Progesterone‐mediated angiogenic activity of endothelial progenitor cell and angiogenesis in traumatic brain injury rats were antagonized by progesterone receptor antagonist

Yu, Peng; Li, Shengjie; Zhang, Zhifei; Wen, Xiaolong; Quan, Wei; Tian, Qilong; Gao, Chuang; Su, Wanqiang; Zhang, Jianning; Jiang, Rongcai

doi:10.1111/cpr.12362

Cited by 28 publications

(27 citation statements)

References 66 publications

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“…In addition, it has been shown that the level of occludin expression in epithelial cells was inversely correlated with paracellular permeability 53–55 . Moreover, administration of progesterone improved brain function through reducing BBB permeability and increasing occludin expression in rats with traumatic brain injury, and progesterone receptor antagonist directly inhibited these functions 23,56 . Braniste et al .…”

Section: Discussionmentioning

confidence: 98%

Progesterone decreases gut permeability through upregulating occludin expression in primary human gut tissues and Caco-2 cells

Zhou

Bian

Luo

et al. 2019

Sci Rep

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Progesterone plays a protective role in preventing inflammation and preterm delivery during pregnancy. However, the mechanism involved is unknown. Microbial product translocation from a permeable mucosa is demonstrated as a driver of inflammation. To study the mechanism of the protective role of progesterone during pregnancy, we investigated the effect of physiologic concentrations of progesterone on tight junction protein occludin expression and human gut permeability in vitro and systemic microbial translocation in pregnant women in vivo . Plasma bacterial lipopolysaccharide (LPS), a representative marker of in vivo systemic microbial translocation was measured. We found that plasma LPS levels were significantly decreased during 24 to 28 weeks of gestation compared to 8 to 12 weeks of gestation. Moreover, plasma LPS levels were negatively correlated with plasma progesterone levels but positively correlated with plasma tumor necrosis factor-alpha (TNF-α) levels at 8 to 12 weeks of gestation but not at 24 to 28 weeks of gestation. Progesterone treatment increased intestinal trans-epithelial electrical resistance (TEER) in primary human colon tissues and Caco-2 cells in vitro through upregulating tight junction protein occludin expression. Furthermore, progesterone exhibited an inhibitory effect on nuclear factor kappa B (NF-κB) activation following LPS stimulation in Caco-2 cells. These results reveal a novel mechanism that progesterone may play an important role in decreasing mucosal permeability, systemic microbial translocation, and inflammation during pregnancy.

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Section: Discussionmentioning

confidence: 98%

Progesterone decreases gut permeability through upregulating occludin expression in primary human gut tissues and Caco-2 cells

Zhou

Bian

Luo

et al. 2019

Sci Rep

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“…During stroke, estrogens exert a protective action due to theirs effect on the cerebral vasculature, increasing endothelial nitric oxide synthase activity, suppressing inflammatory markers like COX-2, and reducing leukocyte adhesion (Suzuki et al, 2009 ). Similarly, in a rat model of traumatic brain injury, progesterone has been described to promote angiogenic activity of endothelial progenitor cells (Yu et al, 2017 ).…”

Section: Introductionmentioning

confidence: 97%

Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair

Zárate

Stevnsner

Gredilla

2017

Front. Aging Neurosci.

210

147

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Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed in all tissues, the brain being the most important one due to its main role in the homeostasis of the organism. As our knowledge about the underlying mechanisms of brain aging increases, potential approaches to preserve brain function rise significantly. Accumulating evidence suggests that loss of genomic maintenance may contribute to aging, especially in the central nervous system (CNS) owing to its low DNA repair capacity. Sex hormones, particularly estrogens, possess potent antioxidant properties and play important roles in maintaining normal reproductive and non-reproductive functions. They exert neuroprotective actions and their loss during aging and natural or surgical menopause is associated with mitochondrial dysfunction, neuroinflammation, synaptic decline, cognitive impairment and increased risk of age-related disorders. Moreover, loss of sex hormones has been suggested to promote an accelerated aging phenotype eventually leading to the development of brain hypometabolism, a feature often observed in menopausal women and prodromal Alzheimer’s disease (AD). Although data on the relation between sex hormones and DNA repair mechanisms in the brain is still limited, various investigations have linked sex hormone levels with different DNA repair enzymes. Here, we review estrogen anti-aging and neuroprotective mechanisms, which are currently an area of intense study, together with the effect they may have on the DNA repair capacity in the brain.

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“…In addition, an adjunct area that can be explored is the hormone therapy in epileptic patients. To this end, convincing data indicate that endothelial cells express estrogen or progesterone receptors, and both of these hormones have been shown to protect from vascular injury/BBB dysfunction in rodent models (Si et al, 2014;Shin et al, 2016;Yu et al, 2017). Therefore, targeting the vascular hormone receptors may serve as another approach to restore BBB defects, as well as for improving the angiogenic outcome in epileptogenesis.…”

Section: Vascular Therapy For Epilepsymentioning

confidence: 99%

Vascular Integrity and Signaling Determining Brain Development, Network Excitability, and Epileptogenesis

2020

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Our understanding of the etiological mechanisms leading up to epilepsy has undergone radical changes over time due to more insights into the complexity of the disease. The traditional hypothesis emphasized network hyperexcitability and an imbalance of inhibition and excitation, eventually leading to seizures. In this context, the contribution of the vascular system, and particularly the interactions between blood vessels and neuronal tissue, came into focus only recently. Thus, one highly exciting causative or contributing factor of epileptogenesis is the disruption of the blood-brain barrier (BBB) in the context of not only posttraumatic epilepsy, but also other etiologies. This hypothesis is now recognized as a synergistic mechanism that can give rise to epilepsy, and BBB repair for restoration of cerebrovascular integrity is considered a therapeutic alternative. Endothelial cells lining the inner surface of blood vessels are an integral component of the BBB system. Sealed by tight junctions, they are crucial in maintaining homeostatic activities of the brain, as well as acting as an interface in the neurovascular unit. Additional potential vascular mechanisms such as inflammation, altered neurovascular coupling, or changes in blood flow that can modulate neuronal circuit activity have been implicated in epilepsy. Our own work has shown how intrinsic defects within endothelial cells from the earliest developmental time points, which preclude neuronal changes, can lead to vascular abnormalities and autonomously support the development of hyperexcitability and epileptiform activity. In this article, we review the importance of vascular integrity and signaling for network excitability and epilepsy by highlighting complementary basic and clinical research studies and by outlining possible novel therapeutic strategies.

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Progesterone‐mediated angiogenic activity of endothelial progenitor cell and angiogenesis in traumatic brain injury rats were antagonized by progesterone receptor antagonist

Abstract: It may suggest that P4-mediated angiogenic activity of EPC and angiogenesis in TBI rats were antagonized by PR antagonist.

Cited by 28 publications

References 66 publications

Progesterone decreases gut permeability through upregulating occludin expression in primary human gut tissues and Caco-2 cells

Progesterone decreases gut permeability through upregulating occludin expression in primary human gut tissues and Caco-2 cells

Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair

Vascular Integrity and Signaling Determining Brain Development, Network Excitability, and Epileptogenesis

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