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Journal articles on the topic 'Lung development'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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1

Pronych, Scott, and Richard Wassersug. "Lung use and development in Xenopus laevis tadpoles." Canadian Journal of Zoology 72, no. 4 (April 1, 1994): 738–43. http://dx.doi.org/10.1139/z94-099.

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Shortly after hatching, Xenopus laevis tadpoles fill their lungs with air. We examined the role played by early lung use in these organisms, since they are able to respire with both their lungs and their gills. We investigated the effect on X. laevis development when the larvae were prevented from inflating their lungs, and whether early lung use influenced the size of the lungs or the tadpole's ability to metamorphose. Tadpoles that were denied access to air had lungs one-half the size of those of controls. This difference in lung size was too large to be explained merely by a stretching of the lung due to inflation. The longer tadpoles were denied access to air, the longer they took to metamorphose, and their probability of completing metamorphosis diminished. One tadpole raised throughout its larval life without access to air successfully metamorphosed but had abnormal, solidified lungs and an enlarged heart. Collectively, these experiments demonstrate that early lung use in tadpoles is important in determining both ultimate lung size and the probability of successfully metamorphosing. Lung use during early larval development in X. laevis is not absolutely necessary for survival through metamorphosis, but its absence severely handicaps growth.

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2

Mullassery, Dhanya, and Nicola P. Smith. "Lung development." Seminars in Pediatric Surgery 24, no. 4 (August 2015): 152–55. http://dx.doi.org/10.1053/j.sempedsurg.2015.01.011.

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3

Chen, Ling, and Graeme R. Zosky. "Lung development." Photochemical & Photobiological Sciences 16, no. 3 (2017): 339–46. http://dx.doi.org/10.1039/c6pp00278a.

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Recent equivocal results in high profile randomised controlled trials suggest that the impact of vitamin D deficiency on lung development is complex. In this narrative review we summarise our current understanding of the link between UV exposure, vitamin D and lung development.

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4

Massaro, Donald, and Gloria DeCarlo Massaro. "Lung Development, Lung Function, and Retinoids." New England Journal of Medicine 362, no. 19 (May 13, 2010): 1829–31. http://dx.doi.org/10.1056/nejme1002366.

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5

Shi, Wei, Saverio Bellusci, and David Warburton. "Lung Development and Adult Lung Diseases." Chest 132, no. 2 (August 2007): 651–56. http://dx.doi.org/10.1378/chest.06-2663.

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6

Copland, Ian, and Martin Post. "Lung development and fetal lung growth." Paediatric Respiratory Reviews 5 (January 2004): S259—S264. http://dx.doi.org/10.1016/s1526-0542(04)90049-8.

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7

Stenmark, Kurt R., and Sarah A. Gebb. "Lung Vascular Development." American Journal of Respiratory Cell and Molecular Biology 28, no. 2 (February 2003): 133–37. http://dx.doi.org/10.1165/rcmb.f259.

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Stovin, P. G. "Early lung development." Thorax 40, no. 6 (June 1, 1985): 401–4. http://dx.doi.org/10.1136/thx.40.6.401.

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9

Shibuya, Soichi, Jessica Allen-Hyttinen, Paolo De Coppi, and Federica Michielin. "In vitro models of fetal lung development to enhance research into congenital lung diseases." Pediatric Surgery International 37, no. 5 (March 31, 2021): 561–68. http://dx.doi.org/10.1007/s00383-021-04864-8.

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AbstractPurposeThis paper aims to build upon previous work to definitively establish in vitro models of murine pseudoglandular stage lung development. These can be easily translated to human fetal lung samples to allow the investigation of lung development in physiologic and pathologic conditions.MethodsLungs were harvested from mouse embryos at E12.5 and cultured in three different settings, i.e., whole lung culture, mesenchyme-free epithelium culture, and organoid culture. For the whole lung culture, extracted lungs were embedded in Matrigel and incubated on permeable filters. Separately, distal epithelial tips were isolated by firstly removing mesothelial and mesenchymal cells, and then severing the tips from the airway tubes. These were then cultured either in branch-promoting or self-renewing conditions.ResultsCultured whole lungs underwent branching morphogenesis similarly to native lungs. Real-time qPCR analysis demonstrated expression of key genes essential for lung bud formation. The culture condition for epithelial tips was optimized by testing different concentrations of FGF10 and CHIR99021 and evaluating branching formation. The epithelial rudiments in self-renewing conditions formed spherical 3D structures with homogeneous Sox9 expression.ConclusionWe report efficient protocols for ex vivo culture systems of pseudoglandular stage mouse embryonic lungs. These models can be applied to human samples and could be useful to paediatric surgeons to investigate normal lung development, understand the pathogenesis of congenital lung diseases, and explore novel therapeutic strategies.

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Wanczyk, Heather, Todd Jensen, Daniel J. Weiss, and Christine Finck. "Advanced single-cell technologies to guide the development of bioengineered lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 320, no. 6 (June 1, 2021): L1101—L1117. http://dx.doi.org/10.1152/ajplung.00089.2021.

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Lung transplantation remains the only viable option for individuals suffering from end-stage lung failure. However, a number of current limitations exist including a continuing shortage of suitable donor lungs and immune rejection following transplantation. To address these concerns, engineering a decellularized biocompatible lung scaffold from cadavers reseeded with autologous lung cells to promote tissue regeneration is being explored. Proof-of-concept transplantation of these bioengineered lungs into animal models has been accomplished. However, these lungs were incompletely recellularized with resulting epithelial and endothelial leakage and insufficient basement membrane integrity. Failure to repopulate lung scaffolds with all of the distinct cell populations necessary for proper function remains a significant hurdle for the progression of current engineering approaches and precludes clinical translation. Advancements in 3D bioprinting, lung organoid models, and microfluidic device and bioreactor development have enhanced our knowledge of pulmonary lung development, as well as important cell-cell and cell-matrix interactions, all of which will help in the path to a bioengineered transplantable lung. However, a significant gap in knowledge of the spatiotemporal interactions between cell populations as well as relative quantities and localization within each compartment of the lung necessary for its proper growth and function remains. This review will provide an update on cells currently used for reseeding decellularized scaffolds with outcomes of recent lung engineering attempts. Focus will then be on how data obtained from advanced single-cell analyses, coupled with multiomics approaches and high-resolution 3D imaging, can guide current lung bioengineering efforts for the development of fully functional, transplantable lungs.

