OGT-related mitochondrial motility is associated with sex differences and exercise effects in depression induced by prenatal exposure to glucocorticoids

Liu, Weina; Wang, Hongmei; Xue, Xiangli; Xia, Jie; Liu, Jiatong; Qi, Zhengtang; Liu, Ji

doi:10.1016/j.jad.2017.09.053

Cited by 16 publications

(16 citation statements)

References 76 publications

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“…Animal studies have also shown that exercise training ameliorates depression-like behavior (Chen et al, 2016; Morgan et al, 2018). Similarly, using several rodent models of depression, we have demonstrated that exercise training reduces depressive behavior (Wang et al, 2016; Liu et al, 2018). Up to now, the biological mechanisms by which exercise ameliorates depression are yet unclear.…”

Section: Introductionmentioning

confidence: 76%

“…Dexamethasone-21-phosphate disodium salt (Sigma-Aldrich, St. Louis, MO, United States) was dissolved in saline to achieve the concentration as 100 μl containing 0.13 mg/kg body weight. The dosage of Dex was chosen on the basis of the literature (Hauser et al, 2006; Liu et al, 2018) and our preliminary study. During gestational days (GD) 14 to 21, rats of DEX group were subcutaneously administered with 0.13 mg/kg dexamethasone-21-phosphate disodium salt (equal to 0.1 mg/kg dexamethasone), while control rats were received vehicle (0.9% saline) once a day for 7 days.…”

Section: Methodsmentioning

confidence: 99%

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Treadmill Exercise Ameliorates Depression-Like Behavior in the Rats With Prenatal Dexamethasone Exposure: The Role of Hippocampal Mitochondria

Huang

Gong

et al. 2019

Front. Neurosci.

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Prenatal exposure to synthetic glucocorticoids (sGCs) can increase the risk of affective disorders, such as depression, in adulthood. Given that exercise training can ameliorate depression and improve mitochondrial function, we sought to investigate whether exercise can ameliorate depression-like behavior induced by prenatal sGC exposure and mitochondria function contributes to that behavior. At first, we confirmed that prenatal dexamethasone (Dex) administration in late pregnancy resulted in depression-like behavior and elevated level of circulatory corticosterone in adult offspring. We then found that mRNA and protein expression of a number of mitochondrial genes was changed in the hippocampus of Dex offspring. Mitochondria in the hippocampus showed abnormal morphology, oxidative stress and dysfunction in Dex offspring. Intracerebroventricular (ICV) injection of the mitochondrial superoxide scavenger mitoTEMPO significantly alleviated depression-like behavior but did not significantly affect circulatory corticosterone level in Dex offspring. The adult Dex offspring treated with treadmill exercise starting at four-weeks of age showed ameliorated depressive-like behavior, improved mitochondrial morphology and function and reduced circulatory corticosterone level. Our data suggest mitochondria dysfunction contributes to depression-like behavior caused by prenatal sGC exposure. Intervention with exercise training in early life can reverse depression caused by prenatal Dex exposure, which is associated with improvement of mitochondrial function in the hippocampus.

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Section: Introductionmentioning

confidence: 76%

Section: Methodsmentioning

confidence: 99%

Treadmill Exercise Ameliorates Depression-Like Behavior in the Rats With Prenatal Dexamethasone Exposure: The Role of Hippocampal Mitochondria

Huang

Gong

et al. 2019

Front. Neurosci.

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“…Dexamethasone-21-phosphate disodium salt (MilliporeSigma, St. Louis, MO, USA) was dissolved in saline to achieve the concentration as 100 ml containing 0.13 mg/kg body weight. The Dex dose was chosen on the basis of the literature (23,24), and this dose was used relevant to that administered to pregnant women at risk of preterm labor (25,26). During gestational days (GD) 14 to 21, 8 rats were subcutaneously administered 0.13 mg/kg dexamethasone-21phosphate disodium salt (equal to 0.1 mg/kg Dex), and 8 rats received vehicle (0.9% saline) once a day for 7 d. The pregnant rats delivered undisturbed to produce the F1 offspring.…”

Section: Animalsmentioning

confidence: 99%

CRH/CRHR1 mediates prenatal synthetic glucocorticoid programming of depression‐like behavior across 2 generations

Sheng

et al. 2018

FASEB j.

