Talk:Respiratory System Development - Revision history

Z8600021 at 16:09, 24 August 2023

2023-08-24T16:09:06Z

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			==2023==

			Bronchial tree of the human embryo: Examination based on a mammalian model

			Sena Fujii 1 , Taiga Muranaka 1 , Jun Matsubayashi 2 , Shigehito Yamada 1 3 , Akio Yoneyama 4 , Tetsuya Takakuwa 1
			Affiliations expand
			PMID: 37602519 DOI: 10.1111/joa.13946
			Abstract

			The symmetry of the right and left bronchi, proposed in a previous comparative anatomical study as the basic model of the mammalian bronchial tree, was examined to determine if it applied to the embryonic human bronchial tree. Imaging data of 41 human embryo specimens at Carnegie stages (CS) 16-23 (equivalent to 6-8 weeks after fertilization) belonging to the Kyoto collection were obtained using phase-contrast X-ray computed tomography. Three-dimensional bronchial trees were then reconstructed from these images. Bronchi branching from both main bronchi were labeled as dorsal, ventral, medial, or lateral systems based on the branching position with numbering starting cranially. The length from the tracheal bifurcation to the branching point of the labeled bronchus was measured, and the right-to-left ratio of the same labeled bronchus in both lungs was calculated. In both lungs, the human embryonic bronchial tree showed symmetry with an alternating pattern of dorsal and lateral systems up to segmental bronchus B9 as the basic shape, with a more peripheral variation. This pattern is similar to that described in adult human lungs. Bronchial length increased with the CS in all labeled bronchi, whereas the right-to-left ratio was constant at approximately 1.0. The data demonstrated that the prototype of the human adult bronchial branching structure is formed and maintained in the embryonic stage. The morphology and branching position of all lobar bronchi and B6, B8, B9, and the subsegmental bronchus of B10 may be genetically determined. On the other hand, no common structures between individual embryos were found in the peripheral branches after the subsegmental bronchus of B10, suggesting that branch formation in this region is influenced more by environmental factors than by genetic factors.

	==2019==		==2019==

Z8600021 at 23:42, 8 October 2019

2019-10-08T23:42:46Z

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	==2019==		==2019==

			===Transcriptional control of lung alveolar type 1 cell development and maintenance by NK homeobox 2-1===

			Gas exchange in the lung relies on passive diffusion of oxygen and carbon dioxide across an extraordinarily thin epithelium that is nearly entirely made of the poorly understood alveolar type 1 (AT1) cell. Our study shows that all AT1 cells express and require NK homeobox 2-1 (Nkx2-1) for their development and maintenance. Nkx2-1 mutant AT1 cells lose their characteristic molecular and cellular features and transform toward a gastrointestinal fate, highlighting remarkable plasticity of an otherwise terminally differentiated cell type. This work establishes NKX2-1 as the first overarching factor in the AT1 cell transcriptional hierarchy and paves the way for unraveling not only the unique biology of AT1 cells but also cell type-specific roles of a lineage transcription factor.


			https://www.pnas.org/content/116/41/20545.abstract?etoc

			See 2012 review paper [https://cshperspectives.cshlp.org/content/4/5/a008318.full Signaling Networks Regulating Development of the Lower Respiratory Tract]


	===New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay===		===New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay===

Z8600021 at 05:58, 19 February 2019

2019-02-19T05:58:18Z

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	==2018==		==2018==


	===How high resolution 3-dimensional imaging changes our understanding of postnatal lung development===		===How high resolution 3-dimensional imaging changes our understanding of postnatal lung development===
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	Alveolar; Bronchi; ESC; Lung disease; Progenitor; Stem cell; iPSC		Alveolar; Bronchi; ESC; Lung disease; Progenitor; Stem cell; iPSC
	PMID: 30111617 PMCID: PMC6124546 DOI: 10.1242/dev.163485		PMID: 30111617 PMCID: PMC6124546 DOI: 10.1242/dev.163485


			===Spatial and temporal changes in extracellular elastin and laminin distribution during lung alveolar development===
			Sci Rep. 2018 May 29;8(1):8334. doi: 10.1038/s41598-018-26673-1.

