scholarly journals Characteristics of pulmonary microvascular structure in postnatal yaks

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ruidong Wan ◽  
Ziqi Zhao ◽  
Min Zhao ◽  
Ke Hu ◽  
Jiaxin Zhai ◽  
...  
Keyword(s):  
Microvessel Density ◽  
Lung Development ◽  
Age Groups ◽  
Alveolar Epithelial Cells ◽  
Morphological Observation ◽  
Alveolar Epithelial ◽  
Microvascular Changes ◽  
Transmission Electron ◽  
Oxygen Requirements ◽  
Interalveolar Septum

AbstractYaks are typical plateau-adapted animals, however the microvascular changes and characteristics in their lungs after birth are still unclear. Pulmonary microvasculature characteristics and changes across age groups were analysed using morphological observation and molecular biology detection in yaks aged 1, 30 and 180 days old in addition to adults. Results: Our experiments demonstrated that yaks have fully developed pulmonary alveolar at birth but that interalveolar thickness increased with age. Immunofluorescence observations showed that microvessel density within the interalveolar septum in the yak gradually increased with age. In addition, transmission electron microscopy (TEM) results showed that the blood–air barrier of 1-day old and 30-days old yaks was significantly thicker than that observed at 180-days old and in adults (P < 0.05), which was caused by the thinning of the membrane of alveolar epithelial cells. Furthermore, Vegfa and Epas1 expression levels in 30-day old yaks were the highest in comparison to the other age groups (P < 0.05), whilst levels in adult yaks were the lowest (P < 0.05). The gradual increase in lung microvessel density can effectively satisfy the oxygen requirements of ageing yaks. In addition, these results suggest that the key period of yak lung development is from 30 to 180 days.

Tenascin in rat lung development: in situ localization and cellular sources

1995 ◽  
Vol 269 (4) ◽  
pp. L482-L491 ◽  
Author(s):  
Y. Zhao ◽  
S. L. Young
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Epithelial Cells ◽  
Lung Tissue ◽  
Lung Development ◽  
Alveolar Epithelial Cells ◽  
Lung Fibroblasts ◽  
Rat Lung ◽  
Alveolar Epithelial

Tenascin (TN) is a hexameric extracellular matrix glycoprotein that may play an important role during lung development. TN protein is temporally and spatially restricted during lung organogenesis. The temporo-spatial and cellular expression of TN mRNA in lung remains unclear. Localization of message expression of TN in rat lung tissue was first investigated by using in situ hybridization performed with an antisense RNA probe. TN mRNA was present primarily within the mesenchyme of day 16 gestational age fetal rat lung tissue, whereas immunoreactive TN protein was found along the basement membrane. In postnatal day 3 rat lung tissue, TN mRNA was detected along alveolar septal walls and was concentrated at secondary septal tips. Expression of TN message was consistent with localization of immunoreactive TN protein. Accumulation of TN mRNA in alveolar septal tips suggests that mesenchyme may be the major source of TN mRNA. To investigate the cellular source of TN in rat lung, we studied the expression of TN in cultured rat lung fibroblasts, endothelial cells, and alveolar epithelial cells. Two TN isoforms having molecular mass of 230 and 180 kDa were in conditioned medium and in cellular extracts of lung fibroblasts and endothelial cells. TN was secreted and deposited in the extracellular matrix closely associated with the surface of lung fibroblasts and endothelial cells. Lung alveolar epithelial cells showed undetectable or barely detectable amounts of TN. These studies demonstrated that TN isoforms are expressed not only by lung fibroblasts but also by lung endothelial cells. The unique spatial localization of TN mRNA during lung development and expression of TN by different lung cell types suggested TN may be involved in matrix organization and cell-cell interactions during lung development.

scholarly journals Breakdown of Epithelial Barrier Integrity and Overdrive Activation of Alveolar Epithelial Cells in the Pathogenesis of Acute Respiratory Distress Syndrome and Lung Fibrosis

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Shigehisa Yanagi ◽  
Hironobu Tsubouchi ◽  
Ayako Miura ◽  
Nobuhiro Matsumoto ◽  
Masamitsu Nakazato
Keyword(s):  
Epithelial Cells ◽  
Lung Development ◽  
Lung Fibrosis ◽  
Initial Step ◽  
Alveolar Epithelial Cells ◽  
Developmental Pathway ◽  
Barrier Integrity ◽  
Alveolar Epithelial ◽  
Triggering Events ◽  
Fibrotic Lung Diseases

