Inflammation-induced fetal growth restriction in rats is associated with increased placental HIF-1α accumulation

Robb, Kevin P.; Cotechini, Tiziana; Allaire, Camille; Sperou, Arissa; Graham, Charles H.

doi:10.1371/journal.pone.0175805

Cited by 40 publications

(34 citation statements)

References 53 publications

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“…Exaggerated maternal inflammation during pregnancy is usually associated with poor trophoblastic invasion, placental malperfusion and IUGR (Anton, Brown, Parry, & Elovitz, ; Robb, Cotechini, Allaire, Sperou, & Graham, ). It is also linked to neurodevelopmental disorders in the child (Angelidou et al, ; Brown, ; Flinkkilä, Keski‐Rahkonen, Marttunen, & Raevuori, ).…”

Section: Models Of Iugr and Fetal Programmingmentioning

confidence: 99%

Models of Intrauterine growth restriction and fetal programming in rabbits

López-Tello

Álvarez

González-Bulnes³

et al. 2019

Molecular Reproduction Devel

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Intrauterine growth restriction (IUGR) affects approximately 10% of human pregnancies globally and has immediate and life‐long consequences for offspring health. However, the mechanisms underlying the pathogenesis of IUGR and its association with later health and disease outcomes are poorly understood. To address these knowledge gaps, the use of experimental animals is critically important. Since the 50's different environmental, pharmacological, and surgical manipulations have been performed in the rabbit to improve our knowledge of the control of fetal growth, fetal responses to IUGR, and mechanisms by which offspring may be programmed by an adverse gestational environment. The purpose of this review is therefore to summarize the utility of the rabbit as a model for IUGR research. It first summarizes the knowledge of prenatal and postnatal development in the rabbit and how these events relate to developmental milestones in humans. It then describes the methods used to induce IUGR in rabbits and the knowledge gained about the mechanisms determining prenatal and postnatal outcomes of the offspring. Finally, it discusses the application of state of the art approaches in the rabbit, including high‐resolution ultrasound, magnetic resonance imaging, and gene targeting, to gain a deeper integrative understanding of the physiological and molecular events governing the development of IUGR. Overall, we hope to engage and inspire investigators to employ the rabbit as a model organism when studying pregnancy physiology so that we may advance our understanding of mechanisms underlying IUGR and its consequences in humans and other mammalian species.

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Section: Models Of Iugr and Fetal Programmingmentioning

confidence: 99%

Models of Intrauterine growth restriction and fetal programming in rabbits

López-Tello

Álvarez

González-Bulnes³

et al. 2019

Molecular Reproduction Devel

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“…Moreover, according to the hypothesis of this research, only the protein expression HIF-1α should be upregulated due to the blocking of degradation. While we also observed the increase expression of HIF-1α in the level of mRNA, which may be related to the influence of pyruvate to inflammation/-ROS in the process of ischemia-reperfusion, the latter were reported to associate with the transcription of HIF-1α [43].…”

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confidence: 44%

Direct Peritoneal Resuscitation with Pyruvate Protects the Spinal Cord and Induces Autophagy via Regulating PHD2 in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury

