Inhibition of Fin Regeneration in Fathead Minnow (Pimephales promelas) by a Potent Synthetic Glucocorticoid and Development of Adverse Outcome Pathway 334 DOI
Alexander R. Cole, Gerald T. Ankley, Jenna E. Cavallin

et al.

Environmental Science & Technology, Journal Year: 2025, Volume and Issue: unknown

Published: May 6, 2025

Despite structural and functional conservation across vertebrate species, the glucocorticoid receptor has been minimally studied in comparison to other biological targets for endocrine-disrupting compounds aquatic systems. Because prolonged use of pharmaceutical glucocorticoids humans linked osteoporosis impaired bone growth, we hypothesized that ability teleost fish regenerate fins following damage may be inhibited by exposure synthetic environment. In present study, examined fin regeneration a 7 days waterborne juvenile fathead minnows (Pimephales promelas) glucocorticoids, fluticasone propionate dexamethasone. Expression several biologically relevant gene products (sgk1, tdgf1, runx2a, lef1, shha, tsc22d3) was measured paired caudal whole-body tissues. Fluticasone dexamethasone significantly at water concentrations 2.62 μg/L 4.62 mg/L, respectively. Changes expression indicated disruption intercellular communication Wnt/β-catenin morphogenetic protein (BMP) signaling pathways after 4.86 propionate. Upregulation tsc22d3, transcription factor responsible suppression anti-inflammatory response, plausible cause repressed cellular signaling. These findings advance development adverse outcome pathway 334─Glucocorticoid Receptor Activation Leads Impaired Fin Regeneration─and elucidate both mechanistic relationship between activation inhibition regeneration, which could plausibly reduce individual fitness

Language: Английский

Inhibition of Fin Regeneration in Fathead Minnow (Pimephales promelas) by a Potent Synthetic Glucocorticoid and Development of Adverse Outcome Pathway 334 DOI
Alexander R. Cole, Gerald T. Ankley, Jenna E. Cavallin

et al.

Environmental Science & Technology, Journal Year: 2025, Volume and Issue: unknown

Published: May 6, 2025

Despite structural and functional conservation across vertebrate species, the glucocorticoid receptor has been minimally studied in comparison to other biological targets for endocrine-disrupting compounds aquatic systems. Because prolonged use of pharmaceutical glucocorticoids humans linked osteoporosis impaired bone growth, we hypothesized that ability teleost fish regenerate fins following damage may be inhibited by exposure synthetic environment. In present study, examined fin regeneration a 7 days waterborne juvenile fathead minnows (Pimephales promelas) glucocorticoids, fluticasone propionate dexamethasone. Expression several biologically relevant gene products (sgk1, tdgf1, runx2a, lef1, shha, tsc22d3) was measured paired caudal whole-body tissues. Fluticasone dexamethasone significantly at water concentrations 2.62 μg/L 4.62 mg/L, respectively. Changes expression indicated disruption intercellular communication Wnt/β-catenin morphogenetic protein (BMP) signaling pathways after 4.86 propionate. Upregulation tsc22d3, transcription factor responsible suppression anti-inflammatory response, plausible cause repressed cellular signaling. These findings advance development adverse outcome pathway 334─Glucocorticoid Receptor Activation Leads Impaired Fin Regeneration─and elucidate both mechanistic relationship between activation inhibition regeneration, which could plausibly reduce individual fitness

Language: Английский

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