Individual alveolar epithelial cells (AECs) collaboratively form a tight barrier between atmosphere and fluid-filled tissue to enable normal gas exchange. The tight junctions of AECs provide intercellular sealing and are integral to the maintenance of the AEC barrier integrity. Disruption and failure of reconstitution of AEC barrier result in catastrophic consequences, leading to alveolar flooding and subsequent devastating fibrotic scarring. Recent evidences reveal that many of the fibrotic lung diseases involve AECs both as a frequent target of injury and as a driver of ongoing pathological processes. Aberrantly activated AECs express most of the growth factors and chemokines responsible for the proliferation, migration, and activation of fibroblasts. Current evidences suggest that AECs may acquire overdrive activation in the initial step of fibrosis by several mechanisms, including abnormal recapitulation of the developmental pathway, defects of the molecules essential for epithelial integrity, and acceleration of aging-related properties. Among these initial triggering events, epithelial Pten, a multiple phosphatase that negatively regulates the PI3K/Akt pathway and is crucial for lung development, is essential for the prevention of alveolar flooding and lung fibrosis through the regulation of AEC barrier integrity after injury. Reestablishment of AEC barrier integrity also involves the deployment of specialized stem/progenitor cells.

Expression of the tyrosine phosphatase LAR-PTP2 is developmentally regulated in lung epithelia

1994 ◽  
Vol 267 (3) ◽  
pp. L263-L270 ◽  
Author(s):  
D. Rotin ◽  
B. J. Goldstein ◽  
C. A. Fladd
Keyword(s):  
Epithelial Cells ◽  
Lung Development ◽  
Tyrosine Phosphatase ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Adult Type ◽  
Alveolar Epithelial

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 in brain, and an alternatively spliced approximately 6.0-kb message (LAR-PTP2B) expressed in brain. In the fetal lung, LAR-PTP2 was preferentially expressed in lung epithelial (but not fibroblast) cells grown briefly in primary culture, and its expression was tightly regulated during lung development, peaking at 20 days of gestational age (term = 22 days), when mature alveolar type II epithelium first appears. Accordingly, immunoblot analysis revealed high expression of endogenous LAR-PTP2 protein in alveolar epithelial cells from 21-day gestation fetuses. LAR-PTP2 was also expressed in lungs of newborn rats, but transcripts (and protein) were barely detectable in adult lungs and in the nonproliferating adult alveolar type II cells. Interestingly, expression was restored in the transformed adult type II-like A549 cells. These results suggest that LAR-PTP2 may play a role in the proliferation and/or differentiation of epithelial cells during lung development.

Glucuronyl C5-epimerase is crucial for epithelial cell maturation during embryonic lung development

Glycobiology ◽  
2020 ◽  
Author(s):  
Hao Cui ◽  
Xiaowen Cheng ◽  
Tahira Batool ◽  
Xiao Zhang ◽  
Jin-Ping Li
Keyword(s):  
Lung Development ◽  
Surfactant Protein ◽  
Branching Morphogenesis ◽  
Sulfated Polysaccharide ◽  
Alveolar Epithelial Cells ◽  
Type I ◽  
Alveolar Epithelial ◽  
Neonatal Lethality ◽  
Key Enzyme ◽  
Distal Lung

Abstract Glucuronyl C5-epimerase (Hsepi) is a key enzyme in the biosynthesis of heparan sulfate that is a sulfated polysaccharide expressed on the cell surface and in the extracellular matrix of alveolar walls and blood vessels. Targeted interruption of the Hsepi gene, Glce, in mice resulted in neonatal lethality, which is most likely due to lung atelectasis. In this study, we examined the potential mechanisms behind the defect in lung development. Histological analysis of the lungs from embryos revealed no difference in the morphology between wild-type and mutant animals up to E16.5. This suggests that the initial events leading to formation of the lung primordium and branching morphogenesis are not disturbed. However, the distal lung of E17.5–18.5 mutants is still populated by epithelial tubules, lacking the typical saccular structural characteristic of a normal E17.5 lung. Immunostaining revealed strong signals of surfactant protein-C, but a weaker signal of T1α in the mutant lungs in comparison to WT littermates, suggesting differentiation of type I alveolar epithelial cells (AT1) is impaired. One of the parameters contributed to the failure of AT1 maturation is reduced vascularization in the developing lungs.