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Moghieb, Ahmed, Geremy Clair, Hugh D. Mitchell, Joseph Kitzmiller, Erika M. Zink, Young-Mo Kim, Vladislav Petyuk, et al. "Time-resolved proteome profiling of normal lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 315, no. 1 (July 1, 2018): L11—L24. http://dx.doi.org/10.1152/ajplung.00316.2017.

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Biochemical networks mediating normal lung morphogenesis and function have important implications for ameliorating morbidity and mortality in premature infants. Although several transcript-level studies have examined normal lung development, corresponding protein-level analyses are lacking. Here we performed proteomics analysis of murine lungs from embryonic to early adult ages to identify the molecular networks mediating normal lung development. We identified 8,932 proteins, providing a deep and comprehensive view of the lung proteome. Analysis of the proteomics data revealed discrete modules and the underlying regulatory and signaling network modulating their expression during development. Our data support the cell proliferation that characterizes early lung development and highlight responses of the lung to exposure to a nonsterile oxygen-rich ambient environment and the important role of lipid (surfactant) metabolism in lung development. Comparison of dynamic regulation of proteomic and recent transcriptomic analyses identified biological processes under posttranscriptional control. Our study provides a unique proteomic resource for understanding normal lung formation and function and can be freely accessed at Lungmap.net.

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12

Rannels, S. R., S. L. Rannels, J. G. Sneyd, and E. G. Loten. "Fetal lung development in rats with a glycogen storage disorder." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 6 (June 1, 1991): L419—L427. http://dx.doi.org/10.1152/ajplung.1991.260.6.l419.

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A New Zealand strain of rats (NZR/Mh) is unable to mobilize liver glycogen due to a deficiency of phosphorylase b kinase. Affected homozygous rats (gsd/gsd) were used to assess the developmental relationship between lung glycogen loss and surfactant phospholipid and protein biosynthesis. Phosphorylase a and phosphorylase b kinase activities were negligible in gsd/gsd fetal lungs compared with controls from gestational day (D18) until postnatal day 1 (D + 1). At D20, tissue glycogen content was 158 +/- 5 and 181 +/- 6 mumol/g lung for control and gsd/gsd, respectively. Control rats mobilized 84% of their lung glycogen by D + 1, whereas the gsd/gsd strain retained 70–80% of D19–20 levels. This apparent fall in gsd/gsd glycogen per gram lung was due to an increase in cellular protein and size. Thus, in controls, total glycogen per lung decreased 65% from D20 to D + 1, whereas DNA doubled. In contrast, gsd/gsd lung growth resulted in a doubling of total lung glycogen, whereas the glycogen-to-DNA ratio remained constant. A lack of cellular glycogenolysis was confirmed by electron microscopy where gsd/gsd type II cells remained large and glycogen-rich over the entire perinatal interval. The potential for glycogen breakdown by a lysosomal alpha-amyloglucosidase in gsd/gsd lungs was estimated in tissue homogenates, whereas rates of hydrolysis of glycogen or p-nitrophenylglucoside were significant and equal to controls at all ages tested. Incorporation of [14C]choline into phosphatidylcholine (PC) of incubated lung slices increased 1.7-fold in control lungs from D20–D21. Over the same interval, PC synthesis in gsd/gsd lungs was 40% lower and did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

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13

Portas, Laura, Miguel Pereira, Seif O. Shaheen, Annah B. Wyss, Stephanie J. London, Peter G. J. Burney, Matthew Hind, Charlotte H. Dean, and Cosetta Minelli. "Lung Development Genes and Adult Lung Function." American Journal of Respiratory and Critical Care Medicine 202, no. 6 (September 15, 2020): 853–65. http://dx.doi.org/10.1164/rccm.201912-2338oc.

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14

Collins, Brendan J., Wolfram Kleeberger, and Douglas W. Ball. "Notch in lung development and lung cancer." Seminars in Cancer Biology 14, no. 5 (October 2004): 357–64. http://dx.doi.org/10.1016/j.semcancer.2004.04.015.

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15

Kalinichenko, Vladimir V., Galina A. Gusarova, Il-Man Kim, Brian Shin, Helena M. Yoder, Jean Clark, Alexander M. Sapozhnikov, Jeffrey A. Whitsett, and Robert H. Costa. "Foxf1 haploinsufficiency reduces Notch-2 signaling during mouse lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 3 (March 2004): L521—L530. http://dx.doi.org/10.1152/ajplung.00212.2003.

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The forkhead box (Fox) f1 transcription factor is expressed in the mouse splanchnic (visceral) mesoderm, which contributes to development of the liver, gallbladder, lung, and intestinal tract. Pulmonary hemorrhage and peripheral microvascular defects were found in approximately half of the newborn Foxf1(+/-) mice, which expressed low levels of lung Foxf1 mRNA [low- Foxf1(+/-) mice]. Microvascular development was normal in the surviving newborn high- Foxf1(+/-) mice, which compensated for pulmonary Foxf1 haploinsufficiency and expressed wild-type Foxf1 levels. To identify expression of genes regulated by Foxf1, we used Affymetrix microarrays to determine embryonic lung RNAs influenced by Foxf1 haploinsufficiency. Embryonic Foxf1(+/-) lungs exhibited diminished expression of hepatocyte growth factor receptor c-Met, myosin VI, the transcription factors SP-3, BMI-1, ATF-2, and glucocorticoid receptor, and cell cycle inhibitors p53, p21Cip1, retinoblastoma, and p107. Furthermore, Notch-2 signaling was decreased in embryonic Foxf1(+/-) lungs, as evidenced by significantly reduced levels of the Notch-2 receptor and the Notch-2 downstream target hairy enhancer of split-1. The severity of the Notch-2-signaling defect in 18-day postcoitus Foxf1(+/-) lungs correlated with Foxf1 mRNA levels. Disruption of pulmonary Notch-2 signaling continued in newborn low- Foxf1(+/-) mice, which died of lung hemorrhage and failed to compensate for Foxf1 haploinsufficiency. In contrast, in newborn high- Foxf1(+/-) lungs, Notch-2 signaling was restored to the level found in wild-type mice, which was associated with normal microvascular formation and survival. Foxf1 haploinsufficiency disrupted pulmonary expression of genes in the Notch-2-signaling pathway and resulted in abnormal development of lung microvasculature.

