Cell-specific expression of group X and group V secretory phospholipases A(2) in human lung airway epithelial cells

• Published in: American journal of respiratory cell and molecular biology Vol. 23; no. 1; pp. 37 - 44
• Main Authors: Seeds, M C, Jones, K A, Duncan Hite, R, Willingham, M C, Borgerink, H M, Woodruff, R D, Bowton, D L, Bass, D A
• Format: Journal Article
• Language: English
• Published: United States 01.07.2000
• Subjects: Animals; Bronchi - cytology; Bronchi - enzymology; Cell Line; Cloning, Molecular; COS Cells; Epithelial Cells - enzymology; Group II Phospholipases A2; Histocytochemistry; Humans; Hydrolysis; In Situ Hybridization; Isoenzymes - genetics; Isoenzymes - metabolism; Lung - cytology; Lung - enzymology; Organ Specificity; Phospholipases A - genetics; Phospholipases A - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Substrate Specificity; Transfection
• ISSN: 1044-1549
• DOI: 10.1165/ajrcmb.23.1.4034

Secretory phospholipase A(2) (sPLA(2)) enzymes contribute to inflammatory injury in human lungs by several mechanisms, including eicosanoid production and hydrolytic damage to surfactant phospholipids. Several distinct sPLA(2) genes have been described in human tissue but little is known regarding their presence, localization, or function(s) within lungs. We hypothesized that sPLA(2)s would have cell-specific distributions within lung. We used reverse transcriptase/polymerase chain reaction to identify sPLA(2) messenger RNAs (mRNAs) in adult human lung tissue. Resulting complementary DNA (cDNA) sequences indicated that total lung extracts contained mRNA for Groups IB, IIA, V, and X sPLA(2). An epithelial cell line, BEAS cells, expressed only Groups IIA, V, and X. We used these cDNAs to clone these enzymes, especially the recently described Group X and Group V enzymes. Digoxigenin-labeled complementary RNA probes were used to determine localization of each sPLA(2) by in situ hybridization of human lung. Hybridization was strongly positive for Group X and Group V in airway epithelial cells, which failed to hybridize Group IB or IIA probes. Although four known mammalian sPLA(2) isotypes were expressed in lung, only Group X and Group V sPLA(2) mRNAs appear uniquely expressed in airway epithelium, suggesting they could provide a mechanism of pulmonary surfactant hydrolysis during lung injury.