			Luo Y1, Li N1, Chen H1, Fernandez GE1, Warburton D1,2, Moats R1,3, Mecham RP4, Krenitsky D5, Pryhuber GS5, Shi W6,7.

			Abstract
			Lung alveolarization requires precise coordination of cell growth with extracellular matrix (ECM) synthesis and deposition. The role of extracellular matrices in alveogenesis is not fully understood, because prior knowledge is largely extrapolated from two-dimensional structural analysis. Herein, we studied temporospatial changes of two important ECM proteins, laminin and elastin that are tightly associated with alveolar capillary growth and lung elastic recoil respectively, during both mouse and human lung alveolarization. By combining protein immunofluorescence staining with two- and three-dimensional imaging, we found that the laminin network was simplified along with the thinning of septal walls during alveogenesis, and more tightly associated with alveolar endothelial cells in matured lung. In contrast, elastin fibers were initially localized to the saccular openings of nascent alveoli, forming a ring-like structure. Then, throughout alveolar growth, the number of such alveolar mouth ring-like structures increased, while the relative ring size decreased. These rings were interconnected via additional elastin fibers. The apparent patches and dots of elastin at the tips of alveolar septae found in two-dimensional images were cross sections of elastin ring fibers in the three-dimension. Thus, the previous concept that deposition of elastin at alveolar tips drives septal inward growth may potentially be conceptually challenged by our data.

			PMID: 29844468 PMCID: PMC5974327 DOI: 10.1038/s41598-018-26673-1

	===PDGF-A signaling is required for secondary alveolar septation and controls epithelial proliferation in the developing lung===		===PDGF-A signaling is required for secondary alveolar septation and controls epithelial proliferation in the developing lung===

Z8600021 at 05:56, 19 February 2019

2019-02-19T05:56:27Z

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	PMID: 30390117 PMCID: PMC6267404 DOI: 10.1007/s00418-018-1749-7		PMID: 30390117 PMCID: PMC6267404 DOI: 10.1007/s00418-018-1749-7


			===Understanding alveolarization to induce lung regeneration===

			Respir Res. 2018 Aug 6;19(1):148. doi: 10.1186/s12931-018-0837-5.

			Rodríguez-Castillo JA1, Pérez DB1, Ntokou A1, Seeger W1,2, Morty RE1,2, Ahlbrecht K3,4.

			Abstract
			BACKGROUND:
			Gas exchange represents the key physiological function of the lung, and is dependent upon proper formation of the delicate alveolar structure. Malformation or destruction of the alveolar gas-exchange regions are key histopathological hallmarks of diseases such as bronchopulmonary dysplasia (BPD), chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis; all of which are characterized by perturbations to the alveolo-capillary barrier structure. Impaired gas-exchange is the primary initial consequence of these perturbations, resulting in severe clinical symptoms, reduced quality of life, and death. The pronounced morbidity and mortality associated with malformation or destruction of alveoli underscores a pressing need for new therapeutic concepts. The re-induction of alveolarization in diseased lungs is a new and exciting concept in a regenerative medicine approach to manage pulmonary diseases that are characterized by an absence of alveoli.

			MAIN TEXT:
			Mechanisms of alveolarization first need to be understood, to identify pathways and mediators that may be exploited to drive the induction of alveolarization in the diseased lung. With this in mind, a variety of candidate cell-types, pathways, and molecular mediators have recently been identified. Using lineage tracing approaches and lung injury models, new progenitor cells for epithelial and mesenchymal cell types - as well as cell lineages which are able to acquire stem cell properties - have been discovered. However, the underlying mechanisms that orchestrate the complex process of lung alveolar septation remain largely unknown.

			CONCLUSION:
			While important progress has been made, further characterization of the contributing cell-types, the cell type-specific molecular signatures, and the time-dependent chemical and mechanical processes in the developing, adult and diseased lung is needed in order to implement a regenerative therapeutic approach for pulmonary diseases.

