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Article ; Online: Histological Analysis of Trophoblast Cells in the Mouse Placental Labyrinth Zone.

Lopez-Tello, Jorge / Sferruzzi-Perri, Amanda

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2781, Page(s) 1–13

Abstract: The mouse is a common animal species used for translational studies. In reproductive studies, this animal is typically preferred over other models as the rodent placenta shows similarities to the human but has a relatively short gestational period. In ... ...

Abstract	The mouse is a common animal species used for translational studies. In reproductive studies, this animal is typically preferred over other models as the rodent placenta shows similarities to the human but has a relatively short gestational period. In mice, the transport of oxygen and nutrients between mother and fetus occurs in a restricted area of the placenta called the labyrinth zone. Here, we provide a detailed protocol to study labyrinth zone trophoblast proliferation and syncytial trophoblast identification using paraffin-embedded histological sections of the mouse placenta and immunohistochemistry. By describing step by step how to collect the mouse placenta and process and analyze the labyrinth zone, we hope to help other scientists understand the contribution of changes in placental transport function in their experimental model and therefore advance our understanding of mechanisms underlying pregnancy complications.
MeSH term(s)	Mice ; Pregnancy ; Female ; Humans ; Animals ; Placenta ; Trophoblasts ; Rodentia
Language	English
Publishing date	2024-03-19
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3746-3_1
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Article ; Online: Early-life exposures and long-term health: adverse gestational environments and the programming of offspring renal and vascular disease.

Oulerich, Zoé / Sferruzzi-Perri, Amanda N

American journal of physiology. Renal physiology

2024

Abstract: According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, exposure to certain environmental influences during early life may be a key determinant of fetal development and short- and long-term offspring health. Indeed, adverse ... ...

Abstract	According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, exposure to certain environmental influences during early life may be a key determinant of fetal development and short- and long-term offspring health. Indeed, adverse conditions encountered during the fetal, perinatal, and early childhood stages can alter normal development and growth, as well as put the offspring at elevated risk of developing long-term health conditions in adulthood, including chronic kidney disease (CKD) and cardiovascular diseases. Of relevance in understanding the mechanistic basis of these long-term health conditions, are previous findings showing low glomerular number in human intrauterine growth restriction and low birth weight - indicators of a sub-optimal intrauterine environment. In different animal models, the main sub-optimal intrauterine conditions studied relate to maternal dietary manipulations, poor micronutrient intake, prenatal ethanol exposure, maternal diabetes, glucocorticoid and chemical exposure, hypoxia, and placental insufficiency. These studies have demonstrated changes in kidney structure, glomerular endowment, and expression of key genes and signalling pathways controlling endocrine, excretion and filtration function of the offspring. This review aims to summarize those studies to uncover the effects and mechanisms by which adverse gestational environments impact offspring renal and vascular health in adulthood. This is important for identifying agents and interventions that can prevent and mitigate the long-term consequences of an adverse intrauterine environment on the subsequent generation.
Language	English
Publishing date	2024-05-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00383.2023
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Article ; Online: Placental inflammation, oxidative stress, and fetal outcomes in maternal obesity.

Zhang, Cindy X W / Candia, Alejandro A / Sferruzzi-Perri, Amanda N

Trends in endocrinology and metabolism: TEM

2024

Abstract: The obesity epidemic has led to a growing body of research investigating the consequences of maternal obesity on pregnancy and offspring health. The placenta, traditionally viewed as a passive intermediary between mother and fetus, is known to play a ... ...

Abstract	The obesity epidemic has led to a growing body of research investigating the consequences of maternal obesity on pregnancy and offspring health. The placenta, traditionally viewed as a passive intermediary between mother and fetus, is known to play a critical role in modulating the intrauterine environment and fetal development, and we now know that maternal obesity leads to increased inflammation, oxidative stress, and altered placental function. Here, we review recent research exploring the involvement of inflammation and oxidative stress as mechanisms impacting the placenta and fetus during obese pregnancy. Understanding them is crucial for informing strategies that can mitigate the adverse health effects of maternal obesity on offspring development and disease risk.
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2024.02.002
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Article ; Online: Placental mitochondria central to gestational diabetes pathogenesis?

Sferruzzi-Perri, Amanda N

The Journal of physiology

2020 Volume 599, Issue 4, Page(s) 1019–1020

MeSH term(s)	Diabetes, Gestational/metabolism ; Female ; Humans ; Mitochondria ; Placenta/metabolism ; Pregnancy ; Trophoblasts/metabolism
Language	English
Publishing date	2020-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP281041
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Article: Characterization of placental endocrine function and fetal brain development in a mouse model of small for gestational age.

Lopez-Tello, Jorge / Sferruzzi-Perri, Amanda N

Frontiers in endocrinology

2023 Volume 14, Page(s) 1116770

Abstract: Conditions such as small for gestational age (SGA), which is defined as birthweight less than ... ...

