Bisphenol-A alters hematopoiesis through EGFR/ERK signaling to induce myeloblastic condition in zebrafish model

Kannan, R.; Sujitha, Mohanan V.; Alphonse, Carlton Ranjith Wilson; Kalaiarasan, Retnamony; Kannan, Rajaretinam Rajesh

doi:10.1016/j.scitotenv.2021.147530

Cited by 21 publications

(11 citation statements)

References 55 publications

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“…2 , 4 ). Generally, this finding is consistent with the literature; however, the exact level of BPA to elicit these effects varies greatly ( Lam et al, 2011 ; Saili et al, 2012 ; Tse et al, 2013 ; Wang et al, 2013 ; Martínez et al, 2018 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Huang et al, 2021 ; Scopel et al, 2021 ; Sundarraj et al, 2021 ; Wu et al, 2021 ). The differences in the reported concentrations of BPA required to elicit deformity and mortality likely result from variation in experimental protocols or the strain of zebrafish used.…”

Section: Discussionsupporting

confidence: 92%

“…The differences in the reported concentrations of BPA required to elicit deformity and mortality likely result from variation in experimental protocols or the strain of zebrafish used. Similar to deformity and mortality, hatching delays have more commonly been reported with higher levels of BPA ( Martínez et al, 2018 ; Scopel et al, 2021 ; but see Olsvik et al, 2019 compared with lower levels of BPA ( Gyimah et al, 2021 ; Huang et al, 2021 ; Gu et al, 2022 ; but see Sundarraj et al, 2021 ). By contrast, very low levels of BPA have been reported to accelerate hatching ( Qiu et al, 2016 ; Coumailleau et al, 2020 ).…”

Section: Discussionmentioning

confidence: 85%

“…It has been found that exposure to relatively high concentrations of BPA early in the zebrafish life cycle increases mortality and deformity, and delays hatching. Interestingly, despite general agreement regarding the adverse effects of high levels of BPA on mortality, body shape, and time of hatching, the reported threshold concentration of BPA for producing these effects varies greatly ( Lam et al, 2011 ; Saili et al, 2012 ; Tse et al, 2013 ; Wang et al, 2013 ; Martínez et al, 2018 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Huang et al, 2021 ; Scopel et al, 2021 ; Sundarraj et al, 2021 ; Wu et al, 2021 ). Furthermore, some studies have found that BPA exposure modifies locomotion in zebrafish, whereas others have not ( Saili et al, 2012 ; Wang et al, 2013 ; Kinch et al, 2015 ; Fraser et al, 2017 ; Olsvik et al, 2019 ; Coumailleau et al, 2020 ; Gyimah et al, 2021 ; Wu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Scaramella

Alzagatiti

Creighton

et al. 2022

eNeuro

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Because of their ex utero development, relatively simple nervous system, translucency, and availability of tools to investigate neural function, larval zebrafish are an exceptional model for understanding neurodevelopmental disorders and the consequences of environmental toxins. Furthermore, early in development, zebrafish larvae easily absorb chemicals from water, a significant advantage over methods required to expose developing organisms to chemical agents in utero . Bisphenol A (BPA) and BPA analogs are ubiquitous environmental toxins with known molecular consequences. All humans have measurable quantities of BPA in their bodies. Most concerning, the level of BPA exposure is correlated with neurodevelopmental difficulties in people. Given the importance of understanding the health-related effects of this common toxin, we have exploited the experimental advantages of the larval zebrafish model system to investigate the behavioral and anatomic effects of BPA exposure. We discovered that BPA exposure early in development leads to deficits in the processing of sensory information, as indicated by BPA’s effects on prepulse inhibition (PPI) and short-term habituation (STH) of the C-start reflex. We observed no changes in locomotion, thigmotaxis, and repetitive behaviors (circling). Despite changes in sensory processing, we detected no regional or whole-brain volume changes. Our results show that early BPA exposure can induce sensory processing deficits, as revealed by alterations in simple behaviors that are mediated by a well-defined neural circuit.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Scaramella

Alzagatiti

Creighton

et al. 2022

eNeuro

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“…We have previously reported that epidermal growth factor receptor (EGFR) could serve as a receptor for REG3A, which can promote activation of JAK2‐STAT3‐REG3A positive feedback loop by EGFR (Liu et al, 2017). EGFR/ERK signalling cascade is one of the major pathways involved in the regulation of various biological processes including cell proliferation, motility and survival (Cheng et al, 2020; Sundarraj et al, 2021; Uchiyama et al, 2019). Hence, we speculate that Reg3g may induce the phosphorylation of STAT3 at Ser727 through affecting the EGFR‐ERK1/2‐pSTAT3 pathway.…”

Section: Discussionmentioning

confidence: 99%

Regenerating islet‐derived protein 3 gamma (Reg3g) ameliorates tacrolimus‐induced pancreatic β‐cell dysfunction in mice by restoring mitochondrial function

