Chronic maternal stress inhibits the capacity to up-regulate placental 11β-hydroxysteroid dehydrogenase type 2 activity

Welberg, Leonie; Thrivikraman, K. V.; Plotsky, Paul M.

doi:10.1677/joe.1.06374

Cited by 200 publications

(131 citation statements)

References 23 publications

(29 reference statements)

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“…In vitro, 11A-HSD2 mRNA is down-regulated by NE and EPI (24), leading to the assumption that chronic activation of the maternal ANS due to stress may weaken 11A-HSD2 activity and, as a result, lead to fetal F excess. Results from the current study reporting a negative association between LF and LF/HF baseline and amniotic E/(E + F) and simultaneously a positive association between LF and LF/HF baseline and amniotic F parallel results of impaired 11A-HSD2 activity in chronically stressed pregnant rats (12,13). Increased baseline levels of stress markers, including LF/HF, have been found to reflect chronic stress exposure in humans (54).…”

Section: Discussionsupporting

confidence: 62%

“…The significant relationship between the acute LF/HF stress response and amniotic E/(E + F) may indicate that higher sympathovagal balance or, in other words, a greater shift to sympathetic activation caused by stress, induces an up-regulation of placental 11A-HSD2 activity in humans and corresponds to findings in acute-stressed pregnant rats (12). Likewise, increased LF/HF and also LF stress responses in our study were associated with lower amniotic fluid F levels.…”

Section: Discussionmentioning

confidence: 90%

“…(11)). In rats, acute maternal stress induces an immediate up-regulation of placental 11A-HSD2 activity, but after maternal chronic stress exposure, this up-regulation is impaired resulting in F excess to the fetus (12,13). A parallel process has been proposed to exist in humans because, from 5 weeks of gestation onward, 11A-HSD2 is also present in the human placental syncytiotrophoblast, the site of maternal-fetal exchange (14).…”

Section: Introductionmentioning

confidence: 99%

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The Acute Autonomic Stress Response and Amniotic Fluid Glucocorticoids in Second-Trimester Pregnant Women

Marca-Ghaemmaghami¹,

Dainese²,

Marca³

et al. 2015

Psychosomatic Medicine

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OBJECTIVE: The maternal autonomic nervous system (ANS) has received little attention in the investigation of biological mechanisms linking prenatal stress to fetal cortisol (F) excess. In vitro, norepinephrine and epinephrine inhibit placental 11-hydroxysteroid dehydrogenase type 2 (11-HSD2), which protects the fetus from F overexposure by inactivating it to cortisone (E). Here, we investigated the acute ANS stress response to an amniocentesis and its association with amniotic fluid F, E, and E/(E + F) as a marker of fetoplacental 11-HSD2 activity. METHODS: An aliquot of amniotic fluid was obtained from 34 healthy, second-trimester pregnant women undergoing amniocentesis. Repeated assessment of mood states served to examine the psychological stress response to amniocentesis. Saliva samples were collected to measure stress-induced changes in salivary -amylase concentrations in response to amniocentesis. Cardiac parameters were measured continuously. RESULTS: Undergoing amniocentesis induced significant psychological and autonomic alterations. Low-frequency (LF)/high-frequency (HF) baseline, suggested to reflect sympathovagal balance, was negatively correlated with amniotic E/(E + F) (r=-0.53, p = .002) and positively with F (r = 0.62, p < .001). In contrast, a stronger acute LF/HF response was positively associated with E/(E + F) (r = 0.44, p = .012) and negatively with F (r=-0.40, p = .025). CONCLUSIONS: These findings suggest that the maternal ANS is involved in the regulation of the fetoplacental barrier to stress. Allostatic processes may have been initiated to counterbalance acute stress effects. In contrast, higher LF/HF baseline values, possibly indicative of chronic stress exposure, may have inhibited 11-HSD2 activity in the fetoplacental unit. These results parallel animal findings of up-regulated placental 11-HSD2 in response to acute stress but impairment under chronic stress. Objective: The maternal autonomic nervous system (ANS) has received little attention in the investigation of biological mechanisms linking prenatal stress to fetal cortisol (F) excess. In vitro, norepinephrine and epinephrine inhibit placental 11A-hydroxysteroid dehydrogenase type 2 (11A-HSD2), which protects the fetus from F overexposure by inactivating it to cortisone (E). Here, we investigated the acute ANS stress response to an amniocentesis and its association with amniotic fluid F, E, and E/(E + F) as a marker of fetoplacental 11A-HSD2 activity. Methods: An aliquot of amniotic fluid was obtained from 34 healthy, second-trimester pregnant women undergoing amniocentesis. Repeated assessment of mood states served to examine the psychological stress response to amniocentesis. Saliva samples were collected to measure stress-induced changes in salivary >-amylase concentrations in response to amniocentesis. Cardiac parameters were measured continuously. Results: Undergoing amniocentesis induced significant psychological and autonomic alterations. Low-frequency (LF)/high-frequency (HF) baseline, suggested to reflect sympa...

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Acute Autonomic Stress Response and Amniotic Fluid Glucocorticoids in Second-Trimester Pregnant Women

Marca-Ghaemmaghami¹,

Dainese²,

Marca³

et al. 2015

Psychosomatic Medicine

View full text Add to dashboard Cite

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“…Por otra parte, la expresión placentaria de 11-beta hidroxiesteroide deshidrogenasa tipo 2, limita la exposición fetal a los glucocorticoides maternos a través de la metabolización de corticosterona en 11-dehidrocorticosterona, un metabolito inactivo 32 . Si bien la exposición reiterada a estrés en el embarazo reduce significativamente la actividad de esta enzima en la barrera placentaria y su expresión génica 33,34 , debe considerarse también que las respuestas del eje HHA materno en situaciones estresantes se reducen drásticamente al final del embarazo, lo que supone minimizar la transmisión de glucocorticoides hacia el feto 34 .…”

Section: Estrés Y Glucocorticoidesunclassified

Efectos neurobiológicos del estrés prenatal sobre el nuevo ser

Cáceres

Martínez-Aguayo

Arancibia

et al. 2017

Rev. chil. neuro-psiquiatr.

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“…This mechanism was extensively reviewed in (Yang, 1997). However in some settings stress was shown to reduce the activity of this enzyme by indirect and direct mechanisms (Welberg et al, 2005), as well as impair placental circulation causing a hypoxic state (Ohkawa et al, 1991) which reduces 11-HSD activity.…”

Section: Maternal Environmental Exposures: Maternal Stressmentioning

confidence: 99%