Abstract	Conditions such as small for gestational age (SGA), which is defined as birthweight less than 10
MeSH term(s)	Humans ; Pregnancy ; Female ; Animals ; Mice ; Birth Weight ; Placenta/metabolism ; Gestational Age ; Fetal Growth Retardation/metabolism ; Fetal Development ; Fetus/metabolism ; Placenta Diseases ; Fetal Weight ; Brain/metabolism
Language	English
Publishing date	2023-02-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1116770
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Article ; Online: Mitochondrial dysfunction in the offspring of obese mothers and it's transmission through damaged oocyte mitochondria: Integration of mechanisms.

Elías-López, A L / Vázquez-Mena, O / Sferruzzi-Perri, A N

Biochimica et biophysica acta. Molecular basis of disease

2023 Volume 1869, Issue 7, Page(s) 166802

Abstract: In vivo and in vitro studies demonstrate that mitochondria in the oocyte, are susceptible to damage by suboptimal pre/pregnancy conditions, such as obesity. These suboptimal conditions have been shown to induce mitochondrial dysfunction (MD) in multiple ... ...

Abstract	In vivo and in vitro studies demonstrate that mitochondria in the oocyte, are susceptible to damage by suboptimal pre/pregnancy conditions, such as obesity. These suboptimal conditions have been shown to induce mitochondrial dysfunction (MD) in multiple tissues of the offspring, suggesting that mitochondria of oocytes that pass from mother to offspring, can carry information that can programme mitochondrial and metabolic dysfunction of the next generation. They also suggest that transmission of MD could increase the risk of obesity and other metabolic diseases in the population inter- and trans-generationally. In this review, we examined whether MD observed in offspring tissues of high energetic demand, is the result of the transmission of damaged mitochondria from the oocytes of obese mothers to the offspring. The contribution of genome-independent mechanisms (namely mitophagy) in this transmission were also explored. Finally, potential interventions aimed at improving oocyte/embryo health were investigated, to see if they may provide an opportunity to halter the generational effects of MD.
MeSH term(s)	Pregnancy ; Female ; Humans ; Mothers ; Mitochondria/metabolism ; Obesity/metabolism ; Oocytes/metabolism ; Mitophagy
Language	English
Publishing date	2023-07-05
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2023.166802
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Article ; Online: Suppression of uterine and placental ferroptosis by N-acetylcysteine in a rat model of polycystic ovary syndrome.

Hu, Min / Zhang, Yuehui / Ma, Shuting / Li, Juanli / Wang, Xu / Liang, Mengmeng / Sferruzzi-Perri, Amanda Nancy / Wu, Xiaoke / Ma, Hongxia / Brännström, Mats / Shao, Linus R / Billig, Håkan

Molecular human reproduction

2021 Volume 27, Issue 12

Abstract: ... of the antioxidant N-acetylcysteine (NAC) in reversing gravid uterine and placental ferroptosis in pregnant rats ...

Abstract	The mechanisms that link hyperandrogenism and insulin (INS) resistance (HAIR) to the increased miscarriage rate in women with polycystic ovary syndrome (PCOS) remain elusive. Previous studies demonstrate that increased uterine and placental ferroptosis is associated with oxidative stress-induced fetal loss in a pre-clinical PCOS-like rat model. Here, we investigated the efficacy and molecular mechanism of action of the antioxidant N-acetylcysteine (NAC) in reversing gravid uterine and placental ferroptosis in pregnant rats exposed to 5α-dihydrotestosterone (DHT) and INS. Molecular and histological analyses showed that NAC attenuated DHT and INS-induced uterine ferroptosis, including dose-dependent increases in anti-ferroptosis gene content. Changes in other molecular factors after NAC treatment were also observed in the placenta exposed to DHT and INS, such as increased glutathione peroxidase 4 protein level. Furthermore, increased apoptosis-inducing factor mitochondria-associated 2 mRNA expression was seen in the placenta but not in the uterus. Additionally, NAC was not sufficient to rescue DHT + INS-induced mitochondria-morphological abnormalities in the uterus, whereas the same treatment partially reversed such abnormalities in the placenta. Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, homeobox A11 mRNA expression and placental estrogen-related receptor beta and trophoblast-specific protein alpha mRNA expression. Collectively, our data provide insight into how NAC exerts beneficial effects on differentially attenuating gravid uterine and placental ferroptosis in a PCOS-like rat model with fetal loss. These results indicate that exogenous administration of NAC represents a potential therapeutic strategy in the treatment of HAIR-induced uterine and placental dysfunction.
MeSH term(s)	Acetylcysteine/pharmacology ; Animals ; Antioxidants/pharmacology ; Dihydrotestosterone ; Disease Models, Animal ; Female ; Ferroptosis/drug effects ; Glutathione/metabolism ; Insulin Resistance ; Iron/metabolism ; Male ; Malondialdehyde/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Oxidative Phosphorylation ; Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism ; Placenta/drug effects ; Placenta/metabolism ; Placenta/ultrastructure ; Polycystic Ovary Syndrome/chemically induced ; Polycystic Ovary Syndrome/metabolism ; Polycystic Ovary Syndrome/pathology ; Polycystic Ovary Syndrome/prevention & control ; Pregnancy ; Rats, Sprague-Dawley ; Signal Transduction ; Uterus/drug effects ; Uterus/metabolism ; Uterus/ultrastructure ; Rats
Chemical Substances	Antioxidants ; Dihydrotestosterone (08J2K08A3Y) ; Malondialdehyde (4Y8F71G49Q) ; Iron (E1UOL152H7) ; Phospholipid Hydroperoxide Glutathione Peroxidase (EC 1.11.1.12) ; glutathione peroxidase 4, rat (EC 1.11.1.9) ; Glutathione (GAN16C9B8O) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2021-11-28
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1324348-2
ISSN	1460-2407 ; 1360-9947
ISSN (online)	1460-2407
ISSN	1360-9947
DOI	10.1093/molehr/gaab067
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Article ; Online: Human placental development and function.

