Bauhinia purpurea lectin (BPA) binding of rat type I pneumocytes: Alveolar epithelial alterations after radiation-induced lung injury

Kasper, Michael; Schuh, Dieter; Müller, Martin

doi:10.1016/s0940-2993(11)80118-1

Cited by 27 publications

(26 citation statements)

References 13 publications

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“…Cells were immunostained for SP-D in acid alcohol-fixed cultures, embedded in paraffin, and localized with polyclonal rabbit anti-rat SP-D IgG and FITC-labeled donkey antirabbit IgG (Jackson ImmunoResearch Laboratories, West Grove, PA) (52). Staining with biotinylated Maclura promifera lectin (Vector Laboratories, Burlingame, CA) was performed as previously described (13,21).…”

Section: Methodsmentioning

confidence: 99%

Maintenance of surfactant protein A and D secretion by rat alveolar type II cells in vitro

Mason

Lewis

Edeen

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Secretion of surfactant proteins A and D (SP-A and SP-D) has been difficult to study in vitro because a culture system for maintaining surfactant secretion has been difficult to establish. We evaluated several growth factors, corticosteroids, rat serum, and a fibroblast feeder layer for the ability to produce and maintain a polarized epithelium of type II cells that secretes SP-A and SP-D into the apical medium. Type II cells were plated on a filter insert coated with an extracellular matrix and were cultured at an air-liquid interface. Keratinocyte growth factor (KGF) stimulated type II cell proliferation and secretion of SP-A and SP-D more than fibroblast growth factor-10 (FGF-10), hepatocyte growth factor (HGF), or heparin-binding epidermal-like growth factor (HB-EGF). Cells cultured in the presence of KGF and rat serum with or without fibroblasts had high surfactant protein mRNA levels and exhibited a high level of SP-A and SP-D secretion. Dexamethasone inhibited type II cell proliferation but increased expression of SP-B. In the presence of KGF, rat serum, and dexamethasone, the mRNAs for the surfactant proteins were maintained at high levels. Secretion of SP-A and SP-D was found to be independent of phospholipid secretion.

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Section: Methodsmentioning

confidence: 99%

Maintenance of surfactant protein A and D secretion by rat alveolar type II cells in vitro

Mason

Lewis

Edeen

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Finally, a group of lectins are able to distinguish between the carbohydrate moieties on the surface of ATI and ATII cells. Lectins such as Ricinus communis agglutinin [82], Lycopersicon esculentum agglutinin [83], Soybean agglutinin [84] and Bauhinia purpurea agglutinin [85] selectively bind to the surface of ATI cells.…”

Section: Group II Alveolar Epithelial Type I Cell-selective Proteinsmentioning

confidence: 99%

The use of alveolar epithelial type I cell-selective markers to investigate lung injury and repair

McElroy

Kasper²

2004

Eur Respir J

116

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Ultrastructural studies demonstrate that alveolar epithelial type I cell damage is frequently observed in acute and chronic lung diseases.This article discusses the use of cell-selective proteins as markers for the investigation of injury and repair of the alveolar epithelium. The utility of proteins specific to alveolar epithelial type I cells as diagnostic markers of alveolar epithelial injury in acute lung injury is considered, and expression of proteins selective for alveolar epithelial type I cells in lungs following injury and in fibrosis are discussed. Eur Respir J 2004; 24: 664-673.