			KEYWORDS:
			Alveolarization; Neo-alveolarization; Regeneration
			PMID: 30081910 PMCID: PMC6090695 DOI: 10.1186/s12931-018-0837-5

	===Development of the pulmonary pleura with special reference to the lung surface morphology: a study using human fetuses===		===Development of the pulmonary pleura with special reference to the lung surface morphology: a study using human fetuses===

Z8600021 at 05:26, 19 February 2019

2019-02-19T05:26:09Z

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			==2019==

			===New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay===

			Microsc Microanal. 2019 Feb 14:1-17. doi: 10.1017/S1431927619000059. [Epub ahead of print]

			Mokhtar DM1, Hussein MT1, Hussein MM1, Abd-Elhafez EA1, Kamel G1.

			Abstract
			This study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood-air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air-blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air-blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air-blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.

			KEYWORDS:
			air–blood barrier; alveolarization; alveoli; electron microscopy; pneumocytes
			PMID: 30761973 DOI: 10.1017/S1431927619000059

Z8600021 at 05:25, 19 February 2019

2019-02-19T05:25:22Z

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	~~==10 Most Recent Papers==~~
	~~{{10 Most Recent}}~~

	==~~=Respiratory System Development=~~==		==2018==

	~~<pubmed limit~~=~~5>Respiratory Embryology<~~/~~pubmed>~~		===How high resolution 3-dimensional imaging changes our understanding of postnatal lung development===
			Histochem Cell Biol. 2018 Dec;150(6):677-691. doi: 10.1007/s00418-018-1749-7. Epub 2018 Nov 2.

	~~<pubmed limit=5>Lung Embryology</pubmed>~~		Schittny JC1.

			Abstract
			During the last 10 + years biologically and clinically significant questions about postnatal lung development could be answered due to the application of modern cutting-edge microscopic and quantitative histological techniques. These are in particular synchrotron radiation based X-ray tomographic microscopy (SRXTM), but also 3Helium Magnetic Resonance Imaging, as well as the stereological estimation of the number of alveoli and the length of the free septal edge. First, the most important new finding may be the following: alveolarization of the lung does not cease after the maturation of the alveolar microvasculature but continues until young adulthood and, even more important, maybe reactivated lifelong if needed to rescue structural damages of the lungs. Second, the pulmonary acinus represents the functional unit of the lung. Because the borders of the acini could not be detected in classical histological sections, any investigation of the acini requires 3-dimensional (imaging) methods. Based on SRXTM it was shown that in rat lungs the number of acini stays constant, meaning that their volume increases by a factor of ~ 11 after birth. The latter is very important for acinar ventilation and particle deposition.

	~~==2018==~~		KEYWORDS:
			Angiogenesis; Lung development; Microvascular maturation; Pulmonary acinus; Pulmonary alveolarization
			PMID: 30390117 PMCID: PMC6267404 DOI: 10.1007/s00418-018-1749-7

Z8600021 at 23:33, 19 November 2018

2018-11-19T23:33:10Z

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	==2018==		==2018==


			===Development of the pulmonary pleura with special reference to the lung surface morphology: a study using human fetuses===
			Anat Cell Biol. 2018 Sep;51(3):150-157. doi: 10.5115/acb.2018.51.3.150. Epub 2018 Sep 28.

			{{#pmid:30310706}}

			Yamamoto M1, Wilting J2, Abe H3, Murakami G1,4, Rodríguez-Vázquez JF5, Abe SI1.
			Author information
			Abstract
			In and after the third trimester, the lung surface is likely to become smooth to facilitate respiratory movements. However, there are no detailed descriptions as to when and how the lung surface becomes regular. According to our observations of 33 fetuses at 9-16 weeks of gestation (crown-rump length [CRL], 39-125 mm), the lung surface, especially its lateral (costal) surface, was comparatively rough due to rapid branching and outward growing of bronchioli at the pseudoglandular phase of lung development. The pulmonary pleura was thin and, beneath the surface mesothelium, no or little mesenchymal tissue was detectable. Veins and lymphatic vessels reached the lung surface until 9 weeks and 16 weeks, respectively. In contrast, in 8 fetuses at 26-34 weeks of gestation (CRL, 210-290 mm), the lung surface was almost smooth because, instead of bronchioli, the developing alveoli faced the external surfaces of the lung. Moreover, the submesothelial tissue became thick due to large numbers of dilated veins connected to deep intersegmental veins. CD34-positive, multilayered fibrous tissue was also evident beneath the mesothelium in these stages. The submesothelial tissue was much thicker at the basal and mediastinal surfaces compared to apical and costal surfaces. Overall, rather than by a mechanical stress from the thoracic wall and diaphragm, a smooth lung surface seemed to be established largely by the thick submesothelial tissue including veins and lymphatic vessels until 26 weeks.
			KEYWORDS:
			Human fetus; Lung surface; Mesothelium; Pulmonary pleura; Submesothelial morphology
			PMID: 30310706 PMCID: PMC6172594 DOI: 10.5115/acb.2018.51.3.150

