Gastrodin Suppresses Pentylenetetrazole-Induced Seizures Progression by Modulating Oxidative Stress in Zebrafish

Jin, Meng; He, Qiuxia; Zhang, Shanshan; Cui, Yan; Han, Liwen; Liu, Kechun

doi:10.1007/s11064-018-2496-9

Cited by 44 publications

(37 citation statements)

References 75 publications

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“…For PTZ treatment, PTZ (10mM) was added directly to the 96 well plate following acclimation period. Final concentration of PTZ was determined from previously published results (Baraban et al, 2005; Afrikanova et al, 2013; Peng et al, 2016; Jin et al, 2018).…”

Section: Methodsmentioning

confidence: 99%

Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Reyes-Nava

Coughlin

et al. 2020

Preprint

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ABSTRACTWe used whole exome sequencing (WES) to determine the genetic etiology of a patient with a multi-system disorder characterized by a seizure phenotype. WES identified a heterozygous de novo missense mutation in the GABRA1 gene (c.875C>T). GABRA1 encodes the alpha subunit of the Gamma-Aminobutyric Acid receptor A (GABAAR). The GABAAR is a ligand gated ion channel that mediates the fast inhibitory signals of the nervous system and mutations in the sub-units that compose the GABAAR have been previously associated with human disease. To understand the mechanisms by which GABRA1 regulates brain development, we developed a zebrafish model of gabra1 deficiency. gabra1 expression is restricted to the nervous system and behavioral analysis of morpholino injected larvae suggests that the knockdown of gabra1 results in hypoactivity and defects in the expression of other sub-units of the GABAAR. Expression the human GABRA1 protein in morphants partially restored the hypomotility phenotype. In contrast, the expression of the c.875C>T variant did not restore these behavioral deficits. Collectively, these results represent a functional approach to understand the mechanisms by which loss of function alleles cause disease.

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Section: Methodsmentioning

confidence: 99%

Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Reyes-Nava

Coughlin

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…For PTZ treatment, PTZ (10 mM) was added directly to the 96-well plate following acclimation period. Final concentration of PTZ was determined from previously published results (Baraban et al, 2005;Afrikanova et al, 2013;Peng et al, 2016;Jin et al, 2018).…”

Section: Behavioral Analysis and Pentylenetetrazol Treatmentmentioning

confidence: 99%

Abnormal expression of GABAA receptor sub-units and hypomotility upon loss of gabra1 in zebrafish

Reyes-Nava

Coughlin

et al. 2020

Biology Open

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We used whole-exome sequencing (WES) to determine the genetic etiology of a patient with a multi-system disorder characterized by a seizure phenotype. WES identified a heterozygous de novo missense mutation in the GABRA1 gene (c.875C>T). GABRA1 encodes the alpha subunit of the gamma-aminobutyric acid receptor A (GABA A R). The GABA A R is a ligand gated ion channel that mediates the fast inhibitory signals of the nervous system, and mutations in the subunits that compose the GABA A R have been previously associated with human disease. To understand the mechanisms by which GABRA1 regulates brain development, we developed a zebrafish model of gabra1 deficiency. gabra1 expression is restricted to the nervous system and behavioral analysis of morpholino injected larvae suggests that the knockdown of gabra1 results in hypoactivity and defects in the expression of other subunits of the GABA A R. Expression of the human GABRA1 protein in morphants partially restored the hypomotility phenotype. In contrast, the expression of the c.875C>T variant did not restore these behavioral deficits. Collectively, these results represent a functional approach to understand the mechanisms by which loss-of-function alleles cause disease.

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“…The embryos were obtained from the natural mating of adult zebrafish bred then maintained in bathing water. Fertilized eggs were collected and transferred to 6-well plates (39). Plates were kept in an incubator with the temperature maintained at 28±0.5˚C and monitored daily until 2 days post-fertilization (dpf).…”

Section: Methodsmentioning

confidence: 99%

Possible involvement of TGF‑β‑SMAD‑mediated epithelial‑mesenchymal transition in pro‑metastatic property of PAX6

et al. 2020

Self Cite

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Paired box 6 (PAX6) is a transcription factor that has oncogenic features. In breast cancer, PAX6 facilitates tumor progression; however, the underlying mechanism is largely unknown. The majority of breast cancer-related mortalities are associated with metastasis of cancer cells. Therefore, the present study aimed to investigate the role of PAX6 in breast tumor metastasis. PAX6 was stably overexpressed in breast cancer cells to perform tumor migration and metastasis assays in vitro and in vivo. In addition, the expression of PAX6 and transforming growth factor β (TGF-β)-SMAD signaling associated proteins on human breast cancer tissue array, as well as key factors involved in epithelial-mesenchymal transition (EMT) were assayed to explore the mechanism underlying metastasis of breast cancer cells. The expression levels of PAX6 were demonstrated to be increased in human breast cancer tissues and associated with poor clinical outcomes. Overexpression of PAX6 markedly promoted metastasis. Further investigation revealed that PAX6 overexpression increased TGF-β-SMAD signaling pathway and induced EMT. These results suggested that highly expressed PAX6 led to EMT through TGF-β-SMAD signaling pathway, thereby promoting cell metastasis and ultimately affecting survival in patients with breast cancer. Taken together, findings indicated that PAX6 may serve as a therapeutic target for the clinical treatment of breast cancer and the underlying mechanism could be used to overcome metastasis of cancer cells.

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Gastrodin Suppresses Pentylenetetrazole-Induced Seizures Progression by Modulating Oxidative Stress in Zebrafish

Cited by 44 publications

References 75 publications

Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Abnormal expression of GABAA receptor sub-units and hypomotility upon loss of gabra1 in zebrafish

Possible involvement of TGF‑β‑SMAD‑mediated epithelial‑mesenchymal transition in pro‑metastatic property of PAX6

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Gastrodin Suppresses Pentylenetetrazole-Induced Seizures Progression by Modulating Oxidative Stress in Zebrafish

Cited by 44 publications

References 75 publications

Abnormal expression of GABAAreceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Abnormal expression of GABAAreceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Abnormal expression of GABAA receptor sub-units and hypomotility upon loss of gabra1 in zebrafish

Possible involvement of TGF‑β‑SMAD‑mediated epithelial‑mesenchymal transition in pro‑metastatic property of PAX6

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Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish

Abnormal expression of GABA_Areceptor sub-units and hypomotility upon loss ofgabra1in zebrafish