• Title/Summary/Keyword: entry inhibition

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Cytoprotective Effects of Polyamines Against Oxidative Stress (산화 스트레스에 대한 폴리아민의 세포보호 효과)

  • Ahn Seoni;Lee Ji Young;Chung Hae Young;Yoo Mi-Ae;Kim Jong-Min;Kim Byeong Gee
    • Journal of Life Science
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    • v.15 no.4 s.71
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    • pp.626-632
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    • 2005
  • The polyamines are essential components of all eukaryotic cells and absolutely necessary for cell growth. In the present study, the cytoprotective role of polyamine was characterized. When $Ac_2F$ rat liver cells were treated with 1M 2,2'-azobis (2-amidinopropane) dehydrochloride (AAPH), a water soluble free radical initiator, viability of the cells was noticeably decreased due to the increase of reactive oxygen species (ROS). The cytotoxic effect of AAPH as well as ROS generation were significantly inhibited by the treatment of polyamines. Among polyamines, especially spermine at $20{\mu}M$ concentration exerted over $45\%$ inhibition of AAPH-induced ROS generation. Western blotting was performed to determine whether superoxide dismutase(SOD) or catalase (CAT) expression was involved in oxidative stress. The AAPH treatment blocked both SOD and CAT protein expressions. Spermine could recover those protein expressions to the untreated control levels. According to the result of cycline E measurement, AAPH might block the entry of the cells into S phase of the cell cycle. The reduced expression of cyclin E protein could be fully recovered by the addition of spermine. The antioxidative effects of spermine was also further proved by the apopotitic morphological analysis using ethidium bromide and acridine orange.

Temporal Transcriptome Analysis of SARS-CoV-2-Infected Lung and Spleen in Human ACE2-Transgenic Mice

  • Jung Ah, Kim;Sung-Hee, Kim;Jung Seon, Seo;Hyuna, Noh;Haengdueng, Jeong;Jiseon, Kim;Donghun, Jeon;Jeong Jin, Kim;Dain, On;Suhyeon, Yoon;Sang Gyu, Lee;Youn Woo, Lee;Hui Jeong, Jang;In Ho, Park;Jooyeon, Oh;Sang-Hyuk, Seok;Yu Jin, Lee;Seung-Min, Hong;Se-Hee, An;Joon-Yong, Bae;Jung-ah, Choi;Seo Yeon, Kim;Young Been, Kim;Ji-Yeon, Hwang;Hyo-Jung, Lee;Hong Bin, Kim;Dae Gwin, Jeong;Daesub, Song;Manki, Song;Man-Seong, Park;Kang-Seuk, Choi;Jun Won, Park;Jun-Won, Yun;Jeon-Soo, Shin;Ho-Young, Lee;Jun-Young, Seo;Ki Taek, Nam;Heon Yung, Gee;Je Kyung, Seong
    • Molecules and Cells
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    • v.45 no.12
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    • pp.896-910
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    • 2022
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and potentially fatal virus. So far, most comprehensive analyses encompassing clinical and transcriptional manifestation have concentrated on the lungs. Here, we confirmed evident signs of viral infection in the lungs and spleen of SARS-CoV-2-infected K18-hACE2 mice, which replicate the phenotype and infection symptoms in hospitalized humans. Seven days post viral detection in organs, infected mice showed decreased vital signs, leading to death. Bronchopneumonia due to infiltration of leukocytes in the lungs and reduction in the spleen lymphocyte region were observed. Transcriptome profiling implicated the meticulous regulation of distress and recovery from cytokine-mediated immunity by distinct immune cell types in a time-dependent manner. In lungs, the chemokine-driven response to viral invasion was highly elevated at 2 days post infection (dpi). In late infection, diseased lungs, post the innate immune process, showed recovery signs. The spleen established an even more immediate line of defense than the lungs, and the cytokine expression profile dropped at 7 dpi. At 5 dpi, spleen samples diverged into two distinct groups with different transcriptome profile and pathophysiology. Inhibition of consecutive host cell viral entry and massive immunoglobulin production and proteolysis inhibition seemed that one group endeavored to survive, while the other group struggled with developmental regeneration against consistent viral intrusion through the replication cycle. Our results may contribute to improved understanding of the longitudinal response to viral infection and development of potential therapeutics for hospitalized patients affected by SARS-CoV-2.

Molecular Miology of the Poliovirus (폴리오바이러스의 분자생물학)

  • 최원상
    • Journal of Life Science
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    • v.7 no.4
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    • pp.392-401
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    • 1997
  • The poliovirus is a small, and non-enveloped virus. The RNA genome of poliovirus is continuous, linear, and has a single open reading frame. This polyprotein precursor is cleaved proteolytically to yield mature products. Most of the cleavages occur by viral protease. The mature proteins derived from the P1 polyprotein precursor are the structural components of the viral capsid. The initial cleavage by 2A protease is indirectly involved in the cleavage of a cellular protein p220, a subunit of the eukaryotic translation initiation factor 4F. This cleavage leads to the shut-off of cap-dependent host cell translation, and allows poliovirus to utilize the host cell machinery exclusively for translation its own RNA, which is initiated by internal ribosome entry via a cap-independent mechanism. The functional role of the 2B, 2C and 2BC proteins are not much known. 2B, 2C, 2BC and 3CD proteins are involved in the replication complex of virus induced vesicles. All newly synthesized viral RNAs are linked with VPg. VPg is a 22 amino acid polypeptide which is derived from 3AB. The 3C and 3CD are protease and process most of the cleavage sites of the polyprotein precursor. The 3C protein is also involved in inhibition of RNA polymerase II and III mediated transcription by converting host transcription factor to an inactive form. The 3D is the RNA dependent RNA polymerase. It is known that poliovirus replication follows the general pattern of positive strand RNA virus. Plus strand RNA is transcribed into complementary minus strand RNA that, in turn, is transcribed for the synthesis of plus strand RNA is transcribed into complementary minus strand RNA that, in turn, is transcribed for the synthesis of plus strand RNA strands. Poliovirus RNA synthesis occurs in a membranous environment but how the template RNA and proteins required for RNA replication assemble in the membrane is not much known. The RNA requirements for the encapsidation of the poliovirus genome (packaging signal) are totally unknown. The poliovirus infection cycle lasts approximately 6 hours.

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