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Zhao, Yun, Stephen L. Young, J. Clarke McIntosh, Mark P. Steele, and Robert Silbajoris. "Ontogeny and localization of TGF-β type I receptor expression during lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 6 (June 1, 2000): L1231—L1239. http://dx.doi.org/10.1152/ajplung.2000.278.6.l1231.

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Transforming growth factor (TGF)-β is a family of multifunctional cytokines controlling cell growth, differentiation, and extracellular matrix deposition in the lung. The biological effects of TGF-β are mediated by type I (TβR-I) and II (TβR-II) receptors. Our previous studies show that the expression of TβR-II is highly regulated in a spatial and temporal fashion during lung development. In the present studies, we investigated the temporal-spatial pattern and cellular expression of TβR-I during lung development. The expression level of TβR-I mRNA in rat lung at different embryonic and postnatal stages was analyzed by Northern blotting. TβR-I mRNA was expressed in fetal rat lungs in early development and then decreased as development proceeded. The localization of TβR-I in fetal and postnatal rat lung tissues was investigated by using in situ hybridization performed with an antisense RNA probe. TβR-I mRNA was present in the mesenchyme and epithelium of gestational day 14 rat lungs. An intense TβR-I signal was observed in the epithelial lining of the developing bronchi. In gestational day 16 lungs, the expression of TβR-I mRNA was increased in the mesenchymal tissue. The epithelium in both the distal and proximal bronchioles showed a similar level of TβR-I expression. In postnatal lungs, TβR-I mRNA was detected in parenchymal tissues and blood vessels. We further studied the expression of TβR-I in cultured rat lung cells. TβR-I was expressed by cultured rat lung fibroblasts, microvascular endothelial cells, and alveolar epithelial cells. These studies demonstrate a differential regulation and localization of TβR-I that is different from that of TβR-II during lung development. TβR-I, TβR-II, and TGF-β isoforms exhibit distinct but overlapping patterns of expression during lung development. This implies a distinct role for TβR-I in mediating TGF-β signal transduction during lung development.

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17

Xi, Jinxiang, Brendan Walfield, Xiuhua April Si, and Alexander A. Bankier. "Lung Physiological Variations in COVID-19 Patients and Inhalation Therapy Development for Remodeled Lungs." SciMedicine Journal 3, no. 3 (September 1, 2021): 198–208. http://dx.doi.org/10.28991/scimedj-2021-0303-1.

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In response to the unmet need for effective treatments for symptomatic patients, research efforts of inhaled therapy for COVID-19 patients have been pursued since the pandemic began. However, inhalation drug delivery to the lungs is sensitive to the lung anatomy and physiology, which can be significantly altered due to the viral infection. The ensued ventilation heterogeneity will change distribution and thus dosimetry of inhaled medications, rendering previous correlations concepts? of pulmonary drug delivery in healthy lungs less reliable. In this study, we first reviewed the recent developments of inhaled therapeutics and vaccines, as well as the latest knowledge of the lung structural variations documented by CT of COVID-19 patients' lungs. We then quantified the volume ratios of the poorly aerated lungs and non-aerated lungs in eight COVID-19 patients, which ranged 2-8% and 0.5-3%, respectively. The need to consider the diseased lung physiologies in estimating pulmonary delivery was emphasized. Diseased lung geometries with varying lesion sites and complexities were reconstructed using Statistical Shape Modeling (SSM). A new segmentation method was applied that could generate patient-specific lung geometries with an increased number of branching generations. The synergy of the CT-based lung segmentation and SSM-based airway variation showed promise for developing representative COVID-infected lung morphological models and investigating inhalation therapeutics in COVID-19 patients. Doi: 10.28991/SciMedJ-2021-0303-1 Full Text: PDF

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18

Kovar, Jana, Karen E. Willet, Alison Hislop, and Peter D. Sly. "Impact of postnatal glucocorticoids on early lung development." Journal of Applied Physiology 98, no. 3 (March 2005): 881–88. http://dx.doi.org/10.1152/japplphysiol.00486.2004.

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Inhaled glucocorticoid treatment during the first 2 yr of life is controversial because this is a period of major structural remodeling of the lung. Rabbits received aerosolized budesonide (Bud; 250 μg/ml) or injected dexamethasone (Dex; 0.05 mg·ml−1·kg−1) between 1 and 5 wk of age. Treatment with Bud caused specific growth retardation of the lung. Dex but not Bud affected the mechanical properties of the lung parenchyma, when corrected for lung volume. Small peripheral airway walls in both glucocorticoid groups were thinner and had fewer alveolar attachment points with greater distance between attachments than controls, but collagen content was not affected by glucocorticoids. Dex led to reduced body weight, lung volume, alveolar number, and surface area. The alveolar size and number and elastin content, when related to lung volume, was not affected by Bud, suggesting normal structural development but inhibition of total growth. Arterial wall thickness and diameter were affected by Bud. This study demonstrates that developing lungs are sensitive to inhaled glucocorticoids. As such, the use of glucocorticoids in young infants and children should be monitored with caution and only the lowest doses that yield significant clinical improvement should be used.