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Pregnant women at risk of preterm labor usually receive synthetic glucocorticoids (sGCs) to promote fetal lung development. Emerging evidence indicates that antenatal sGC increases the risk of affective disorders in offspring. Data from animal studies show that such disorders can be transmitted to the second generation. However, the molecular mechanisms underlying the intergenerational effects of prenatal sGC remain largely unknown. Here we show that prenatal dexamethasone (Dex) administration in late pregnancy induced depression-like behavior in first-generation (F1) offspring, which could be transmitted to second-generation (F2) offspring with maternal dependence. Moreover, corticotropin-releasing hormone (CRH) and CRH receptor type 1 (CRHR1) expression in the hippocampus was increased in F1 Dex offspring and F2 offspring from F1 Dex female rats. Administration of a CRHR1 antagonist to newborn F1 Dex offspring alleviated depression-like behavior in these rats at adult. Furthermore, we demonstrated that increased CRHR1 expression in F1 and F2 offspring was associated with hypomethylation of CpG islands in Crhr1 promoter. Our results revealed that prenatal sGC exposure could program Crh and Crhr1 gene expression in hippocampus across 2 generations, thereby leading to depression-like behavior. Our study indicates that prenatal sGC can cause epigenetic instability, which increases the risk of disease development in the offspring's later life.-Xu, Y.-J., Sheng, H., Wu, T.-W., Bao, Q.-Y., Zheng, Y., Zhang, Y.-M., Gong, Y.-X., Lu, J.-Q., You, Z.-D., Xia, Y., Ni, X. CRH/CRHR1 mediates prenatal synthetic glucocorticoid programming of depression-like behavior across 2 generations.

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“…A deleterious consequence of maternal stress on offspring includes depression. Adult female rats displayed sex-specific depressive-like behavior when submitted to an intrauterine stress environment as offspring, while males did not display these symptoms ( Liu et al, 2018 ). Interestingly, when these animals were subjected to a swimming exercise, depression symptoms were ameliorated, and this improvement was associated with OGT-related mitochondrial motility.…”

Section: O- Glcnac During Pregnancymentioning

confidence: 99%

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

et al. 2018

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Successful placentation is a key event for fetal development, which commences following embryo implantation into the uterine wall, eliciting decidualization, placentation, and remodeling of blood vessels to provide physiological exchange between embryo-fetus and mother. Several signaling pathways are recruited to modulate such important processes and specific proteins that regulate placental function are a target for the glycosylation with O-linked β-N-acetylglucosamine (O-GlcNAc), or O-GlcNAcylation. This is a reversible post-translational modification on nuclear and cytoplasmic proteins, mainly controlled by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). O-GlcNAcylation has been implicated as a modulator of proteins, both in physiological and pathological conditions and, more recently, O-GlcNAc has also been shown to be an important modulator in placental tissue. In this mini-review, the interplay between O-GlcNAcylation of proteins and placental function will be addressed, discussing the possible implications of this post-translational modification through placental development and pregnancy.

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OGT-related mitochondrial motility is associated with sex differences and exercise effects in depression induced by prenatal exposure to glucocorticoids

Cited by 16 publications

References 76 publications

Treadmill Exercise Ameliorates Depression-Like Behavior in the Rats With Prenatal Dexamethasone Exposure: The Role of Hippocampal Mitochondria

Treadmill Exercise Ameliorates Depression-Like Behavior in the Rats With Prenatal Dexamethasone Exposure: The Role of Hippocampal Mitochondria

CRH/CRHR1 mediates prenatal synthetic glucocorticoid programming of depression‐like behavior across 2 generations

O-GlcNAc Modification During Pregnancy: Focus on Placental Environment

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