Cindrova-Davies, Tereza / Sferruzzi-Perri, Amanda N

Seminars in cell & developmental biology

2022 Volume 131, Page(s) 66–77

Abstract: The placenta is a transient fetal organ that plays a critical role in the health and wellbeing of both the fetus and its mother. Functionally, the placenta sustains the growth of the fetus as it facilitates delivery of oxygen and nutrients and removal of ...

Abstract	The placenta is a transient fetal organ that plays a critical role in the health and wellbeing of both the fetus and its mother. Functionally, the placenta sustains the growth of the fetus as it facilitates delivery of oxygen and nutrients and removal of waste products. Not surprisingly, defective early placental development is the primary cause of common disorders of pregnancy, including recurrent miscarriage, fetal growth restriction, pre-eclampsia and stillbirth. Adverse pregnancy conditions will also affect the life-long health of the fetus via developmental programming[1]. Despite its critical importance in reproductive success and life-long health, our understanding of placental development is not extensive, largely due to ethical limitations to studying early or chronological placental development, lack of long-term in vitro models, or comparative animal models. In this review, we examine current knowledge of early human placental development, discuss the critical role of the maternal endometrium and of the fetal-maternal dialogue in pregnancy success, and we explore the latest models of trophoblast and endometrial stem cells. In addition, we discuss the role of oxygen in placental formation and function, how nutrient delivery is mediated during the periods of histotrophic nutrition (uptake of uterine secretions) and haemotrophic nutrition (exchange between the maternal and fetal circulations), and how placental endocrine function facilitates fetal growth and development.
MeSH term(s)	Animals ; Female ; Fetal Development ; Humans ; Maternal-Fetal Exchange ; Oxygen ; Placenta ; Placentation ; Pregnancy
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2022-04-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2022.03.039
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Article ; Online: Assessment of Placental Transport Function in Studies of Disease Programming.

Sferruzzi-Perri, Amanda N

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1735, Page(s) 239–250

Abstract: Environmental conditions during pregnancy affect fetal growth and development and program the offspring for poor future health. These effects may be mediated by the placenta, which develops to transfer nutrients from the mother to the fetus for growth. ... ...

Abstract	Environmental conditions during pregnancy affect fetal growth and development and program the offspring for poor future health. These effects may be mediated by the placenta, which develops to transfer nutrients from the mother to the fetus for growth. The ability to measure the unidirectional maternofetal transfer of non-metabolizable radio-analogues of glucose and amino acid by the placenta in vivo has thus been invaluable to our understanding of the regulation of fetal growth, particularly in small animal models. Herein, I describe the method by which in vivo placental transfer function can be quantified in the mouse, an animal model widely used in studies of in utero disease programming.
MeSH term(s)	Animals ; Biological Transport ; Disease Susceptibility ; Female ; Fetal Development ; Male ; Maternal-Fetal Exchange ; Mice ; Placenta/metabolism ; Pregnancy
Language	English
Publishing date	2018-01-30
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7614-0_14
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Article ; Online: Correction to: Developmental programming of offspring adipose tissue biology and obesity risk.

Rodgers, Amanda / Sferruzzi-Perri, Amanda N

International journal of obesity (2005)

2021 Volume 45, Issue 8, Page(s) 1861

Language	English
Publishing date	2021-11-07
Publishing country	England
Document type	Published Erratum
ZDB-ID	752409-2
ISSN	1476-5497 ; 0307-0565
ISSN (online)	1476-5497
ISSN	0307-0565
DOI	10.1038/s41366-021-00828-z
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