p146 type II alveolar epithelial cell antigen is identical to aminopeptidase N

1991 ◽  
Vol 260 (4) ◽  
pp. L274-L279 ◽  
Author(s):  
J. D. Funkhouser ◽  
S. D. Tangada ◽  
M. Jones ◽  
S. J. O ◽  
R. D. Peterson
Keyword(s):  
Alveolar Epithelial Cell ◽  
Limited Proteolysis ◽  
Aminopeptidase N ◽  
Lung Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Protein Amino Acid ◽  
Differentiation Antigens ◽  
Alveolar Epithelial ◽  
Type Ii Alveolar Cells

A prominent membrane protein of rat type II alveolar cells, p146, was originally identified by one of many mouse monoclonal antibodies that were produced to rat lung cells in the course of a search for differentiation antigens that might prove useful in studying lung differentiation. We report here results from analysis of the primary structure of this molecule and, based on this knowledge, the elucidation of the function of the protein. Amino acid sequencing of the NH2-terminal portion of the p146 protein, plus partial sequencing of several peptides obtained by limited proteolysis, indicates it is identical to aminopeptidase N. Further, the immunoaffinity purified p146 protein has aminopeptidase N activity. The discussion includes references to other molecules such as CD 13 and CD 10 (CALLA) that were recognized as differentiation antigens and subsequently found to be peptidases. The possible biological implications of such a peptidase on the luminal surface of type II alveolar cells are also considered.

scholarly journals Simultaneous isolation of endothelial and alveolar epithelial type I and type II cells during mouse lung development in the absence of a transgenic reporter

2020 ◽  
Vol 318 (4) ◽  
pp. L619-L630 ◽  
Author(s):  
Yves Donati ◽  
Sanja Blaskovic ◽  
Isabelle Ruchonnet-Métrailler ◽  
Josefina Lascano Maillard ◽  
Constance Barazzone-Argiroffo
Keyword(s):  
Epithelial Cell ◽  
De Novo ◽  
Morphological Changes ◽  
Alveolar Epithelial Cell ◽  
Mouse Lung ◽  
Cell Populations ◽  
Type I ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial

Mouse lung developmental maturation and final alveolarization phase begin at birth. During this dynamic process, alveolar cells modify their morphology and anchorage to the extracellular matrix. In particular, alveolar epithelial cell (AEC) type I undergo cytoplasmic flattening and folding to ensure alveoli lining. We developed FACS conditions for simultaneous isolation of alveolar epithelial and endothelial cells in the absence of specific reporters during the early and middle alveolar phase. We evidenced for the first time a pool of extractable epithelial cell populations expressing high levels of podoplanin at postnatal day (pnd)2, and we confirmed by RT-qPCR that these cells are already differentiated but still immature AEC type I. Maturation causes a decrease in isolation yields, reflecting the morphological changes that these cell populations are undergoing. Moreover, we find that major histocompatibility complex II (MHCII), reported as a good marker of AEC type II, is poorly expressed at pnd2 but highly present at pnd8. Combined experiments using LysoTracker and MHCII demonstrate the de novo acquisition of MCHII in AEC type II during lung alveolarization. The lung endothelial populations exhibit FACS signatures from vascular and lymphatic compartments. They can be concomitantly followed throughout alveolar development and were obtained with a noticeable increased yield at the last studied time point (pnd16). Our results provide new insights into early lung alveolar cell isolation feasibility and represent a valuable tool for pure AEC type I preparation as well as further in vitro two- and three-dimensional studies.