Migration and gelatinases in cultured fetal, adult, and hyperoxic alveolar epithelial cells

2001 ◽  
Vol 281 (2) ◽  
pp. L427-L434 ◽  
Author(s):  
S. Buckley ◽  
B. Driscoll ◽  
W. Shi ◽  
K. Anderson ◽  
D. Warburton
Keyword(s):  
Growth Factor ◽  
Lung Development ◽  
Alveolar Epithelial Cell ◽  
Lung Cancer Cell Line ◽  
Alveolar Epithelial Cells ◽  
Migratory Activity ◽  
Alveolar Epithelial ◽  
Control Adult

Alveolar epithelial cell (AEC) migration mediated by matrix metalloproteinases (MMPs) is required for lung development and repair after injury such as hyperoxia. Of specific interest in lung remodeling are the gelatinases, which are upregulated in AEC after hyperoxia. We correlated migration and gelatinase production in AEC cultured from fetal, adult, and hyperoxic rats. Fetal AEC (19–20 days) had higher MMP-2 and MMP-9 gelatinase expression than adult AEC, with fivefold higher MMP-9 activity, and were migratory through gelatin, responding to epidermal growth factor, keratinocyte growth factor, and fibroblast growth factor-10. MMP-2 and MMP-9 expression and migratory activity could be detected from the time of plating. In contrast, adult AEC migrated and expressed MMP-2 and MMP-9 proteins only after 48 h of culture. AEC from hyperoxic rats were significantly more migratory through gelatin than control adult AEC, with significantly higher MMP-9 activity. Inhibition of MMPs with doxycycline reduced the migration of AEC from hyperoxic rats to the level of control adult AEC. Fibronectin-cultured “hyperoxic” AEC acquired a temporary capacity for migration similar to the A549 lung cancer cell line, which is both highly migratory and invasive and is derived from the AEC type 2 lineage. These data suggest that MMP activity is associated with a migratory phenotype in fetal, hyperoxic, and transformed AEC in vitro, and we speculate that MMPs may play a key mechanistic role in AEC migration in vivo during lung development and repair.

scholarly journals Research article expression of surfactant protein-A and D, and CD9 in lungs of 1 and 30 day old foals

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Tara Bocking ◽  
Laura Johnson ◽  
Amitoj Singh ◽  
Atul Desai ◽  
Gurpreet Kaur Aulakh ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Protein A ◽  
Age Groups ◽  
Surfactant Protein ◽  
Alveolar Epithelial Cells ◽  
Western Blots ◽  
Alveolar Epithelial ◽  
Research Article ◽  
Bronchiolar Epithelium ◽  
Alveolar Septa

Abstract Background Respiratory diseases are a major cause of morbidity and mortality in the horses of all ages including foals. There is limited understanding of the expression of immune molecules such as tetraspanins and surfactant proteins (SP) and the regulation of the immune responses in the lungs of the foals. Therefore, the expression of CD9, SP-A and SP-D in foal lungs was examined. Results Lungs from one day old (n = 6) and 30 days old (n = 5) foals were examined for the expression of CD9, SP-A, and SP-D with immunohistology and Western blots. Western blot data showed significant increase in the amount of CD9 protein (p = 0.0397) but not of SP-A and SP-D at 30 days of age compared to one day. Immunohistology detected CD9 in the alveolar septa and vascular endothelium but not the bronchiolar epithelium in the lungs of the foals in both age groups. SP-A and SP-D expression was localized throughout the alveolar septa including type II alveolar epithelial cells and the vascular endothelium of the lungs in all the foals. Compared to one day old foals, the expression of SP-A and SP-D appeared to be increased in the bronchiolar epithelium of 30 day old foals. Pulmonary intravascular macrophages were also positive for SP-A and SP-D in 30 days old foals and these cells are not developed in the day old foals. Conclusions This is the first data on the expression of CD9, SP-A and SP-D in the lungs of foals.

scholarly journals miR-184 mediates hyperoxia-induced injury by targeting cell death and angiogenesis signalling pathways in the developing lung

2020 ◽  
pp. 1901789 ◽  
Author(s):  
Dilip Shah ◽  
Karmyodh Sandhu ◽  
Pragnya Das ◽  
Zubair H. Aghai ◽  
Sture Andersson ◽  
...  
Keyword(s):  
Lung Development ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Alveolar Epithelial Cells ◽  
Therapeutic Interventions ◽  
Normal Lung ◽  
Alveolar Epithelial ◽  
Fetal Mice ◽  
And Function ◽  
Neonatal Lungs