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Kim, Jae Yeol, Jong Sung Park, Derek Strassheim, Ivor Douglas, Fernando Diaz del Valle, Karim Asehnoune, Sanchayita Mitra, et al. "HMGB1 contributes to the development of acute lung injury after hemorrhage." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 5 (May 2005): L958—L965. http://dx.doi.org/10.1152/ajplung.00359.2004.

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High mobility group box 1 (HMGB1) is a novel late mediator of inflammatory responses that contributes to endotoxin-induced acute lung injury and sepsis-associated lethality. Although acute lung injury is a frequent complication of severe blood loss, the contribution of HMGB1 to organ system dysfunction in this setting has not been investigated. In this study, HMGB1 was detected in pulmonary endothelial cells and macrophages under baseline conditions. After hemorrhage, in addition to positively staining endothelial cells and macrophages, neutrophils expressing HMGB1 were present in the lungs. HMGB1 expression in the lung was found to be increased within 4 h of hemorrhage and then remained elevated for more than 72 h after blood loss. Neutrophils appeared to contribute to the increase in posthemorrhage pulmonary HMGB1 expression since no change in lung HMGB1 levels was found after hemorrhage in mice made neutropenic with cyclophosphamide. Plasma concentrations of HMGB1 also increased after hemorrhage. Blockade of HMGB1 by administration of anti-HMGB1 antibodies prevented hemorrhage-induced increases in nuclear translocation of NF-κB in the lungs and pulmonary levels of proinflammatory cytokines, including keratinocyte-derived chemokine, IL-6, and IL-1β. Similarly, both the accumulation of neutrophils in the lung as well as enhanced lung permeability were reduced when anti-HMGB1 antibodies were injected after hemorrhage. These results demonstrate that hemorrhage results in increased HMGB1 expression in the lungs, primarily through neutrophil sources, and that HMGB1 participates in hemorrhage-induced acute lung injury.

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20

Schuger, Lucia. "Laminins in Lung Development." Experimental Lung Research 23, no. 2 (January 1997): 119–29. http://dx.doi.org/10.3109/01902149709074025.

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21

Mariani, Thomas J., Stephanie Sandefur, and Richard A. Pierce. "Elastin in Lung Development." Experimental Lung Research 23, no. 2 (January 1997): 131–45. http://dx.doi.org/10.3109/01902149709074026.

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22

Bush, Andrew. "Lung Development and Aging." Annals of the American Thoracic Society 13, Supplement_5 (December 2016): S438—S446. http://dx.doi.org/10.1513/annalsats.201602-112aw.

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23

Chytil, Frank. "Retinoids in lung development." FASEB Journal 10, no. 9 (July 1996): 986–92. http://dx.doi.org/10.1096/fasebj.10.9.8801181.

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24

Lick, S. D., S. K. Alpard, P. Montoya, D. J. Deyo, J. B. Jayroe, and J. B. Zwischenberger. "ARTIFICIAL LUNG PROTOTYPE DEVELOPMENT." ASAIO Journal 46, no. 2 (March 2000): 230. http://dx.doi.org/10.1097/00002480-200003000-00319.

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25

Schittny, Johannes C. "Development of the lung." Cell and Tissue Research 367, no. 3 (January 31, 2017): 427–44. http://dx.doi.org/10.1007/s00441-016-2545-0.

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26

Joshi, Suchita, and Sailesh Kotecha. "Lung growth and development." Early Human Development 83, no. 12 (December 2007): 789–94. http://dx.doi.org/10.1016/j.earlhumdev.2007.09.007.

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Hislop, A. A. "Advances in lung development." Paediatric Respiratory Reviews 11 (January 2010): S10. http://dx.doi.org/10.1016/s1526-0542(10)70013-0.

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Chinoy, Mala R. "Lung growth and development." Frontiers in Bioscience 8, no. 4 (2003): d392–415. http://dx.doi.org/10.2741/974.

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Raghu, Srikanti. "Disorders of lung development." Journal of Dr. NTR University of Health Sciences 4, no. 2 (2015): 65. http://dx.doi.org/10.4103/2277-8632.158571.

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Stephenson, J. "Smog Slows Lung Development." JAMA: The Journal of the American Medical Association 284, no. 19 (November 15, 2000): 2445—c—2445. http://dx.doi.org/10.1001/jama.284.19.2445-c.

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Stephenson, Joan. "Smog Slows Lung Development." JAMA 284, no. 19 (November 15, 2000): 2445. http://dx.doi.org/10.1001/jama.284.19.2445-jha00011-4-1.

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Maritz, Gert S. "Nicotine and lung development." Birth Defects Research Part C: Embryo Today: Reviews 84, no. 1 (2008): 45–53. http://dx.doi.org/10.1002/bdrc.20116.

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Khoshgoo, Naghmeh, Ramin Kholdebarin, Barbara Maria Iwasiow, and Richard Keijzer. "MicroRNAs and lung development." Pediatric Pulmonology 48, no. 4 (December 31, 2012): 317–23. http://dx.doi.org/10.1002/ppul.22739.

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Li, Jiao, and Nan Tang. "Empowering human lung development." Cell Stem Cell 30, no. 1 (January 2023): 5–6. http://dx.doi.org/10.1016/j.stem.2022.12.012.

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Ardini-Poleske, Maryanne E., Robert F. Clark, Charles Ansong, James P. Carson, Richard A. Corley, Gail H. Deutsch, James S. Hagood, et al. "LungMAP: The Molecular Atlas of Lung Development Program." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 5 (November 1, 2017): L733—L740. http://dx.doi.org/10.1152/ajplung.00139.2017.