Demonstration of Microtubules in Type II Alveolar Cells

1977 ◽  
Vol 35 ◽  
pp. 464-465
Author(s):  
Frederick J. Stone ◽  
Yutaka Kikkawa
Keyword(s):  
Secretory Granules ◽  
Alveolar Epithelial Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Type Ii Alveolar Cells ◽  
Probable Role ◽  
Secretory Products

Two lines of evidence indicate a probable role for microtubules in the secretory processes of type II alveolar epithelial cells. These are: (1) The inhibition of the release of disaturated lecithins (the major component of putative type II cell secretory products) by lung slices pretreated and then incubated with antimicrotubular agents colchicine and vinblastine (Delahunty, J.J. and Johnston, J.M.: J. Lipid Res., 17:112,1976); and (2) The abnormality of the secretory granules, lamellar bodies, in the type II cells of beige mice (Chi, E.Y. Prueitt, J.L., and Lagunoff, D: J. Histochem. Cytochem., 23:863-869, 1975) in which microtubular function is abnormal (Oliver, J.M.: Amer. J. Pathol., 85:395, 1976). Our failure to morphologically identify the expected microtubules in type II cells from lungs prepared for electron microscopy by conventional fixations led us to attempt their visualization by the application of the tannic acid- glutaraldehyde fixative of Futaesakie, et. al. (Histochemistry and Cytochemistry, 1972.).

Surfactant Bodies: The New Look o£ the Lamellar Inclusions from Type II Alveolar Pneumocytes

1975 ◽  
Vol 33 ◽  
pp. 320-321
Author(s):  
R. M. Wagner ◽  
K. Miyai
Keyword(s):  
Complete Characterization ◽  
Male Rats ◽  
Type Ii ◽  
Alveolar Cells ◽  
Alveolar Epithelial ◽  
Epithelial Regeneration ◽  
Lamellar Inclusions ◽  
Type Ii Alveolar Cells ◽  
Mammalian Lung

Lamellar bodies, inclusions unique to type II alveolar cells, have an essential role in the metabolism of the surface-active lipoproteins of the mammalian lung. Most recent investigations have shown that the type II alveolar cell also functions as a progenitor of alveolar epithelial regeneration in certain types of alveolar injury, thus emphasizing the need for complete characterization of this cell and its lamellar inclusions. This paper presents a new appearance for the lamellar inclusion in situ as well as in isolated fraction and suggests a correlation between the improved appearance and the biochemical composition of the inclusion.The lungs from adult male rats were removed and 1 mm3 blocks were cut from the peripheral lung regions for the in situ studies. This tissue was fixed in 1% OSO4 in 0.15 M isotonic buffered saline at 4°C for 2 hours then dehydrated with a graded series of acetone at 4°C and embedded in Luft's Epon.

scholarly journals Senescence associated long non-coding RNA 1 regulates cigarette smoke-induced senescence of type II alveolar epithelial cells through sirtuin-1 signaling

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098604
Author(s):  
Dong Yuan ◽  
Yuanshun Liu ◽  
Mengyu Li ◽  
Hongbin Zhou ◽  
Liming Cao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Sirtuin 1 ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Objective The primary aim of our study was to explore the mechanisms through which long non-coding RNA (lncRNA)-mediated sirtuin-1 (SIRT1) signaling regulates type II alveolar epithelial cell (AECII) senescence induced by a cigarette smoke-media suspension (CSM). Methods Pharmacological SIRT1 activation was induced using SRT2104 and senescence-associated lncRNA 1 (SAL-RNA1) was overexpressed. The expression of SIRT1, FOXO3a, p53, p21, MMP-9, and TIMP-1 in different groups was detected by qRT-PCR and Western blotting; the activity of SA-β gal was detected by staining; the binding of SIRT1 to FOXO3a and p53 gene transcription promoters was detected by Chip. Results We found that CSM increased AECII senescence, while SAL-RNA1 overexpression and SIRT1 activation significantly decreased levels of AECII senescence induced by CSM. Using chromatin immunoprecipitation, we found that SIRT1 bound differentially to transcriptional complexes on the FOXO3a and p53 promoters. Conclusion Our results suggested that lncRNA-SAL1-mediated SIRT1 signaling reduces senescence of AECIIs induced by CSM. These findings suggest a new therapeutic target to limit the irreversible apoptosis of lung epithelial cells in COPD patients.

scholarly journals TRIM72 is required for effective repair of alveolar epithelial cell wounding

2014 ◽  
Vol 307 (6) ◽  
pp. L449-L459 ◽  
Author(s):  
Seong Chul Kim ◽  
Thomas Kellett ◽  
Shaohua Wang ◽  
Miyuki Nishi ◽  
Nagaraja Nagre ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Molecular Mechanisms ◽  
Striated Muscle ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Lung Cells ◽  
Alveolar Epithelial ◽  
High Tidal Volume Ventilation

