Expression and location of mRNAs encoding multiple forms of secretory phospholipase A2 in the rat retina

Low‐molecular‐weight secretory phospholipases A2 (sPLA2s) are a subgroup of PLA2s, which are secreted, bind to receptors, and may act as intercellular signaling modulators. At least 10 different groups have been characterized in mammals, and there is expanding evidence of the significance of sPLA2s...

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Veröffentlicht in:Journal of neuroscience research 2004-08, Vol.77 (4), p.517-524
Hauptverfasser: Kolko, Miriam, Christoffersen, Nanna R., Barreiro, Sebastian G., Bazan, Nicolas G.
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Sprache:eng
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Zusammenfassung:Low‐molecular‐weight secretory phospholipases A2 (sPLA2s) are a subgroup of PLA2s, which are secreted, bind to receptors, and may act as intercellular signaling modulators. At least 10 different groups have been characterized in mammals, and there is expanding evidence of the significance of sPLA2s in neuronal signaling and survival [Kolko et al. (1996) J. Biol. Chem. 271: 32722–32728]. To date, no retinal sPLA2s have been cloned or characterized. We evaluated the existence and abundance of sPLA2 subtypes in rat retina and explored their possible involvement in light‐induced retinal damage. We designed primers to identify the sPLA2s in rat retina, based on known sequences of sPLA2‐specific mRNAs in other tissues. RNA was isolated from rat retina, and cDNA was produced and used for PCR cloning to identify the novel subtypes of sPLA2. Our study revealed the presence of mRNAs encoding sPLA2‐IB, ‐X, ‐V, ‐IIE, ‐IIA, and ‐IIF in the retina, and quantification by real‐time PCR revealed different abundances of the sPLA2s. We showed a time‐dependent gene induction of sPLA2‐X, ‐IB, and ‐V in light‐induced retinal damage. We further explored the location of sPLA2‐IB by in situ hybridization and immunohistochemistry. This study is the first to reveal the presence, abundance, and induction of mRNAs encoding sPLA2s in rat retina. We suggest that these enzymes are themselves intercellular signaling modulators of retinal cell function and perhaps also of retinal degeneration. © 2004 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.20187