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“…Alveolar brush (type III) cells lack surfactant proteins and are selectively decorated with cytokeratin 18-and villin-specific antibodies [3,4]. Type I pneumocytes, in contrast to type II pneumocytes, bind various lectins (Lycopersicon esculentum agglutinin (LEA), Erythrina cristagalli agglutinin (ECA) or Bauhinia purpurea agglutinin (BPA)) [5][6][7], express the leukocytic intercellular adhesion molecule-1 (ICAM-1) [8,9] as well as caveolin, a structural protein of caveolae, and antigens recognized by other type I cell-specific monoclonal antibodies [10][11][12]. One of the type I cell-specific monoclonal antibodies recognizes a 40-42 kDa apical plasma membrane integral protein (RTI40) that was detected in the alveolar fluid of injured lungs [13].…”

mentioning

confidence: 99%

“…The binding to the alveolar surface has been shown to be stable even under conditions of lung injury, compared with the immunoreactions of antibodies against type I cell-specific antigens [7,12].…”

mentioning

confidence: 99%

Loss of immunoreactivity for RTI40, a type I cell-specific protein in the alveolar epithelium of rat lungs with bleomycin-induced fibrosis

Koslowski

Dobbs²,

Wenzel³

et al. 1998

Eur Respir J

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The rat alveolar epithelium comprises three different epithelial cell types: the large squamous type I cells, the cuboidal type II pneumocytes and the bottle-shaped alveolar brush (type III) cells. Various biochemical markers have been used to distinguish type I from type II cells. Most of these markers are not unique for either cell type, but are helpful in defining the different phenotypes of type I and type II cells. Type II pneumocytes may be distinguished from type I cells by their cytokeratin pattern, by the presence of certain enzymes (e.g. alkaline phosphatase, carbonic anhydrase II, carbonyl reductase, protein disulphide isomerase and catalase), by the presence of surfactant apoproteins (SP-A, SP-B, SP-C and SP-D) and by different lectin binding (Maclura pomifera agglutinin (MPA)) (reviewed in [1,2]). Alveolar brush (type III) cells lack surfactant proteins and are selectively decorated with cytokeratin 18-and villin-specific antibodies [3,4]. Type I pneumocytes, in contrast to type II pneumocytes, bind various lectins (Lycopersicon esculentum agglutinin (LEA), Erythrina cristagalli agglutinin (ECA) or Bauhinia purpurea agglutinin (BPA)) [5][6][7], express the leukocytic intercellular adhesion molecule-1 (ICAM-1) [8,9] as well as caveolin, a structural protein of caveolae, and antigens recognized by other type I cell-specific monoclonal antibodies [10][11][12]. One of the type I cell-specific monoclonal antibodies recognizes a 40-42 kDa apical plasma membrane integral protein (RTI40) that was detected in the alveolar fluid of injured lungs [13]. Another type I cellspecific monoclonal antibody is .In the present study, the distribution of RTI40, MEP-1 antigen and the BPA lectin-binding glycoprotein was investigated in bleomycin-injured rat lungs and compared with that in normal adult and foetal lung tissue. The binding to the alveolar surface has been shown to be stable even under conditions of lung injury, compared with the immunoreactions of antibodies against type I cell-specific antigens [7,12]. Materials and methodsMale Wistar rats weighing 350-400 g were given a single dose of 7 units of bleomycin sulphate in phosphatebuffered saline (PBS)·kg body weight -1 by intratracheal instillation. Controls received PBS alone. Different animals were killed at 7, 14, 21, 28, 35 and 42 days after bleomycin application and the lungs were prepared and lavaged via the trachea with PBS [17].Sections of formalin-fixed, paraffin-embedded lung tissue (normal, n=5; injured tissue, 4 weeks after bleomycin administration, n=12) were dewaxed. In addition, sections These results suggest RTI40 as a tool for the evaluation of alveolar epithelial type I cell behaviour during re-epithelialization processes.

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Bauhinia purpurea lectin (BPA) binding of rat type I pneumocytes: Alveolar epithelial alterations after radiation-induced lung injury

Cited by 27 publications

References 13 publications

Maintenance of surfactant protein A and D secretion by rat alveolar type II cells in vitro

Maintenance of surfactant protein A and D secretion by rat alveolar type II cells in vitro

The use of alveolar epithelial type I cell-selective markers to investigate lung injury and repair

Loss of immunoreactivity for RTI40, a type I cell-specific protein in the alveolar epithelium of rat lungs with bleomycin-induced fibrosis

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