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The National Heart, Lung, and Blood Institute is funding an effort to create a molecular atlas of the developing lung (LungMAP) to serve as a research resource and public education tool. The lung is a complex organ with lengthy development time driven by interactive gene networks and dynamic cross talk among multiple cell types to control and coordinate lineage specification, cell proliferation, differentiation, migration, morphogenesis, and injury repair. A better understanding of the processes that regulate lung development, particularly alveologenesis, will have a significant impact on survival rates for premature infants born with incomplete lung development and will facilitate lung injury repair and regeneration in adults. A consortium of four research centers, a data coordinating center, and a human tissue repository provides high-quality molecular data of developing human and mouse lungs. LungMAP includes mouse and human data for cross correlation of developmental processes across species. LungMAP is generating foundational data and analysis, creating a web portal for presentation of results and public sharing of data sets, establishing a repository of young human lung tissues obtained through organ donor organizations, and developing a comprehensive lung ontology that incorporates the latest findings of the consortium. The LungMAP website ( www.lungmap.net ) currently contains more than 6,000 high-resolution lung images and transcriptomic, proteomic, and lipidomic human and mouse data and provides scientific information to stimulate interest in research careers for young audiences. This paper presents a brief description of research conducted by the consortium, database, and portal development and upcoming features that will enhance the LungMAP experience for a community of users.

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Liao, Zhengchang, Xiaocheng Zhou, Ziqiang Luo, Huiyi Huo, Mingjie Wang, Xiaohe Yu, Chuanding Cao, Ying Ding, Zeng Xiong, and Shaojie Yue. "N-Methyl-D-aspartate Receptor Excessive Activation Inhibited Fetal Rat Lung DevelopmentIn VivoandIn Vitro." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/5843981.

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Background. Intrauterine hypoxia is a common cause of fetal growth and lung development restriction. Although N-methyl-D-aspartate receptors (NMDARs) are distributed in the postnatal lung and play a role in lung injury, little is known about NMDAR’s expression and role in fetal lung development.Methods. Real-time PCR and western blotting analysis were performed to detect NMDARs between embryonic days (E) 15.5 and E21.5 in fetal rat lungs. NMDAR antagonist MK-801’s influence on intrauterine hypoxia-induced retardation of fetal lung development was testedin vivo, and NMDA’s direct effect on fetal lung development was observed using fetal lung organ culturein vitro.Results. All seven NMDARs are expressed in fetal rat lungs. Intrauterine hypoxia upregulated NMDARs expression in fetal lungs and decreased fetal body weight, lung weight, lung-weight-to-body-weight ratio, and radial alveolar count, whereas MK-801 alleviated this damagein vivo.In vitroexperiments showed that NMDA decreased saccular circumference and area per unit and downregulated thyroid transcription factor-1 and surfactant protein-C mRNA expression.Conclusions. The excessive activation of NMDARs contributed to hypoxia-induced fetal lung development retardation and appropriate blockade of NMDAR might be a novel therapeutic strategy for minimizing the negative outcomes of prenatal hypoxia on lung development.

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Patrone, Cesare, Tobias N. Cassel, Katarina Pettersson, Yun-Shang Piao, Guojun Cheng, Paolo Ciana, Adriana Maggi, Margaret Warner, Jan-Åke Gustafsson, and Magnus Nord. "Regulation of Postnatal Lung Development and Homeostasis by Estrogen Receptor β." Molecular and Cellular Biology 23, no. 23 (December 1, 2003): 8542–52. http://dx.doi.org/10.1128/mcb.23.23.8542-8552.2003.

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ABSTRACT Estrogens have well-documented effects on lung development and physiology. However, the classical estrogen receptor α (ERα) is undetectable in the lung, and this has left many unanswered questions about the mechanism of estrogen action in this organ. Here we show, both in vivo and in vitro, that ERβ is abundantly expressed and biologically active in the lung. Comparisons of lungs from wild-type mice and mice with an inactivated ERβ gene (ERβ−/−) revealed decreased numbers of alveoli in adult female ERβ−/− mice and findings suggesting deficient alveolar formation as well as evidence of surfactant accumulation. Platelet-derived growth factor A (PDGF-A) and granulocyte-macrophage colony-stimulating factor (GM-CSF), key regulators of alveolar formation and surfactant homeostasis, respectively, were decreased in lungs of adult female ERβ−/− mice, and direct transcriptional regulation of these genes by ERβ was demonstrated. This suggests that estrogens act via ERβ in the lung to modify PDGF-A and GM-CSF expression. These results provide a potential molecular mechanism for the gender differences in alveolar structure observed in the adult lung and establish ERβ as a previously unknown regulator of postnatal lung development and homeostasis.

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Haberthür, David, Eveline Yao, Sébastien F. Barré, Tiziana P. Cremona, Stefan A. Tschanz, and Johannes C. Schittny. "Pulmonary acini exhibit complex changes during postnatal rat lung development." PLOS ONE 16, no. 11 (November 8, 2021): e0257349. http://dx.doi.org/10.1371/journal.pone.0257349.

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Pulmonary acini represent the functional gas-exchanging units of the lung. Due to technical limitations, individual acini cannot be identified on microscopic lung sections. To overcome these limitations, we imaged the right lower lobes of instillation-fixed rat lungs from postnatal days P4, P10, P21, and P60 at the TOMCAT beamline of the Swiss Light Source synchrotron facility at a voxel size of 1.48 μm. Individual acini were segmented from the three-dimensional data by closing the airways at the transition from conducting to gas exchanging airways. For a subset of acini (N = 268), we followed the acinar development by stereologically assessing their volume and their number of alveoli. We found that the mean volume of the acini increases 23 times during the observed time-frame. The coefficients of variation dropped from 1.26 to 0.49 and the difference between the mean volumes of the fraction of the 20% smallest to the 20% largest acini decreased from a factor of 27.26 (day 4) to a factor of 4.07 (day 60), i.e. shows a smaller dispersion at later time points. The acinar volumes show a large variation early in lung development and homogenize during maturation of the lung by reducing their size distribution by a factor of 7 until adulthood. The homogenization of the acinar sizes hints at an optimization of the gas-exchange region in the lungs of adult animals and that acini of different size are not evenly distributed in the lungs. This likely leads to more homogeneous ventilation at later stages in lung development.