	===Human lung development: recent progress and new challenges===		===Human lung development: recent progress and new challenges===

Z8600021 at 02:28, 7 October 2018

2018-10-07T02:28:27Z

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	==2018==		==2018==

			===Human lung development: recent progress and new challenges===
			{{#pmid:30111617}}

			Nikolić MZ1,2, Sun D1, Rawlins EL3.
			Author information
			Abstract
			Recent studies have revealed biologically significant differences between human and mouse lung development, and have reported new in vitro systems that allow experimental manipulation of human lung models. At the same time, emerging clinical data suggest that the origins of some adult lung diseases are found in embryonic development and childhood. The convergence of these research themes has fuelled a resurgence of interest in human lung developmental biology. In this Review, we discuss our current understanding of human lung development, which has been profoundly influenced by studies in mice and, more recently, by experiments using in vitro human lung developmental models and RNA sequencing of human foetal lung tissue. Together, these approaches are helping to shed light on the mechanisms underlying human lung development and disease, and may help pave the way for new therapies.
			KEYWORDS:
			Alveolar; Bronchi; ESC; Lung disease; Progenitor; Stem cell; iPSC
			PMID: 30111617 PMCID: PMC6124546 DOI: 10.1242/dev.163485

	===PDGF-A signaling is required for secondary alveolar septation and controls epithelial proliferation in the developing lung===		===PDGF-A signaling is required for secondary alveolar septation and controls epithelial proliferation in the developing lung===

Z8600021 at 02:23, 7 October 2018

2018-10-07T02:23:57Z

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	==2018==		==2018==
			===PDGF-A signaling is required for secondary alveolar septation and controls epithelial proliferation in the developing lung===

			{{#pmid:29636361}}

			Gouveia L1, Betsholtz C1,2, Andrae J3.
			Author information
			Abstract
			Platelet-derived growth factor A (PDGF-A) signaling through PDGF receptor α is essential for alveogenesis. Previous studies have shown that Pdgfa-/- mouse lungs have enlarged alveolar airspace with absence of secondary septation, both distinctive features of bronchopulmonary dysplasia. To study how PDGF-A signaling is involved in alveogenesis, we generated lung-specific Pdgfa knockout mice (Pdgfafl/-; Spc-cre) and characterized their phenotype postnatally. Histological differences between mutant mice and littermate controls were visible after the onset of alveogenesis and maintained until adulthood. Additionally, we generated Pdgfafl/-; Spc-cre; PdgfraGFP/+ mice in which Pdgfra+ cells exhibit nuclear GFP expression. In the absence of PDGF-A, the number of PdgfraGFP+ cells was significantly decreased. In addition, proliferation of PdgfraGFP+ cells was reduced. During alveogenesis, PdgfraGFP+ myofibroblasts failed to form the α-smooth muscle actin rings necessary for alveolar secondary septation. These results indicate that PDGF-A signaling is involved in myofibroblast proliferation and migration. In addition, we show an increase in both the number and proliferation of alveolar type II cells in Pdgfafl/-; Spc-cre lungs, suggesting that the increased alveolar airspace is not caused solely by deficient myofibroblast function.
			KEYWORDS:
			Alveogenesis; Lung development; PDGF-A; PDGFRα
			PMID: 29636361 DOI: 10.1242/dev.161976

Z8600021 at 23:56, 1 September 2018

2018-09-01T23:56:42Z

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 b Own unpublished observation
 ==2016==