Zhou

Xie

et al. 2022

British J Pharmacology

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Background and Purpose Tacrolimus a first‐line medication used after transplantation can induce β‐cell dysfunction, causing new‐onset diabetes mellitus (NODM). Regenerating islet‐derived protein 3 gamma (Reg3g), a member of the pancreatic regenerative gene family, has been reported to improve type 1 diabetes by promoting β‐cell regeneration. We aim to investigate the role of Reg3g in reversing tacrolimus‐induced β‐cell dysfunction and NODM in mice. Experimental Approach Circulating REG3A (the human homologue of mouse Reg3g) in heart transplantation patients treated with tacrolimus was detected. The glucose‐stimulated insulin secretion and mitochondrial functions, including mitochondria membrane potential (MMP), mitochondria calcium, ATP production, oxygen consumption rate and mitochondrial morphology were investigated in β‐cells. Additionally, effects of Reg3g on tacrolimus‐induced NODM in mice were analysed. Key Results Circulating REG3A level in heart transplantation patients with NODM significantly decreased compared with those without diabetes. Tacrolimus down‐regulated Reg3g via inhibiting STAT3‐mediated transcription activation. Moreover, Reg3g restored glucose‐stimulated insulin secretion suppressed by tacrolimus in β‐cells by improving mitochondrial functions, including increased MMP, mitochondria calcium uptake, ATP production, oxygen consumption rate and contributing to an intact mitochondrial morphology. Mechanistically, Reg3g increased accumulation of pSTAT3(Ser727) in mitochondria by activating ERK1/2‐STAT3 signalling pathway, leading to restoration of tacrolimus‐induced mitochondrial impairment. Reg3g overexpression also effectively mitigated tacrolimus‐induced NODM in mice. Conclusion and Implications Reg3g can significantly ameliorate tacrolimus‐induced β‐cell dysfunction by restoring mitochondrial function in a pSTAT3(Ser727)‐dependent manner. Our observations identify a novel Reg3g‐mediated mechanism that is involved in tacrolimus‐induced NODM and establish the novel role of Reg3g in reversing tacrolimus‐induced β‐cell dysfunction.

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“…Accumulating evidence has shown that low levels of BPA have been detected in a variety of human breast milk, blood, as well as urine samples, 4–6 indicating that the kidney is a potential target organ for BPA. Several studies have also revealed that BPA had nephrotoxicity, for example, BPA induced apoptosis, oxidative stress, and DNA damage in cultured rhesus monkey embryo renal epithelial Marc‐145 cells, 7 and BPA induced‐mitochondrial dysfunction caused kidney damage in rats, 8 and kidneys from BPA‐exposed zebrafish showed abnormal myeloid blast cells along with severe morphological changes in erythrocytes 9 …”

Section: Introductionmentioning

confidence: 99%

Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

Chen

Zhang

et al. 2022

Environmental Toxicology

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Bisphenol A (BPA), a phenolic compound, is harmful to humans and animals as its residue in the water threatens multiple organs, especially the kidney. Low selenium (Se) diets are consumed in many regions of the world, and poor Se status has exacerbating effect on toxicity of several environmental chemicals. Here, we described the discovery path of Se deficiency aggravation on autophagy in BPA treated chicken kidney through regulating nitric oxide (NO) and adenosine monophosphate activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathways.The actual dietary Se intake for chickens was 0.30 mg/kg in control group and 0.03 mg/kg in Low-Se group, and BPA exposure concentration for chickens was 0.05 g/kg. Chicken embryo kidney (CEK) cells were used in vitro and the BPA exposure concentration for CEK cells was 150 nM. We found that BPA significantly increased levels of NO and inducible nitric oxide synthase, activated AMPK/mTOR signaling pathways, thereby triggering p62/LC3/Beclin1 signaling, resulting in formations of autophagosome and autolysosome, and finally stimulating autophagy in the chicken kidney. Additionally, Se deficiency promoted the occurrence of autophagy in BPA-treated kidneys. Altogether, our findings showed that Se deficiency exacerbates BPA-induced renal autophagy in chickens via regulation of NO and AMPK/mTOR signaling pathways. These findings will improve our understandings of the mechanisms of nephrotoxicity of BPA and detoxification by Se in chickens. In addition, further work is required to determine if Se status of exposed populations needs to be considered in future epidemiological assessments.

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Bisphenol-A alters hematopoiesis through EGFR/ERK signaling to induce myeloblastic condition in zebrafish model

Cited by 21 publications

References 55 publications

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Bisphenol A Exposure Induces Sensory Processing Deficits in Larval Zebrafish during Neurodevelopment

Regenerating islet‐derived protein 3 gamma (Reg3g) ameliorates tacrolimus‐induced pancreatic β‐cell dysfunction in mice by restoring mitochondrial function

Selenium deficiency aggravates bisphenol A‐induced autophagy in chicken kidney through regulation of nitric oxide and adenosine monophosphate activated protein kinase/mammalian target of rapamycin signaling pathway

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