Increased oxidative stress and cancer biomarkers in the ventral prostate of older rats submitted to maternal malnutrition

Portela, Luiz Marcos Frediani; Santos, Sérgio A. A.; Constantino, Flávia Bessi; Camargo, Ana Carolina Lima; Colombelli, Ketlin T.; Fioretto, Matheus Naia; Barquilha, Caroline N.; Périco, Larissa Lucena; Hiruma-Lima, Clélia Akiko; Scarano, Wellerson Rodrigo; Zambrano, Elena; Justulin, Luis Antônio

doi:10.1016/j.mce.2020.111148

Cited by 20 publications

(17 citation statements)

References 65 publications

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“…The expression pro le of miRNA extracted from PRAD-TCGA demonstrated the downregulation of miR-206 in patients with PCa. Interestingly, we observed a reduction in the expression pro le of miR-206 and an increase in Plg gene expression in the VP of older offspring rats from the GLLP groups, which developed prostate carcinoma in situ[21][22][23]. Functional validation con rmed the modulation negative correlation of the miR-206/PLG expression, as well as their participation in modulating cell migration and invasion in PNT2 cells.…”

mentioning

confidence: 57%

“…Over the past decades, the DOHaD concept has provided causal relationships between early-life exposure to environmental risk factors and the developmental origins of non-communicable chronic diseases, including PCa [7,21,22]. Although the molecular mechanisms involved in this process remain elusive, the imbalance of sex hormones in both dams and offspring submitted to maternal malnutrition has been pointed to as a key factor related to prostate carcinogenesis in the progeny [6, 9,10,21,22].…”

Section: Discussionmentioning

confidence: 99%

“…The diets followed the AIN-93 standards described by Reeves et al (1993) and were provided by PragSoluções (PragSoluções, SP, Brazil) [25]. The diets were previously used in other studies [15,21,22]. Litters were reduced to eight pups (four males and four females) on a postnatal day (PND) 1 to maximize lactation performance [26].…”

Section: Animals and Dietsmentioning

confidence: 99%

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Early-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats

Portela

Constantino

Camargo

et al. 2022

Preprint

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The Developmental Origins of Health and Disease (DOHaD) has provided the framework to assess how early life experiences can shape health and disease throughout the life course. While maternal malnutrition has been proposed as a risk factor for the developmental programming of prostate cancer (PCa), the molecular mechanisms remain poorly understood. Here, we found an association between deregulation of steroidogenesis and impairment of the ventral prostate (VP) growth in young offspring rats exposed to maternal low protein diet (LPD) during gestation and lactation. Reanalysis of RNA-seq data demonstrated that miR-206 was upregulated in the VP of young maternally malnourished offspring. Target prediction and in vitro studies identified Plasminogen (PLG) as a direct target of miR-206. To give further insights into the participation of the miR-206-PLG network in prostate carcinogenesis in the progeny submitted to maternal LPD. RT-qPCR analysis revealed deregulation of the miR-206-PLG network in the VP of older rats that developed prostate carcinoma in situ. Furthermore, mimic studies revealed a negative correlation between miR-206 and estrogen receptor α (ESR1) expression in PNT2 cells. Together, we demonstrate that early life estrogenization associated with deregulation of miR-206-networks can contribute to the developmental origins of PCa in maternally malnourished offspring. Understanding the molecular mechanisms by which early life malnutrition affects offspring health can encourage the adoption of a governmental policy for the prevention of non-communicable chronic diseases related to the DOHaD concept.

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confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Early-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats

Portela

Constantino

Camargo

et al. 2022

Preprint

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“…Maternal liver and two placentas from each litter (one from female newborns and the other from one of the male newborns were randomly assigned) were removed and quickly frozen in liquid nitrogen and stored in a freezer at -80°C until homogenates were performed. The liver homogenate (modified from Spada et al, 2014 ) was used for redox status evaluation, and the placental homogenate (modified from Portela et al, 2021 ) was used for leptin and adiponectin determinations. Newborns were sexed and all male and female newborns from each litter were euthanized and killed by decapitation for blood collection (pool).…”

Section: Methodsmentioning

confidence: 99%

Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring

Sinzato

Paula

Gallego

et al. 2022

Front. Cell Dev. Biol.

