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BOR - Papers in Press, published online ahead of print September 13, 2006.
Biol Reprod 2006, 10.1095/biolreprod.106.053322
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BIOLOGY OF REPRODUCTION 75, 940–947 (2006)
DOI: 10.1095/biolreprod.106.053322
© 2006 by the Society for the Study of Reproduction, Inc.

research-article

Adrenomedullin 2 Antagonist Infusion to Rats During Midgestation Causes Fetoplacental Growth Restriction Through Apoptosis1

Madhu Chauhan , Uma Yallampalli , Luckey Reed , and Chandrasekhar Yallampalli 2

Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas 77555

ABSTRACT

Adrenomedullin 2 (ADM2) is a recently discovered member of the calcitonin/calcitonin gene-related peptide family with an exon-intron structure similar to that of ADM. The mRNA of ADM2 is expressed in several tissues, including uterus and ovary. The present study was designed to assess the effects of ADM2 antagonist (ADM217–47) infusion to pregnant rats on fetal and placental growth. On Day 15 of gestation, rats were implanted s.c. with osmotic minipumps delivering 50 and 200 µg per rat per day of ADM217–47 and were killed on Gestational Day 18. In ADM217–47-treated rats, placental weights were significantly inhibited in a dose-related manner, with an 11% reduction in the group of rats receiving 200 µg/day, whereas the fetal weights were reduced by 17% without significant differences between the two doses. 2 In ADM217–47-infused rats, increased apoptosis was demonstrated in the labyrinth and junctional zones of rat placenta by the TUNEL method compared with the control animals. Western blot analysis demonstrated that in ADM217–47-treated rats Bcl-2, mitochondrial cytochrome c, and active caspase-9 and caspase-3 were significantly increased compared with the controls. No significant treatment-associated changes were observed in Bax, Bid, p53, and caspase-8 and caspase-10 proteins in the treated placentas. In addition, infusion of ADM217–47 caused a significant decline in the transcripts of nitric oxide synthase 3 (NOS3) and NOS2. These findings show that ADM217–47 infusion in rats during midpregnancy cause fetoplacental growth restriction through the activation of mitochondrial apoptotic pathways. This study demonstrates for the first time (to our knowledge) a potential role for ADM2 in placental functions during pregnancy.

ADM, ADM2, apoptosis, fetus, placenta, pregnancy

FOOTNOTES

1Supported by grants HL-58144 and HL-72650 from the National Institutes of Health.

Correspondence: 2 Chandrasekhar Yallampalli, Department of Obstetrics and Gynecology, 301 University Boulevard, MRB, 11.138, Route 1062, Galveston, TX 77555-1062. FAX: 409 747 0475; e-mail: chyallam{at}utmb.edu






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Copyright © 2006 by the Society for the Study of Reproduction.