lung tissue, a process that ultimately destroys the three-dimensional (3-D) anatomy of the tissue. In comparison, a novel X-ray-based imaging method that allows nondestructive sectioning and imaging of fixed lungs at multiple resolutions can overcome this limitation. Scanning of the

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Ong, Tan, Ler, Gunaratne, Choi, Seet, and Chow. "Insights into Early Recovery from Influenza Pneumonia by Spatial and Temporal Quantification of Putative Lung Regenerating Cells and by Lung Proteomics." Cells 8, no. 9 (August 26, 2019): 975. http://dx.doi.org/10.3390/cells8090975.

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During influenza pneumonia, the alveolar epithelial cells of the lungs are targeted by the influenza virus. The distal airway stem cells (DASCs) and proliferating alveolar type II (AT2) cells are reported to be putative lung repair cells. However, their relative spatial and temporal distribution is still unknown during influenza-induced acute lung injury. Here, we investigated the distribution of these cells, and concurrently performed global proteomic analysis of the infected lungs to elucidate and link the cellular and molecular events during influenza pneumonia recovery. BALB/c mice were in

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Popova, N. V., and L. Rossi. "Nitrosomethylurea disturbs differentiation of mouse embryonic lungs in organ cultures." Russian Journal of Developmental Biology 31, no. 3 (May 2000): 166–70. http://dx.doi.org/10.1007/bf02758821.

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OBERT, MARTIN, STEFANIE HAGNER, GABRIELE A. KROMBACH, SELCUK INAN, and HARALD RENZ. "FRACTAL GEOMETRY ENABLES CLASSIFICATION OF DIFFERENT LUNG MORPHOLOGIES IN A MODEL OF EXPERIMENTAL ASTHMA." Fractals 23, no. 03 (July 31, 2015): 1550024. http://dx.doi.org/10.1142/s0218348x15500243.

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Animal models represent the basis of our current understanding of the pathophysiology of asthma and are of central importance in the preclinical development of drug therapies. The characterization of irregular lung shapes is a major issue in radiological imaging of mice in these models. The aim of this study was to find out whether differences in lung morphology can be described by fractal geometry. Healthy and asthmatic mouse groups, before and after an acute asthma attack induced by methacholine, were studied. In vivo flat-panel-based high-resolution Computed Tomography (CT) was used for mic

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