• Title/Summary/Keyword: Chrysaora pacifica

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Distribution of the Sea Nettle Chrysaora pacifica (Goette, 1886) (Semaeostomeae; Pelagiidae) in Korea Using Molecular Markers (커튼원양해파리 Chrysaora pacifica (Goette, 1886) (Semaeostomeae; Pelagiidae)의 분자 마커를 이용한 한국내 지리적 분포)

  • Seo, Yoseph;Kim, Dae-Hyun;Chae, Jinho;Ki, Jang-Seu
    • Ocean and Polar Research
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    • v.42 no.3
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    • pp.263-270
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    • 2020
  • The distribution and genotypes of the sea nettle Chrysaora pacifica have been reported in the South Sea of Korea; however, little research work has been attempted in the East Sea. Here, we collected similar jellyfishes from the East Sea coasts (Goseong, Yangyang and Sokcho), and identified them to the sea nettle morphologically. In addition, the genotypes of these sea nettle were compared with those from the South Sea (Tongyeong and Geoje). Phylogenetic analysis by using the mitochondrial COI sequences showed that the genus Chrysaora was clearly separated from other taxa to be formed a monophyletic group, with each species distinctly separated. C. pacifica in the East and South Seas was separated geographically by the COI phylogeography, representing potentially different populations. The COI gene of the Korean C. pacifica had approximately 7 times more genetic variation than the nuclear ITS rDNA, and thus it might be considered as a useful marker for genetic analysis of the jellyfish population.

Re-description of Chrysaora pacifica (Goette, 1886) (Cnidaria, Scyphozoa) from Korean Coastal Waters: Morphology and Molecular Comparisons

  • Lee, Hye Eun;Yoon, Won Duk;Chae, Jinho;Ki, Jang-Seu
    • Ocean and Polar Research
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    • v.38 no.4
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    • pp.295-301
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    • 2016
  • The nomenclature of the sea nettle jellyfish from Korea was initially described as Dactylometra quinquecirrha Agassiz, 1862. However its identity has been questioned on the basis of its local distribution and molecular data. Here, we examined morphology and DNA sequences of nuclear rDNA using specimens collected from southern Korean waters in August 2014. Based on morphological characteristics (bell size, umbrella pattern, number of tentacles and lappets) and distribution locality, we reassign the Korean D. quinquecirrha to Chrysaora pacifica (Goette, 1886), and provide a re-description accordingly. The molecular identity of C. pacifica was further confirmed by comparison of nuclear ribosomal DNA sequences.

The venom of jellyfish, Chrysaora pacifica, induces neurotoxicity via activating Ca2+-mediated ROS signaling in HT-22 cells

  • Yang, Yoon-Sil;Kang, Young-Joon;Kim, Hye-Ji;Kim, Min-Soo;Jung, Sung-Cherl
    • Journal of Applied Biological Chemistry
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    • v.62 no.4
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    • pp.347-353
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    • 2019
  • Stings of jellyfish, which frequently occur in a warm season, cause severe pain, inflammation and sometimes irreversible results such as the death. Harmful venoms from jellyfish, therefore, have been studied for finding the therapeutic agents to relieve pain or to neutralize toxic components. However, it is still unclear if and how jellyfish venom reveal neuronal toxicity even though pain induction seems to result from the activation of nociceptors such as nerve endings. In this study, using HT-22 cell line, we investigated neurotoxic effects of the venom of Chrysaora pacifica (CpV) which appears in South-East ocean of Korea. In 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, CpV significantly reduced the viability of HT-22 cells in a dose-dependent manner. Additionally, in 2',7'-Dichlorofluorescin diacetate fluorescence test under the culture condition lacking dominant inflammatory factors, CpV remarkably increased the production of intracellular reactive oxygen species (ROS). Reduced responsive fluorescence to Rhodamine123 and increased expression of intracellular cytochrome c were also observed in HT-22 cells treated with CpV. These indicate that CpV-reduced viability of HT-22 cells may be due to the activation of apoptotic signalings mediated with oxidative stress and mitochondrial dysfunction. Furthermore, removing Ca2+ ion or adding N-acetyl-Lcystein remarkably blocked the CpV effect to reduce the viability of HT-22 cells. The findings in this study clearly demonstrate that CpV may activate Ca2+-mediated ROS signalings and mitochondrial dysfunction resulting in neuronal damage or death, and suggest that blocking Ca2+ pathway is a therapeutic approach to possibly block toxic effects of jellyfish venoms.