Xiong

Xia

Deng

et al. 2020

Oxidative Medicine and Cellular Longevity

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Direct peritoneal resuscitation with pyruvate (Pyr-PDS) has emerged as an interesting candidate to alleviate injury in diverse organs, while the potential mechanism has yet to be fully elucidated. To explore the effect of autophagy in the spinal cord ischemia-reperfusion (SCIR) injury and the underlying mechanism, we established a model of SCIR in vivo and in vitro. In vivo, male SD rats underwent aortic occlusion for 60 min and then followed by intraperitoneally infused with 20 mL of pyruvate or normal saline for 30 min, and the spinal cords were removed for analysis after 48 h of reperfusion. The functional and morphological results showed that Pyr-PDS alleviated SCIR injury; meanwhile, the expression of autophagy-related genes and transmission electron microscopy displayed autophagy was activated by SCIR injury, and Pyr-PDS treatment could further upregulate the degree of autophagy which plays a protective part in the SCIR injury, while there is no significant difference after treatment with saline. In addition, SCIR injury inhibited expression of PHD2, which results to activate its downstream HIF-1α/BNIP3 pathway to promote autophagy. In the Pyr-PDS, the results revealed PHD2 was further inhibited compared to the SCIR group, which could further activate the HIF-1α/BNIP3 signaling pathway. Additionally, oxygen-glucose deprivation and reoxygenation were applied to SH-SY5Y cells to mimic anoxic conditions in vitro, and the expression of autophagy-related genes, PHD2, and its downstream HIF-1α/BNIP3 pathway showed the same trend as the results in vivo. Besides, IOX2, a specific inhibitor of PHD2 was also treated to SH-SY5Y cells during reoxygenation, in which the result is as same as the pyruvate group. Then, we observed the expression of autophagy-related genes and the HIF-1α signal pathway in the process of reoxygenation; the results showed that as the reoxygenation goes, the expression of the HIF-1α signal pathway and degree of autophagy came to decrease gradually, while treated with pyruvate could maintain autophagy high and stable through keeping PHD2 at a lower level during reoxygenation, and the latter was observed downregulated during reoxygenation process from 0 to 24 hours in a time-effect way. The above results indicated that direct peritoneal resuscitation with pyruvate showed effective protection to ischemia-reperfusion of the spinal cord through activating autophagy via acting on PHD2 and its downstream HIF-1α/BNIP3 pathway.

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“…Haemodynamic changes in the maternal uterine circulation are characterized by a significant decrease in the resistance of the uterine vessels, which in turn, is due to vessel growth and vasodilation [20]. It was reported in rats that intrauterine growth restriction was associated with altered utero-placental perfusion [21]. These may explain the increased number of foetal loss during parturition (Table 4) and the decreased weight of the uteroplacental swelling on day 16 of pregnancy ( Table 6).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Nicotine on Foetal Loss, Postnatal Growth and Plasma Oestrogen and Progesterone Levels in Rats

Tambeh¹,

Ghosh²,

Rajikin³

2019

JCHS

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Introduction: The present study aims to investigate the effects of nicotine on foetal loss, postnatal growth and corresponding levels of oestrogen and progesterone in pregnant rats. Method: Subcutaneous injection of nicotine tartrate (7.5 mg/kg/day) was administered to groups of pregnant rats; with treatment scheduled from day 1 through day 5, day 5 through day 9 or day 1 through day 9 of pregnancy. On day 10 of pregnancy, laparotomy was performed to count the number of blastocyst implantation sites. During parturition, the number of viable pups was recounted and statistically compared with the controls. One group of rats which received nicotine from day 1 through day 9 of pregnancy was sacrificed on day 16 of pregnancy, and circulating levels of oestrogen and progesterone were measured. Upon delivery, the birth weight of the pups was measured, and their weights were recorded until weaning. Result: There was a significant increase in foetal loss particularly in rats which received nicotine from day 5 through day 9 and from day 1 through day 9 of pregnancy. There was also significantly lower birth weight of pups in all groups; however, this pattern did not continue until weaning. Plasma oestrogen level was significantly elevated with a significant decrease in the plasma progesterone level. Conclusion: Nicotine administration during pregnancy showed an increase in foetal loss with a corresponding increase in oestrogen and decrease in progesterone levels. Although the birth weight of the pups was low, there was catch-up growth in the pups.

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Inflammation-induced fetal growth restriction in rats is associated with increased placental HIF-1α accumulation

Cited by 40 publications

References 53 publications

Models of Intrauterine growth restriction and fetal programming in rabbits

Models of Intrauterine growth restriction and fetal programming in rabbits

Direct Peritoneal Resuscitation with Pyruvate Protects the Spinal Cord and Induces Autophagy via Regulating PHD2 in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury

The Effects of Nicotine on Foetal Loss, Postnatal Growth and Plasma Oestrogen and Progesterone Levels in Rats

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