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Yang, Yu-Chen S. H., Hsiu-Chu Chou, Yun-Ru Liu, and Chung-Ming Chen. "Uteroplacental Insufficiency Causes Microbiota Disruption and Lung Development Impairment in Growth-Restricted Newborn Rats." Nutrients 14, no. 20 (October 19, 2022): 4388. http://dx.doi.org/10.3390/nu14204388.

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Preclinical studies have demonstrated that intrauterine growth retardation (IUGR) is associated with reduced lung development during the neonatal period and infancy. Uteroplacental insufficiency (UPI), affecting approximately 10% of human pregnancies, is the most common cause of IUGR. This study investigated the effects of UPI on lung development and the intestinal microbiota and correlations in newborn rats with IUGR, using bilateral uterine artery ligation to induce UPI. Maternal fecal samples were collected on postnatal day 0. On postnatal days 0 and 7, lung and intestinal microbiota samples were collected from the left lung and the lower gastrointestinal tract. The right lung was harvested for histological assessment and Western blot analysis. Results showed that UPI through bilateral uterine artery ligation did not alter the maternal gut microbiota. IUGR impaired lung development and angiogenesis in newborn rats. Moreover, on postnatal day 0, the presence of Acinetobacter and Delftia in the lungs and Acinetobacter and Nevskia in the gastrointestinal tract was negatively correlated with lung development. Bacteroides in the lungs and Rodentibacter and Romboutsia in the gastrointestinal tract were negatively correlated with lung development on day 7. UPI may have regulated lung development and angiogenesis through the modulation of the newborn rats’ intestinal and lung microbiota.

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40

Sozo, Foula, Megan J. Wallace, Valerie A. Zahra, Caitlin E. Filby, and Stuart B. Hooper. "Gene expression profiling during increased fetal lung expansion identifies genes likely to regulate development of the distal airways." Physiological Genomics 24, no. 2 (February 2006): 105–13. http://dx.doi.org/10.1152/physiolgenomics.00148.2005.

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Growth and development of the fetal lungs is critically dependent on the degree to which the lungs are expanded by liquid; increases in fetal lung expansion accelerate lung growth, whereas reductions in lung expansion cause lung growth to cease. The mechanisms mediating expansion-induced lung growth are unknown but likely include alterations in the expression of genes that regulate lung cell proliferation. Our aim was to isolate and identify genes that are up- or downregulated by increased fetal lung expansion. In chronically catheterized fetal sheep at 126 days gestational age (GA), the left lung was expanded for 36 h, while the right lung remained at a control level of expansion. Subtraction hybridization was used to isolate genes differentially expressed between the left and right lungs. Screening of ∼6,000 clones identified 1,138 and 118 cDNA fragments that were up- and downregulated by increased lung expansion, respectively. Northern blot analyses in separate groups of control fetuses and fetuses exposed to increased lung expansion were used to verify differential expression. Increased fetal lung expansion upregulated heat shock protein 47, thrombospondin-1, TROP2, tropoelastin, and tubulin-α3 in fetal lung tissue by ∼200–300%; connective tissue growth factor and cysteine-rich angiogenic inducer 61 were increased by 20–30%. Genes downregulated by increased fetal lung expansion included CCSP-related protein-1, elongation factor-1α and vitamin D3 upregulated protein 1. We conclude that an increase in fetal lung expansion differentially regulates the expression of numerous genes in lung tissue, many of which have important putative roles in lung development, while the functions of others are currently unknown.

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Riccio, Veronica Del, Minke Van Tuyl, and Martin Post. "Apoptosis in Lung Development and Neonatal Lung Injury." Pediatric Research 55, no. 2 (February 2004): 183–89. http://dx.doi.org/10.1203/01.pdr.0000103930.93849.b2.

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42

Driscoll, Barbara, Susan Buckley, Kim Chi Bui, Kathryn D. Anderson, and David Warburton. "Telomerase in alveolar epithelial development and repair." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (December 1, 2000): L1191—L1198. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1191.

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Telomerase expression and activity were examined in the developing lung and in the adult lung during repair after injury. Both whole lung tissue and primary cultures of type 2 alveolar epithelial cells (AEC2) isolated from fetal and adult rodents were analyzed for 1) telomerase expression by immunohistochemistry and 2) telomerase activity with a telomerase repeat amplification protocol. We found that telomerase was expressed in a temporally regulated manner in fetal lung through the late stages of gestation, with peak expression just before birth. Expression persisted for a brief period in neonates, then decreased to nearly undetectable levels by postnatal day 9. Telomerase expression and activity were reinduced in normally quiescent adult lung by in vivo treatment with hyperoxia. In populations of AEC2 isolated from both developing and repairing lungs, telomerase expression and activity showed a strong correlation with the proliferation marker proliferating cell nuclear antigen. It has been suggested that telomerase expression and activity are hallmarks of stem or progenitor cells. Our observations suggest that a telomerase-positive subpopulation is present within the general AEC2 population. Telomerase may act as a marker for the proliferative status of this subpopulation.

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43

Rasky, Andrew, David M. Habiel, Susan Morris, Matthew Schaller, Bethany B. Moore, Sem Phan, Steven L. Kunkel, Martin Phillips, Cory Hogaboam, and Nicholas W. Lukacs. "Inhibition of the stem cell factor 248 isoform attenuates the development of pulmonary remodeling disease." American Journal of Physiology-Lung Cellular and Molecular Physiology 318, no. 1 (January 1, 2020): L200—L211. http://dx.doi.org/10.1152/ajplung.00114.2019.

