Effects of 17α‑ethinylestradiol on caudal fin regeneration in zebrafish larvae

Sun, Liwei; Gu, Linqi; Tan, Hao; Liu, Pan; Gao, Gan; Tian, Li; Chen, Hui; Lu, Tao; Qian, Haifeng; Fu, Zhengwei; Pan, Xiangliang

doi:10.1016/j.scitotenv.2018.10.275

Cited by 22 publications

(8 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, endocrine disruption was not associated with zebrafish fin regeneration (this study, Fig. 2J) and estrogen does not affect the rate of fin regeneration in zebrafish larvae (Sun et al 2019).…”

Section: Journal Of Endocrinologymentioning

confidence: 50%

Estrogen accelerates heart regeneration by promoting the inflammatory response in zebrafish

Xie

Tian

et al. 2020

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

Sexual differences have been observed in the onset and prognosis of human cardiovascular diseases, but the underlying mechanisms are not clear. Here, we found that zebrafish heart regeneration is faster in females, can be accelerated by estrogen and is suppressed by the estrogen-antagonist tamoxifen. Injuries to the zebrafish heart, but not other tissues, increased plasma estrogen levels and the expression of estrogen receptors, especially esr2a. The resulting endocrine disruption induces the expression of the female-specific protein vitellogenin in male zebrafish. Transcriptomic analyses suggested heart injuries triggered pronounced immune and inflammatory responses in females. These responses, previously shown to elicit heart regeneration, could be enhanced by estrogen treatment in males and reduced by tamoxifen in females. Furthermore, a prior exposure to estrogen preconditioned the zebrafish heart for an accelerated regeneration. Altogether, this study reveals that heart regeneration is modulated by an estrogen-inducible inflammatory response to cardiac injury. These findings elucidate a previously unknown layer of control in zebrafish heart regeneration and provide a new model system for the study of sexual differences in human cardiac repair.

show abstract

Section: Journal Of Endocrinologymentioning

confidence: 50%

Estrogen accelerates heart regeneration by promoting the inflammatory response in zebrafish

Xie

Tian

et al. 2020

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

show abstract

“…We now show that the unique role of estrogen in heart repair is evolutionarily conserved. For example, endocrine disruption was not associated with zebrafish fin regeneration (this study) and estrogen (17α ethinylestradiol) does not affect the rate of fin regeneration in zebrafish larvae (Sun et al, 2019).…”

mentioning

confidence: 51%

Estrogen accelerates heart regeneration by promoting inflammatory responses in zebrafish

Xie

Fallah

et al. 2019

Preprint

View full text Add to dashboard Cite

Sexual differences are observed in the onset and prognosis of human cardiovascular diseases, but the underlying mechanisms are not clear. Here, we report that zebrafish heart regeneration is faster in females, can be accelerated by estrogen and suppressed by estrogen-antagonist tamoxifen. Injuries to the heart, but not other tissues, increased plasma estrogen level and expression of estrogen receptors, especially esr2a, in zebrafish hearts. The resulting endocrine disruption induces the expression of femalespecific protein vitellogenin in male zebrafish. Transcriptomic analyses suggested heart injuries triggered more pronounced immune and inflammatory responses in females. These responses, previously shown to enhance heart regeneration, could be enhanced by estrogen treatment in males and reduced by tamoxifen in female.Furthermore, a brief exposure to estrogen could precondition zebrafish for an accelerated heart regeneration. Altogether, this study reveals that heart regeneration is modulated by an estrogen-inducible inflammatory response to heart injury. These findings elucidate a previously unknown layer of control in zebrafish heart regeneration and provides a new model system for the study of sexual differences in human cardiac repair.

show abstract

“…Shikonin is a naphthoquinone drug, and the molecular formula is illustrated in Figure 1 A. In our study, we selected 3 dpf healthy zebrafish larvae with consistent size for tail amputation ( Figure 1 A) and performed shikonin treatment immediately on operated zebrafish larvae as described in the References [ 14 , 15 ]. We determined the concentrations of shikonin based on the phenotype of defective fin regeneration in zebrafish larvae and the literature described by He et al [ 17 ].…”

Section: Resultsmentioning

confidence: 99%

“…Fin amputation and drug treatments were performed as described in References [ 14 , 15 ]. The caudal fins of 3 dpf larvae were amputated (just posterior to the notochord) with sterilized blades ( Figure 1 A), and fish were then transferred in a six-well polystyrene plate, with 15 fish in each well, and allowed to regenerate in shikonin solutions or shikonin-free embryonic medium (EM) for various times.…”

Section: Methodsmentioning

confidence: 99%

Shikonin Inhibits Fin Regeneration in Zebrafish Larvae

Cao

Guo

Chen

et al. 2022

Cells

View full text Add to dashboard Cite

Shikonin is a naphthoquinone compound extracted from Chinese comfrey for treating cancer. However, there are few reports on its research on vertebrate tissue regeneration. Zebrafish is an ideal model for studying organ regeneration. In this study, we found that 3-dpf of zebrafish larvae exposed to shikonin at concentrations of 0.2, 0.3, and 0.4 mg/L showed increasingly inhibited regeneration of the tail fin. Immunohistochemical staining showed that shikonin exposure from 6 to 12 hpa increased the number of apoptotic cells in the caudal fin wound of larvae and decreased the number of proliferating cells. Shikonin exposure was found to up-regulate oxidative stress, increase ROS levels, and reduce neutrophil recruitment in the early stage of wound repair. Moreover, shikonin exposure caused disordered expression of fin regeneration blastemal-related genes. The use of astaxanthin to down-regulate oxidative stress was found to significantly reduce the inhibition of caudal fin regeneration. Mixed exposure of AMPK inhibitors or fullerenes (C60) with shikonin also showed the similar rescue effect. Collectively, our study showed that shikonin inhibited fin regeneration in zebrafish larvae by the upregulation of oxidative stress level and AMPK signaling pathway. This research provides valuable information on the mechanism of action of shikonin for its safe application.

show abstract

Effects of 17α‑ethinylestradiol on caudal fin regeneration in zebrafish larvae

Cited by 22 publications

References 60 publications

Estrogen accelerates heart regeneration by promoting the inflammatory response in zebrafish

Estrogen accelerates heart regeneration by promoting the inflammatory response in zebrafish

Estrogen accelerates heart regeneration by promoting inflammatory responses in zebrafish

Shikonin Inhibits Fin Regeneration in Zebrafish Larvae

Contact Info

Product

Resources

About