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Nerve Growth Factor and its Functional Receptor TrkA are Up-regulated in Murine Decidual Tissue of Stress-triggered and Substance P-mediated Abortion

Authors


Address reprint requests to PD Dr Petra Clara Arck, Biomedizinisches Forschungszentrum, Raum 2.0549, Augustenburger Platz 1, 13353 Berlin, Germany.
E-mail: petra.arck@charite.de

Abstract

Problem:  Stress, elicited by environmental and social conditions, is known to affect the homeostasis of the nervous, endocrine and immune systems. In pregnancy, perceived stress results in a predomination of inflammatory abortion-associated Th1 cytokines over immunosuppressive, pregnancy-protective-associated Th2 cytokines, putatively via neuropeptide substance P (SP). Nerve growth factor (NGF), an important trophic factor for sympathetic neurons, has been implicated in the responsiveness of immune-competent cells through its functional receptor, tropomyosin receptor kinase (TrkA). Thus, the aim of the present study was to identify a cross-talk between distinct neurotrophic and immune mediators in pregnancy maintenance.

Method of Study:  Using immune fluorescence, we evaluated decidual and placental expression of NGF and TrkA on gestation day (gd) 13.5 in the abortion-prone mouse model CBA/J × DBA/2J in (1) CBA/J female control mice; (2) CBA/J mice exposed to stress on gd 5.5; and (3) CBA/J mice injected with SP on gd 5.5 to mimick stress perception.

Results: Stress and SP injection significantly increased the abortion rate and up-regulated decidual NGF and TrkA expression compared with the control. Stress, but not SP injection down-regulated placental NGF, whereas no changes in placental TrkA were observed.

Conclusion:  Our data suggest a functional role for NGF in stress-triggered, SP-mediated abortion.

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