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J. Biol. Chem., Vol. 278, Issue 33, 31352-31360, August 15, 2003

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Pulmonary Inflammation and Edema Induced by Phospholipase A₂

GLOBAL GENE ANALYSIS AND EFFECTS ON AQUAPORINS AND Na⁺/K⁺-ATPase^*

Charmian D. N. Cher  , Arunmozhiarasi Armugam , Ramkumar Lachumanan ¶, Marelyn-Wintour Coghlan || and Kandiah Jeyaseelan  **

From the Department of Biochemistry, Faculty of Medicine, National University of Singapore, S117597, Singapore, the ^¶Research Instruments Pte Ltd., S139944, Singapore, and the ^||Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria 3052, Australia

Victims of snakebite quickly succumb to severe respiratory failure, which can be fatal if left untreated. One of the most toxic components of snake venom is phospholipase A₂ (PLA₂; EC 3.1.1.4). PLA₂ isolated from the elapid, Naja sputatrix, induced pulmonary inflammation and edema when administered intravenously and intratracheally to rats. Analysis of pulmonary gene expression profiles using oligonucleotide microarrays revealed 60 genes whose expression was altered by at least 3-fold in response to intratracheal instillation of PLA₂ for 3 h as compared with controls. In addition to genes encoding cytokines and chemokines responsible for inflammatory processes, the Na⁺/K⁺-ATPase gene has been found to be involved in edema formation. Real-time PCR, Western blot, and immunohistochemical analyses confirmed that the expression of AQP1 and AQP5 mRNAs and proteins was decreased. Besides providing an experimental model for studies on the pathophysiology of the lung, this investigation yields a clue to the mechanisms by which endogenous PLA₂s could mediate inflammation in conditions such as allergy and rheumatoid arthritis.

Received for publication, March 10, 2003 , and in revised form, April 23, 2003.

^* This work was supported in part by research Grant RP-183-000-067-213 from the National Medical Research Council, Singapore. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by a research scholarship from the National University of Singapore.

^** To whom correspondence should be addressed: Dept. of Biochemistry, Faculty of Medicine, National University of Singapore, 8 Medical Dr., Singapore 117597. Tel.: 6568743248; Fax: 6567791453; E-mail: bchjeya{at}nus.edu.sg.

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