The molecular mechanisms for lung cell repair are largely unknown. Previous studies identified tripartite motif protein 72 (TRIM72) from striated muscle and linked its function to tissue repair. In this study, we characterized TRIM72 expression in lung tissues and investigated the role of TRIM72 in repair of alveolar epithelial cells. In vivo injury of lung cells was introduced by high tidal volume ventilation, and repair-defective cells were labeled with postinjury administration of propidium iodide. Primary alveolar epithelial cells were isolated and membrane wounding and repair were labeled separately. Our results show that absence of TRIM72 increases susceptibility to deformation-induced lung injury whereas TRIM72 overexpression is protective. In vitro cell wounding assay revealed that TRIM72 protects alveolar epithelial cells through promoting repair rather than increasing resistance to injury. The repair function of TRIM72 in lung cells is further linked to caveolin 1. These data suggest an essential role for TRIM72 in repair of alveolar epithelial cells under plasma membrane stress failure.

scholarly journals Bradykinin Stimulates Type II Alveolar Cells to Release Neutrophil and Monocyte Chemotactic Activity and Inflammatory Cytokines

1998 ◽  
Vol 153 (6) ◽  
pp. 1885-1893 ◽  
Author(s):  
Sekiya Koyama ◽  
Etsuro Sato ◽  
Hiroshi Nomura ◽  
Keishi Kubo ◽  
Masakazu Miura ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Chemotactic Activity ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

PM2.5-induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

2017 ◽  
Vol 37 (10) ◽  
pp. 1203-1218 ◽  
Author(s):  
Miao He ◽  
Takamichi Ichinose ◽  
Seiichi Yoshida ◽  
Tomohiro Ito ◽  
Cuiying He ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Lung Inflammation ◽  
Type Ii ◽  
Alveolar Cells ◽  
Type Ii Alveolar Cells

scholarly journals Paracrine Regulation of Alveolar Epithelial Damage and Repair Responses by Human Lung-Resident Mesenchymal Stromal Cells

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2860
Author(s):  
Dennis M. L. W. Kruk ◽  
Marissa Wisman ◽  
Jacobien A. Noordhoek ◽  
Mehmet Nizamoglu ◽  
Marnix R. Jonker ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mesenchymal Stromal Cells ◽  
Lung Tissue ◽  
Stromal Cells ◽  
Wound Repair ◽  
Lung Cells ◽  
Alveolar Type ◽  
Type Ii ◽  
Epithelial Damage ◽  
Alveolar Epithelial

COPD is characterized by irreversible lung tissue damage. We hypothesized that lung-derived mesenchymal stromal cells (LMSCs) reduce alveolar epithelial damage via paracrine processes, and may thus be suitable for cell-based strategies in COPD. We aimed to assess whether COPD-derived LMSCs display abnormalities. LMSCs were isolated from lung tissue of severe COPD patients and non-COPD controls. Effects of LMSC conditioned-medium (CM) on H2O2-induced, electric field- and scratch-injury were studied in A549 and NCI-H441 epithelial cells. In organoid models, LMSCs were co-cultured with NCI-H441 or primary lung cells. Organoid number, size and expression of alveolar type II markers were assessed. Pre-treatment with LMSC-CM significantly attenuated oxidative stress-induced necrosis and accelerated wound repair in A549. Co-culture with LMSCs supported organoid formation in NCI-H441 and primary epithelial cells, resulting in significantly larger organoids with lower type II-marker positivity in the presence of COPD-derived versus control LMSCs. Similar abnormalities developed in organoids from COPD compared to control-derived lung cells, with significantly larger organoids. Collectively, this indicates that LMSCs’ secretome attenuates alveolar epithelial injury and supports epithelial repair. Additionally, LMSCs promote generation of alveolar organoids, with abnormalities in the supportive effects of COPD-derived LMCS, reflective of impaired regenerative responses of COPD distal lung cells.

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