Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications

Hu, Xiang‐Qun; Zhang, Li

doi:10.3390/antiox10030405

Cited by 43 publications

(40 citation statements)

References 331 publications

(209 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The suppression of NFκB activation and its translocation into nucleus of cells in mice uterus was found to delay the process of implantation confirmed in animal models whereas the complete loss of NFκB activity in knockout mice results in death [ 31 , 32 ]. As implantation proceeds, the oxygen level in the environment increases; this steers trophoblast differentiation toward remodeling of the maternal spiral artery and allows the placenta to mature into an exchange organ [ 33 , 34 ]. The inflammatory reaction is gradually slowed, thus allowing the development of an immunosuppression stage needed to maintain pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…In this process, the p53/RSK1 complex plays a dominant role, being responsible for the phosphorylation of NFκB at Serine536 [ 19 , 49 ]. It is known that preeclampsia is related to the accumulation of ROS and inflammatory factors in maternal blood, and that the HTR8/SVneo cell line generates mitochondrial ROS in hypoxic condition [ 34 , 50 , 51 , 52 ]. Therefore, in the present study, the combination of maternal serum and hypoxic conditions certainly influenced the generation of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line

Sakowicz

Bralewska

Pietrucha

et al. 2021

IJMS

View full text Add to dashboard Cite

Preeclampsia is a pregnancy disorder associated with shallow placentation, forcing placental cells to live in hypoxic conditions. This activates the transcription factor kappa B (NFκB) in maternal and placental cells. Although the role of NFκB in preeclampsia is well documented, its mechanism of activation in trophoblastic cells has been never studied. This study investigates the mechanism of NFκB activation in a first trimester trophoblastic cell line (HTR8/SVneo) stimulated by a medium containing serum from preeclamptic (PE) or normotensive (C) women in hypoxic (2% O2) or normoxic (8% O2) conditions. The results indicate that in HTR8/SVneo cells, the most widely studied NFκB pathways, i.e., canonical, non-canonical and atypical, are downregulated in environment PE 2% O2 in comparison to C 8% O2. Therefore, other pathways may be responsible for NFκB activation. One such pathway depends on the activation of NFκB by the p53/RSK1 complex through its phosphorylation at Serine 536 (pNFκB Ser536). The data generated by our study show that inhibition of the p53/RSK1 pathway by p53-targeted siRNA results in a depletion of pNFκB Ser536 in the nucleus, but only in cells incubated with PE serum at 2% O2. Thus, the p53/RSK1 complex might play a critical role in the activation of NFκB in trophoblastic cells and preeclamptic placentas.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line

Sakowicz

Bralewska

Pietrucha

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…In addition, overproduced ROS would overwhelm the endogenous defense mechanisms (SOD, etc. ), further leading to the accumulation of ROS [ 14 , 15 ]. ROS is considered to play a critical role in disease progression after MI [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

An antioxidant system through conjugating superoxide dismutase onto metal-organic framework for cardiac repair

Guo

Yang

et al. 2022

Bioactive Materials

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) remains a dominant origin of morbidity, mortality and disability worldwide. Increases in reactive oxygen species (ROS) are key contributor to excessive cardiac injury after AMI. Here we developed an immobilized enzyme with Superoxide Dismutase (SOD) activity cross-link with Zr-based metal-organic framework (ZrMOF) (SOD-ZrMOF) for mitigate ROS-caused injury. In vitro and in vivo evidence indicates that SOD-ZrMOF exhibits excellent biocompatibility. By efficiently scavenging ROS and suppressing oxidative stress, SOD-ZrMOF can protect the function of mitochondria, reduce cell death and alleviate inflammation. More excitingly, long-term study using an animal model of AMI demonstrated that SOD-ZrMOF can reduce the infarct area, protect cardiac function, promote angiogenesis and inhibit pathological myocardial remodeling. Therefore, SOD-ZrMOF holds great potential as an efficacious and safe nanomaterial treatment for AMI.

show abstract

“…Here, we showed that padlock assay is a robust method to map the distribution of the SARS-CoV-2 genome in infected tissues, and, most importantly, for the first time we provided images visualizing the in situ co-localization of SARS-CoV-2 RNA and mitochondria in host cells. Furthermore, in the context of pregnancy complications, mitochondrial dysfunction appears a critical feature in the pathogenesis of preeclampsia [10]. To note, pregnant women with COVID-19 are more likely to develop preeclampsia [11].…”

Section: Introductionmentioning

confidence: 99%

Exploring Mitochondrial Localization of SARS-CoV-2 RNA by Padlock Assay. A Pilot Study in Human Placenta

Certo¹,

Gabanella²,

Barbato³

et al. 2022

Preprint

View full text Add to dashboard Cite

The ongoing COVID-19 pandemic dictated new priorities in biomedicine research. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of COVID-19, is a single-stranded positive-sense RNA virus. In this pilot study, we optimized our padlock assay to visualize genomic/subgenomic regions using formalin-fixed paraffin-embedded placental samples obtained from a confirmed case of COVID-19. SARS-CoV-2 RNA was localized in trophoblastic cells. We also checked the presence of the virion by immunolocalization of its glycoprotein spike. In addition, we imaged mitochondria of placental villi keeping in mind that the mitochondrion has been suggested as a potential residence of the SARS-CoV-2 genome. Indeed, we observed a substantial overlapping of SARS-CoV-2 RNA and mitochondria in trophoblastic cells. This intriguing linkage correlated with an aberrant mitochondrial network. Overall, to our knowledge, this is the first study that provides the evidence of a co-localization of the SARS-CoV-2 genome and mitochondria in SARS-CoV-2 infected tissue. These findings also support the notion that SARS-CoV-2 infection could reprogram mitochondrial activity in highly specialized maternal/fetal interface.

show abstract

Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications

Cited by 43 publications

References 331 publications

The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line

The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line

An antioxidant system through conjugating superoxide dismutase onto metal-organic framework for cardiac repair

Exploring Mitochondrial Localization of SARS-CoV-2 RNA by Padlock Assay. A Pilot Study in Human Placenta

Contact Info

Product

Resources

About