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Stem cell factor (SCF) and its receptor c-kit have been implicated in inflammation, tissue remodeling, and fibrosis. Ingenuity Integrated Pathway Analysis of gene expression array data sets showed an upregulation of SCF transcripts in idiopathic pulmonary fibrosis (IPF) lung biopsies compared with tissue from nonfibrotic lungs that are further increased in rapid progressive disease. SCF248, a cleavable isoform of SCF, was abundantly and preferentially expressed in human lung fibroblasts and fibrotic mouse lungs relative to the SCF220 isoform. In fibroblast-mast cell coculture studies, blockade of SCF248 using a novel isoform-specific anti-SCF248 monoclonal antibody (anti-SCF248), attenuated the expression of COL1A1, COL3A1, and FN1 transcripts in cocultured IPF but not normal lung fibroblasts. Administration of anti-SCF248 on days 8 and 12 after bleomycin instillation in mice significantly reduced fibrotic lung remodeling and col1al, fn1, acta2, tgfb, and ccl2 transcript expression. In addition, bleomycin increased numbers of c-kit+ mast cells, eosinophils, and ILC2 in lungs of mice, whereas they were not significantly increased in anti-SCF248-treated animals. Finally, mesenchymal cell-specific deletion of SCF significantly attenuated bleomycin-mediated lung fibrosis and associated fibrotic gene expression. Collectively, these data demonstrate that SCF is upregulated in diseased IPF lungs and blocking SCF248 isoform significantly ameliorates fibrotic lung remodeling in vivo suggesting that it may be a therapeutic target for fibrotic lung diseases.

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44

Srinivasan, Hari B., Stephen M. Vogel, Dharmapuri Vidyasagar, and Asrar B. Malik. "Protective effect of lung inflation in reperfusion-induced lung microvascular injury." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 3 (March 1, 2000): H951—H957. http://dx.doi.org/10.1152/ajpheart.2000.278.3.h951.

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We used the isolated-perfused rat lung model to study the influence of pulmonary ventilation and surfactant instillation on the development of postreperfusion lung microvascular injury. We hypothesized that the state of lung inflation during ischemia contributes to the development of the injury during reperfusion. Pulmonary microvascular injury was assessed by continuously monitoring the wet lung weight and measuring the vessel wall125I-labeled albumin (125I-albumin) permeability-surface area product ( PS). Sprague-Dawley rats ( n = 24) were divided into one control group and five experimental groups ( n = 4 rats per group). Control lungs were continuously ventilated with 20% O2and perfused for 120 min. All lung preparations were ventilated with 20% O2before the ischemia period and during the reperfusion period. The various groups differed only in the ventilatory gas mixtures used during the flow cessation: group I, ventilated with 20% O2; group II, ventilated with 100% N2; group III, lungs remained collapsed and unventilated; group IV, same as group IIIbut pretreated with surfactant (4 ml/kg) instilled into the airway; and group V, same as group III but saline (4 ml/kg) was instilled into the airway. Control lungs remained isogravimetric with baseline125I-albumin PS value of 4.9 ± 0.3 × 10−3ml ⋅ min−1⋅ g wet lung wt−1. Lung wet weight in group III increased by 1.45 ± 0.35 g and albumin PSincreased to 17.7 ± 2.3 × 10−3, indicating development of vascular injury during the reperfusion period. Lung wet weight and albumin PS did not increase in groups I and II, indicating that ventilation by either 20% O2or 100% N2prevented vascular injury. Pretreatment of collapsed lungs with surfactant before cessation of flow also prevented the vascular injury, whereas pretreatment with saline vehicle had no effect. These results indicate that the state of lung inflation during ischemia (irrespective of gas mixture used) and supplementation of surfactant prevent reperfusion-induced lung microvascular injury.

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Barrios, R., A. Pardo, C. Ramos, M. Montano, R. Ramirez, and M. Selman. "Upregulation of acidic fibroblast growth factor during development of experimental lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 2 (August 1, 1997): L451—L458. http://dx.doi.org/10.1152/ajplung.1997.273.2.l451.

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Fibroblast proliferation and extracellular matrix accumulation are crucial in the pathogenesis of lung fibrosis. Fibroblast growth factor (FGF)-1 participates in both processes, but its role in lung fibrogenesis has not been evaluated. We analyzed the expression of FGF-1 and of FGF receptor (FGFR) in a model of lung fibrosis induced in rats with paraquat plus hyperoxia. Experimental and control animals were killed at 48 h and 2, 4, and 8 wk, and the lungs were studied by in situ hybridization, immunohistochemistry, and Northern blot. In normal lungs, scattered macrophages contained FGF-1. In contrast, at all times examined, the injured lungs exhibited FGF-1 transcript and the immunoreactive protein, mainly in alveolar epithelial cells and macrophages. In advanced fibrotic lesions, fibroblasts also appeared stained. Northern blot corroborated the upregulation of FGF-1 mRNA. FGFR was not observed in normal lungs, whereas it was strongly increased in the damaged lungs and was virtually immunolocalized in the same cell types as the corresponding ligand. These findings suggest that FGF-1 and FGFR are actively synthesized during the development of pulmonary fibrosis.

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46

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 inflammation and prevent optimal lung development and repair. Wild-type C57BL6J mice were intraperitoneally administered 3, 6, or 10 mg/kg of LPS or a vehicle once daily on postnatal days (PNDs) 3–5. The lungs were collected for proteomic and genomic analyses and flow cytometric detection on PND6. The impact of LPS on lung development, cell proliferation, and apoptosis was determined on PND7. Finally, we determined differences in the LPS effects between the saccular and alveolar lungs. LPS decreased the survival and growth rate and lung development in a dose-dependent manner. These effects were associated with a decreased expression of proteins regulating cell proliferation and differentiation and increased expression of those mediating inflammation. While the lung macrophage population of LPS-treated mice increased, the T-regulatory cell population decreased. Furthermore, LPS-induced inflammatory and apoptotic response and interruption of cell proliferation and alveolarization was greater in alveolar than in saccular lungs. Collectively, the data support our hypothesis and reveal several potential therapeutic targets for sepsis-mediated BPD in infants.

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Ghorayeb, Sleiman R., Matthew J. Blitz, and Luis A. Bracero. "Recent developments in fetal lung ultrasound." Journal of the Acoustical Society of America 151, no. 4 (April 2022): A111. http://dx.doi.org/10.1121/10.0010816.

