Developmental low-dose exposure to bisphenol A induces chronic inflammation, bone marrow fibrosis and reduces bone stiffness in female rat offspring only

Lind, Thomas; Lejonklou, Margareta Halin; Dunder, Linda; Kushnir, Mark M.; Öhman‐Mägi, Caroline; Larsson, Sune; Melhus, Håkan; Lind, P. Monica

doi:10.1016/j.envres.2019.108584

Cited by 43 publications

(31 citation statements)

References 87 publications

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“…However, the fibrosis was more prominent in 20 ppm BPA. Previously, BPA shown to upregulate the expression of marker for fibrosis such as interleukin-6 (IL-6) and collagen type 1 66,67 . In here, our result is the first to suggest that BPA exposure during prenatal life may altered cardiac miRNAs and induced fibrosis.…”

Section: Main Textmentioning

confidence: 99%

The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

Rasdi

Kamaludin

Ab‐Rahim

et al. 2020

Sci Rep

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this study aimed to examine the impact of BpA exposure on pregnancy and foetuses on cardiac tissues and the expression of cardiac microRnAs (miRnAs) related to heart development and diseases. Pregnancy is known to be the "critical windows" in determining the offspring physical and cells development in their life after birth. The increment of the risk of cardiovascular disease (CVD) in a later stage of life has been reported by few studies demonstrated from prenatal exposure of BpA. BpA has been shown to alter miRNAs expression profiles for organ development, regeneration and metabolic functions. These alterations have been associated with the risk of CVDs. However, the associations between pregnancy outcomes and miRnAs expression in cardiac of mother-and foetuses-exposed to BPA are still not entirely explored. In BPA-exposed pregnant rat groups, a significant weight gained was observed in comparison to control (p < 0.05). Interestingly, significant changes in systolic and diastolic blood pressure between the first and third trimester of BPA-exposed pregnant rats were also observed (p < 0.05). In BPA-exposed pregnant rats, miR-499-5p was significantly altered in the heart (p < 0.01). Meanwhile, altered miR-17-5p,-208-3p, and-210-3p expressions were observed in all heart of the foetuses from BpA-exposed pregnant rats (p < 0.05). In H&E staining, BPA-exposed foetal hearts showed a sign of fibrosis while BPA-exposed pregnant rats showed muscle remnant. Masson trichrome staining further confirmed the presence of fibrosis observed in BPA-exposed foetal heart and reduced expression of cardiac troponin I (cTnI) was also observed in BPA-exposed foetal heart. In summary, altered cardiac miRnAs with histological changes were observed in both mother-and foetus-exposed BPA These findings put forward the importance of future work to further understand how prenatal BPA exposure affect foetuses in their later stage of life. Altered foetal development "programming" may predispose certain individuals to the risk of chronic disease development later in their life. This was suggested by Barker and co-worker who presented the first finding on the increased risk of cardiovascular disease (CVD) in children of malnourished mothers 1. Barker then further extended his theory and linked the CVD development and insulin resistance to the environment of the placenta. His findings have attracted another study to report on the insufficiency of uteroplacental of malnutrition mothers increases the risk of the offspring to type 2 diabetes 2. Another study demonstrated that miR-208, a

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Section: Main Textmentioning

confidence: 99%

The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

Rasdi

Kamaludin

Ab‐Rahim

et al. 2020

Sci Rep

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“…These alterations in cortical thickness seen in our study and others is most likely due to interrupted estrogen signaling through ERa, which plays a significant role in periosteal expansion in male mice [174]. In addition, a recent study showed that morphological alterations seen at 13 weeks in the male offspring exposed to BPA during gestation and lactation only were no longer present at 52 weeks [249], implying that the changes could be reversible with time. This encourages further exploration into the mechanisms behind the morphological alterations seen in younger animals.…”

Section: Discussionsupporting

confidence: 62%

“…In one study, female offspring had decreased energy-to-failure at 13 weeks of age, which could not be explained by any morphological differences in the bone [63]. In another, female offspring at 52 weeks of age had decreased whole-bone stiffness, which also could not be explained by morphological changes [249].…”

Section: Introductionmentioning

confidence: 91%

Hormonal regulation of bone health: novel understandings of xenoestrogens and estrogen receptor-[alpha]

Dirkes¹

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Estrogen is one of the most influential hormones on bone growth and maintenance throughout the life cycle in both men and women, but there are still unknown roles of estrogen and the estrogen receptors in males. In addition, exposure to xenoestrogens, or environmental compounds that have anti-estrogenic qualities, is increasing in industrial countries, but the impact of these compounds on skeletal health in males and females remains unknown. In this dissertation, we used animal models to explore a, the importance of estrogen receptor-[alpha] (ER[alpha]) in male mice at different points in the life cycle and b, the long-term impact of gestational exposure to xenoestrogens, specifically bisphenol-A (BPA) and bisphenol-S (BPS), on male and female offspring. We found that both young and aged male ER[alpha] knockout (ERKO) animals had impaired measures of cortical geometry, but improved measures of trabecular microarchitecture, implying differential roles for ER[alpha] in different bone compartments. We also found that ERKO could lead to increased expression of sclerostin, a bone growth inhibitor, in aged, male mice. In younger, male ERKO mice we found that ERa is not required for an osteogenic response to exercise, which is in direct contrast with females. Finally, we found that gestational and lactational exposure to BPA, but not BPS, had significant negative impacts on the skeleton of adult male, but not female, mice. Male offspring exposed to BPA had significantly lower measures of both cortical geometry and trabecular microarchitecture, indicating long-term effects of interrupted estrogen signaling during uterine and early childhood on skeletal development. These findings further our understandings of the importance of estrogen on skeletal health across the lifespan and could have significant public health impacts if they are translatable to humans.

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“…COL1A1 is a bone matrix protein gene; it is regulated by Runx2. BPA exposure increased the plasma levels of procollagen type I N-terminal propeptide (P1NP) associated with the risk of bone metastasis (Lind et al 2019). Further studies are needed to understand further the molecular mechanisms of BPA in osteosarcoma.…”

Section: Osteosarcomamentioning

confidence: 99%

A comprehensive review on the carcinogenic potential of bisphenol A: clues and evidence

Khan

Correia

Adiga

et al. 2021

Environ Sci Pollut Res

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Bisphenol A [BPA; (CH3)2C(C6H4OH)2] is a synthetic chemical used as a precursor material for the manufacturing of plastics and resins. It gained attention due to its high chances of human exposure and predisposing individuals at extremely low doses to diseases, including cancer. It enters the human body via oral, inhaled, and dermal routes as leach-out products. BPA may be anticipated as a probable human carcinogen. Studies using in vitro cell lines, rodent models, and epidemiological analysis have convincingly shown the increasing susceptibility to cancer at doses below the oral reference dose set by the Environmental Protection Agency for BPA. Furthermore, BPA exerts its toxicological effects at the genetic and epigenetic levels, influencing various cell signaling pathways. The present review summarizes the available data on BPA and its potential impact on cancer and its clinical outcome.

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Developmental low-dose exposure to bisphenol A induces chronic inflammation, bone marrow fibrosis and reduces bone stiffness in female rat offspring only

Cited by 43 publications

References 87 publications

The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

The impacts of intrauterine Bisphenol A exposure on pregnancy and expression of miRNAs related to heart development and diseases in animal model

Hormonal regulation of bone health: novel understandings of xenoestrogens and estrogen receptor-[alpha]

A comprehensive review on the carcinogenic potential of bisphenol A: clues and evidence

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