Literature DB >> 9761749

Expression of Fas (CD95) and FasL (CD95L) in human airway epithelium.

K J Hamann1, D R Dorscheid, F D Ko, A E Conforti, A I Sperling, K F Rabe, S R White.   

Abstract

The cell surface molecule Fas (CD95) is a member of the tumor necrosis factor receptor family. Ligation of the Fas receptor can lead to induction of apoptosis in inflammatory cells. It has been suggested that expression of the Fas receptor and its ligand (FasL) in airway epithelium may modulate the inflammatory response commonly found in asthmatic lungs. We examined Fas and FasL expression on primary human tissues, on bronchial epithelial cells in primary culture, and on the immortalized human airway epithelial cell line, 1HAEo-. Receptor and ligand expression were demonstrated using multiple antibodies and multiple techniques, including immunohistochemistry, flow cytometry, Western blots, and reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical staining demonstrated that both columnar and basal cells of intact human lung tissues expressed cell surface Fas and FasL. In addition, both primary cultured and immortalized 1HAEo- cells expressed cell surface Fas and FasL, as demonstrated by flow cytometry; expression of Fas and FasL was confirmed at the transcription level using RT-PCR and, for additional confirmation of FasL, using Western blots. We demonstrate that both Fas and FasL are expressed by human airway epithelial cell subtypes. Expression of these molecules may play an important role in regulation of the inflammatory response.

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Year:  1998        PMID: 9761749     DOI: 10.1165/ajrcmb.19.4.3100

Source DB:  PubMed          Journal:  Am J Respir Cell Mol Biol        ISSN: 1044-1549            Impact factor:   6.914


  35 in total

1.  Effect of cigarette smoke extract on the proliferation of human airway epithelial cells and expression and activation of FAK.

Authors:  Li Xu; Zhenxiang Zhang; Yongjian Xu
Journal:  J Huazhong Univ Sci Technolog Med Sci       Date:  2005

Review 2.  Roles of apoptosis in airway epithelia.

Authors:  Yohannes Tesfaigzi
Journal:  Am J Respir Cell Mol Biol       Date:  2006-01-26       Impact factor: 6.914

Review 3.  Epithelium: at the interface of innate and adaptive immune responses.

Authors:  Robert P Schleimer; Atsushi Kato; Robert Kern; Douglas Kuperman; Pedro C Avila
Journal:  J Allergy Clin Immunol       Date:  2007-10-18       Impact factor: 10.793

4.  Fas and fas ligand are up-regulated in pulmonary edema fluid and lung tissue of patients with acute lung injury and the acute respiratory distress syndrome.

Authors:  Kurt H Albertine; Matthew F Soulier; Zhengming Wang; Akitoshi Ishizaka; Satoru Hashimoto; Guy A Zimmerman; Michael A Matthay; Lorraine B Ware
Journal:  Am J Pathol       Date:  2002-11       Impact factor: 4.307

Review 5.  RNAi therapeutic strategies for acute respiratory distress syndrome.

Authors:  Melissa L Jagrosse; David A Dean; Arshad Rahman; Bradley L Nilsson
Journal:  Transl Res       Date:  2019-07-27       Impact factor: 7.012

Review 6.  Cell Death in the Lung: The Apoptosis-Necroptosis Axis.

Authors:  Maor Sauler; Isabel S Bazan; Patty J Lee
Journal:  Annu Rev Physiol       Date:  2018-11-28       Impact factor: 19.318

7.  Enhanced expression of Fas and FasL modulates apoptosis in the lungs of severe P. falciparum malaria patients with pulmonary edema.

Authors:  Chuchard Punsawad; Parnpen Viriyavejakul; Chayanee Setthapramote; Sarawoot Palipoch
Journal:  Int J Clin Exp Pathol       Date:  2015-09-01

8.  Fas (CD95) induces rapid, TLR4/IRAK4-dependent release of pro-inflammatory HMGB1 from macrophages.

Authors:  Feng Wang; Ziyue Lu; Michael Hawkes; Huan Yang; Kevin C Kain; W Conrad Liles
Journal:  J Inflamm (Lond)       Date:  2010-06-17       Impact factor: 4.981

Review 9.  Beyond inflammation: airway epithelial cells are at the interface of innate and adaptive immunity.

Authors:  Atsushi Kato; Robert P Schleimer
Journal:  Curr Opin Immunol       Date:  2007-10-24       Impact factor: 7.486

10.  Fas-ligand-induced apoptosis of respiratory epithelial cells causes disruption of postcanalicular alveolar development.

Authors:  Monique E De Paepe; Sravanthi Gundavarapu; Umadevi Tantravahi; John R Pepperell; Sheila A Haley; Francois I Luks; Quanfu Mao
Journal:  Am J Pathol       Date:  2008-06-05       Impact factor: 4.307

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