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Maternal diabetes-induced fetal programming predisposes offspring to type 2 diabetes, cardiovascular disease, and obesity in adulthood. However, lifelong health and disease trajectories depend on several factors and nutrition is one of the main ones. We intend to understand the role of maternal diabetes-induced fetal programming and its association with a high-fat diet during lifelong in the female F1 generation focusing on reproductive outcomes and the possible changes in physiological systems during pregnancy as well as the repercussions on the F2 generation at birth. For this, we composed four groups: F1 female pups from control (OC) or from diabetic dams (OD) and fed with standard (SD) or high-fat diet from weaning to full-term pregnancy. During pregnancy, glucose intolerance and insulin sensitivity were evaluated. In a full-term pregnancy, the maternal blood and liver were collected to evaluate redox status markers. The maternal blood, placental tissue, and fetal blood (pool) were collected to evaluate adiponectin and leptin levels. Maternal reproductive parameters were evaluated as well. Maternal diabetes and high-fat diet consumption, in isolation, were both responsible for increased infertility rates and fasting glucose levels in the F1 generation and fetal growth restriction in the F2 generation. The association of both conditions showed, in addition to those, increased lipoperoxidation in maternal erythrocytes, regardless of the increased endogenous antioxidant enzyme activities, glucose intolerance, decreased number of implantation sites and live fetuses, decreased litter, fetal and placental weight, increased preimplantation losses, and increased fetal leptin serum levels. Thus, our findings show that fetal programming caused by maternal diabetes or lifelong high-fat diet consumption leads to similar repercussions in pregnant rats. In addition, the association of both conditions was responsible for glucose intolerance and oxidative stress in the first generation and increased fetal leptin levels in the second generation. Thus, our findings show both the F1 and F2 generations harmed health after maternal hyperglycemic intrauterine environment and exposure to a high-fat diet from weaning until the end of pregnancy.

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“…The presence of alternative receptors and proteases for SARS-CoV-2 entry into STB cells has been suggested [ 114 ]. Recently proposed alternative receptors are DPP4 (CD26) and CD147 [ 115 , 116 ]. Whereas, furin and trypsin, both expressed on placental tissues through gestation, have been suggested as SARS-CoV-2 entry proteases [ 113 , 117 , 118 ].…”

Section: Covid 19—placentamentioning

confidence: 99%

The Immunological Role of the Placenta in SARS-CoV-2 Infection—Viral Transmission, Immune Regulation, and Lactoferrin Activity

Bukowska-Ośko

Popiel

Kowalczyk

2021

IJMS

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A pandemic of acute respiratory infections, due to a new type of coronavirus, can cause Severe Acute Respiratory Syndrome 2 (SARS-CoV-2) and has created the need for a better understanding of the clinical, epidemiological, and pathological features of COVID-19, especially in high-risk groups, such as pregnant women. Viral infections in pregnant women may have a much more severe course, and result in an increase in the rate of complications, including spontaneous abortion, stillbirth, and premature birth—which may cause long-term consequences in the offspring. In this review, we focus on the mother-fetal-placenta interface and its role in the potential transmission of SARS-CoV-2, including expression of viral receptors and proteases, placental pathology, and the presence of the virus in neonatal tissues and fluids. This review summarizes the current knowledge on the anti-viral activity of lactoferrin during viral infection in pregnant women, analyzes its role in the pathogenicity of pandemic virus particles, and describes the potential evidence for placental blocking/limiting of the transmission of the virus.

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Increased oxidative stress and cancer biomarkers in the ventral prostate of older rats submitted to maternal malnutrition

Cited by 20 publications

References 65 publications

Early-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats

Early-life origin of prostate cancer through deregulation of miR-206 networks in maternally malnourished offspring rats

Maternal Diabetes and Postnatal High-Fat Diet on Pregnant Offspring

The Immunological Role of the Placenta in SARS-CoV-2 Infection—Viral Transmission, Immune Regulation, and Lactoferrin Activity

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