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Fetal ultrasound has been employed for years to help evaluate fetal growth and development and to monitor pregnancy. Furthermore, fetal lung maturity has been assessed pre-natally by examination of the amniotic fluid, usually obtained by transabdominal amniocentesis, for lecithin, lecithin/sphingomyelin ratio, or “P” factor (fluorescent polarization measurement for lipids.) Quantitative ultrasound texture analysis of fetal lung has been proposed in previous studies as a promising noninvasive method to predict fetal lung maturity, fetal lung hypoplasia, and neonatal respiratory morbidity. This technique utilizes standard fetal lung images, which are easily obtained by sonographers during routine ultrasound examinations. Additional information then can be extracted from these images by applying quantitative processing methods that characterize the tissue. This presentation discusses how to differentiate preterm (<37 weeks of gestation) from term (≥37 weeks of gestation) fetal lungs by quantitative texture analysis of ultrasound images. This quantification is based on the extent of heterogeneity associated with lung maturity by employing a unique, novel noninvasive technique to determine the Heterogeneity Index (HI) in ultrasound images. The HI values are then compared in sonograms of immature lungs with mature lungs. Conceptual advances for the possibility of integrating this technology in handheld ultraportable systems for point-of-care ultrasound (POCUS) are also presented.

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48

Berg, Tove, Lukas Didon, and Magnus Nord. "Ectopic expression of C/EBPα in the lung epithelium disrupts late lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 4 (October 2006): L683—L693. http://dx.doi.org/10.1152/ajplung.00497.2005.

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The lung develops from the endoderm through a process of branching morphogenesis. This process is highly active during the pseudoglandular stage of lung development and continues into the canalicular stage, resulting in the formation of terminal sacs. CCAAT/enhancer binding proteins (C/EBPs) are transcription factors regulating central aspects of differentiation and proliferation. We report here the developmental expression of C/EBPα, -β, and -δ in the lung. C/EBPα exhibits a dynamic expression pattern and is first detected during the late pseudoglandular stage. At this stage, expression is observed in a subset of epithelial cells in the distal parts of the branching tubules. The expression of C/EBPα is confined to nonproliferating cells. To examine the role of C/EBPα in lung development, we generated transgenic mice ectopically expressing C/EBPα in the lung epithelium using the human surfactant protein C promoter. Lungs from these mice were of normal size but exhibited a phenotype characterized by fewer and larger developing epithelial tubules, indicating that the branching process was affected. No effects on overall proliferation or cellular differentiation were observed. When this phenotype was compared with that of mice carrying a targeted mutation of the Cebpa gene, the Cebpa −/− mice exhibited a similar developmental phenotype. In conclusion, our results show a role for C/EBPα in lung development and suggest a function in the later stages of lung branching morphogenesis.

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van Tuyl, Minke, Jason Liu, Freek Groenman, Ross Ridsdale, Robin N. N. Han, Vikram Venkatesh, Dick Tibboel, and Martin Post. "Iroquoisgenes influence proximo-distal morphogenesis during rat lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 4 (April 2006): L777—L789. http://dx.doi.org/10.1152/ajplung.00293.2005.

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Lung development is a highly regulated process directed by mesenchymal-epithelial interactions, which coordinate the temporal and spatial expression of multiple regulatory factors required for proper lung formation. The Iroquois homeobox ( Irx) genes have been implicated in the patterning and specification of several Drosophila and vertebrate organs, including the heart. Herein, we investigated whether the Irx genes play a role in lung morphogenesis. We found that Irx1– 3 and Irx5 expression was confined to the branching lung epithelium, whereas Irx4 was not expressed in the developing lung. Antisense knockdown of all pulmonary Irx genes together dramatically decreased distal branching morphogenesis and increased distention of the proximal tubules in vitro, which was accompanied by a reduction in surfactant protein C-positive epithelial cells and an increase in β-tubulin IV and Clara cell secretory protein positive epithelial structures. Transmission electron microscopy confirmed the proximal phenotype of the epithelial structures. Furthermore, antisense Irx knockdown resulted in loss of lung mesenchyme and abnormal smooth muscle cell formation. Expression of fibroblast growth factors (FGF) 1, 7, and 10, FGF receptor 2, bone morphogenetic protein 4, and Sonic hedgehog (Shh) were not altered in lung explants treated with antisense Irx oligonucleotides. All four Irx genes were expressed in Shh- and Gli2-deficient murine lungs. Collectively, these results suggest that Irx genes are involved in the regulation of proximo-distal morphogenesis of the developing lung but are likely not linked to the FGF, BMP, or Shh signaling pathways.

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Shifren, Adrian, Anthony G. Durmowicz, Russell H. Knutsen, Eiichi Hirano, and Robert P. Mecham. "Elastin protein levels are a vital modifier affecting normal lung development and susceptibility to emphysema." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 3 (March 2007): L778—L787. http://dx.doi.org/10.1152/ajplung.00352.2006.

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Cigarette smoking is the strongest risk factor for emphysema. However, sensitivity to cigarette smoke-induced emphysema is highly variable, and numerous genetic and environmental factors are thought to mitigate lung response to injury. We report that the quantity of functional elastin in the lung is an important modifier of both lung development and response to injury. In mice with low levels of elastin, lung development is adversely affected, and mice manifest with congenital emphysema. Animals with intermediate elastin levels exhibit normal alveolar structure but develop worse emphysema than normal mice following cigarette smoke exposure. Mechanical testing demonstrates that lungs with low levels of elastin experience greater tissue strains for any given tissue stress compared with wild-type lungs, implying that force-mediated propagation of lung injury through alveolar wall failure may worsen the emphysema after an initial enzymatic insult. Our findings suggest that quantitative deficiencies in elastin predispose to smoke-induce emphysema in animal models and suggest that humans with altered levels of functional elastin could have relatively normal lung function while being more susceptible to smoke-induced lung injury.

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