MicroRNAs (miRs) have been shown to disrupt normal lung development and function by interrupting alveolarization and vascularisation leading to development of bronchopulmonary dysplasia (BPD). Here we report that miR-184 has a critical role in the induction of BPD phenotype characterised by abnormal alveolarization and pulmonary angiogenesis in the developing lung. We observed an increased expression of miR-184 in BPD clinical specimens: tracheal aspirates (TA), human neonatal lungs with BPD and in fetal human lung Type II alveolar epithelial cells (TIIAECs) exposed to hyperoxia. Consistent with this, we also detected an upregulated miR-184-3p expression in whole lungs, in freshly isolated TIIAECs from lungs of hyperoxia-induced experimental BPD mice and in fetal mice lung TIIAECs exposed to hyperoxia. We demonstrate that overexpression of miR-184-3p exacerbates the BPD pulmonary phenotype, while downregulation of miR-184-3p expression ameliorated the BPD phenotype and also improved respiratory function. We identified miR-184 specific targets: platelet-derived growth factor-beta (Pdgf-β) and friend of Gata 2 (Fog2), also known as zinc finger protein family member (Zfpm2), and show that they are critically involved in pulmonary alveolarization and angiogenesis. Using cell-based luciferase analysis, downregulation of miR-184-3p expression and gene knockdown of miR-184-3p targets Pdgf-β and Fog2 in lung TIIAECs and endothelial cells, we mechanistically show that inhibition of miR-184-3p expression improves pulmonary alveolarization by regulating PDGF-β/AKT/Foxo3/Bax, Bcl2 signalling and enhances angiogenesis by Fog2/VEGF-A/Angiopoietin-1/2 pathway. Collectively, these data suggest that the use of miR-184-3p specific inhibitors may act as novel therapeutic interventions to control the adverse effects of hyperoxia on lung development and function.

scholarly journals Autophagy Activation by Rapamycin Before Hypoxia-Reoxygenation Reduces Endoplasmic Reticulum Stress in Alveolar Epithelial Cells

2017 ◽  
Vol 41 (1) ◽  
pp. 79-90 ◽  
Author(s):  
Tao Fan ◽  
Lei Chen ◽  
Zhixin Huang ◽  
Wei Wang ◽  
Boyou Zhang ◽  
...  
Keyword(s):  
Western Blot ◽  
Lung Diseases ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Beclin 1 ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Promising Agent ◽  
Transmission Electron ◽  
Hypoxia Reoxygenation

Background: To determine potential effects of autophagy activation on hypoxia-reoxygenation (H/R) induced damage of a rat alveolar epithelial cell line. Methods: CCL149 cells were subjected to autophagy agonist (rapamycin, Rap), autophagy inhibitor (3-methyladenine, 3-MA) or PBS for 1 h before H/R treatment for 2 h, 4 h and 6 h. The optimal concentration of Rap (150 nM, 200 nM and 250 nM) or 3-MA (5 mM, 10 mM and 15 mM) was obtained from MTT assay. Autophagy was determined by fluorescence microscopy of eRFP-LC3 positive cells, transmission electron microscopy of autophagosome, western blot of LC3, AMPK, Beclin-1, HDAC6 and p62 proteins. Endoplasmatic reticulum stress was indicated by detecting expressions of BIP, XBP-1 and CHOP via western blot. Results: Rap at concentration of 250 nM before H/R increased the autophagy formation with more eRFP-LC3 positive cells and higher expressions of LC3-II, Beclin-1, HDAC6 and p62, but lower expressions of BIP, XBP-1 and CHOP in H/R treated CCL149. This effect seemed to be still obvious after H/R exposure for 6 h. The contrary results were obtained by treatment with 5 mM 3-MA. Conclusion: Rap might be a promising agent before mechanical ventilation or reperfusion to prevent re-damage in hypoxia related lung diseases.

Development of 200 kV Scanning-Transmission Electron Microscope

1974 ◽  
Vol 32 ◽  
pp. 410-411
Author(s):  
H. Koike ◽  
S. Sakurai ◽  
K. Ueno ◽  
M. Watanabe
Keyword(s):  
Electron Microscopy ◽  
Electron Microscope ◽  
Scanning Transmission Electron Microscope ◽  
The Other ◽  
Morphological Observation ◽  
Magnetic Domains ◽  
Transmission Electron ◽  
Scanning Transmission ◽  
Backscattered Electron ◽  
Increasing Demand

In recent years, there has been increasing demand for higher voltage SEMs, in the field of surface observation, especially that of magnetic domains, dislocations, and electron channeling patterns by backscattered electron microscopy. On the other hand, the resolution of the CTEM has now reached 1 ∼ 2Å, and several reports have recently been made on the observation of atom images, indicating that the ultimate goal of morphological observation has beem nearly achieved.

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