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Mutations in SOHLH1 gene associate with nonobstructive Azoospermia
Choi, Youngsok,Jeon, Sanghyun,Choi, Mikyung,Lee, Min-ho,Park, Miseon,Lee, Dong Ryul,Jun, Kyu-Yeon,Kwon, Youngjoo,Lee, Ok-Hee,Song, Seung-Hun,Kim, Ji-Young,Lee, Kyung-Ah,Yoon, Tae Ki,Rajkovic, Aleksand Wiley Subscription Services, Inc., A Wiley Company 2010 Human mutation Vol.31 No.7
<P>In a previous study, we found SOHLH1 (spermatogenesis and oogenesis-specific basic helix-loop-helix 1) as the first testis-specific basic helix-loop-helix transcription factor essential for spermatogonial differentiation. SOHLH1 therefore represents an excellent candidate gene for testicular failure such as nonobstructive azoospermia (NOA). We analyzed whether there were mutations in the SOHLH1 gene in 96 Korean patients with NOA. The sequence analysis discovered three novel variations: one intronic variant (c.346−1G>A), and two nonsynonymous exonic variants (c.91T>C and c.529C>A) with known single nucleotide polymorphisms (SNPs), which included six intronic variants, two synonymous, and two nonsynonymous variants. We examined the consequences of mutations in SOHLH1 using in vivo and in vitro assays. Analysis of transcripts from minigenes carrying the c.346−1G>A revealed that splicing site variation leads to the partial deletion at a cryptic splicing site within exon 4. This deletion results in SOHLH1 with a truncated bHLH domain. Transient transfection assay showed that the SOHLH1 mutant with the truncated domain disrupted the transcriptional activity of KIT promoter, whereas two missense mutations harboring either p.Arg37Gln or p.Pro269Ser did not have a significant effect on its transactivation. Our findings indicate that a splice-acceptor site mutation that probably causes a nonfunctional SOHLH1 protein results in nonobstructive azoospermia by the lack of normal spermatogenesis. Hum Mutat 31:788–793, 2010. © 2010 Wiley-Liss, Inc.</P>
Choi, Mikyung,Lee, Ok-Hee,Jeon, Sanghyun,Park, Miseon,Lee, Dong Ryul,Ko, Jeong-Jae,Yoon, Tae Ki,Rajkovic, Aleksandar,Choi, Youngsok Elsevier 2010 FEBS letters Vol.584 No.16
<P><B>Abstract</B></P><P>Nobox is an oocyte-specific transcriptional regulator. <I>Nobox</I> deficiency disrupts early folliculogenesis and the expression of oocyte-specific genes in mice. In the present study, we found that peptidylarginine deiminase 6 (<I>Pad6</I>) was downregulated in <I>Nobox</I>-null ovaries. <I>Pad6</I> is preferentially expressed in oocytes and its transcript is detectable at embryonic day 16.5. In addition, we identified one Nobox DNA-binding element (NBE) within the mouse <I>Pad6</I> promoter. The NBE includes a core sequence TAATTA. Sequence-specific binding of Nobox to the TAATTA motif was confirmed. <I>Nobox</I> overexpression augmented transcriptional activity of a <I>luciferase</I> reporter driven by mouse Pad6. Our findings indicate that Nobox is a critical regulator that orchestrates oocyte-specific genes such as <I>Pad6</I> during folliculogenesis.</P>
최미선(Miseon Choi),이상혁(Sanghyuk Lee),박성준(Sungjun Park),남해곤(Haekon Nam),송성근(SungGeun Song) 전력전자학회 2009 전력전자학술대회 논문집 Vol.2009 No.1
최근 산업고도화로 인한 정보기기의 폭발적인 증가, 컴퓨터 보급의 확산에 따라 무정전 전원공급장치(UPS) 보급의 중요성이 높아가고 있다. 하지만 이 UPS의 제어방식에 몇 가지의 문제점을 가지고 있기에 본 논문에서는 고효율 및 고전력 밀도를 위해 push-pull 컨버터방식의 소프트 스위칭이 가능하고 효율을 개선한 새로운 타입의 DC/DC 컨버터를 제안한다. 제안된 DC/DC 컨버터는 새로운 개념의 DC 무정전 전원공급장치(UPS)를 대상으로 하여 시뮬레이션으로 인해 그 타당성을 입증하였다.
Effects of NOX1 on fibroblastic changes of endothelial cells in radiation-induced pulmonary fibrosis
CHOI, SEO-HYUN,KIM, MISEON,LEE, HAE-JUNE,KIM, EUN-HO,KIM, CHUN-HO,LEE, YOON-JIN SPANDIDOS PUBLICATIONS 2016 MOLECULAR MEDICINE REPORTS Vol.13 No.5
<P>Lung fibrosis is a major complication in radiation-induced lung damage following thoracic radiotherapy, while the underlying mechanism has remained to be elucidated. The present study performed immunofluorescence and immunoblot assays on irradiated human pulmonary artery endothelial cells (HPAECs) with or without pre-treatment with VAS2870, a novel NADPH oxidase (NOX) inhibitor, or small hairpin (sh)RNA against NOX1, -2 or -4. VAS2870 reduced the cellular reactive oxygen species content induced by 5 Gy radiation in HPAECs and inhibited phenotypic changes in fibrotic cells, including increased alpha smooth muscle actin and vimentin, and decreased CD31 and vascular endothelial cadherin expression. These fibrotic changes were significantly inhibited by treatment with NOX1 shRNA, but not by NOX2 or NOX4 shRNA. Next, the role of NOX1 in pulmonary fibrosis development was assessed in the lung tissues of C57BL/6J mice following thoracic irradiation using trichrome staining. Administration of an NOX1-specific inhibitor suppressed radiation-induced collagen deposition and fibroblastic changes in the endothelial cells (ECs) of these mice. The results suggested that radiation-induced pulmonary fibrosis may be efficiently reduced by specific inhibition of NOX1, an effect mediated by reduction of fibrotic changes of ECs.</P>
( Miseon Bang ),( Cheng-chung Yong ),( Hyeok-jin Ko ),( In-geol Choi ),( Sejong Oh ) 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.10
Lactobacillus rhamnosus GG (LGG) is a probiotic commonly used in fermented dairy products. In this study, RNA-sequencing was performed to unravel the effects of acid stress on LGG. The transcriptomic data revealed that the exposure of LGG to acid at pH 4.5 (resembling the final pH of fermented dairy products) for 1 h or 24 h provoked a stringent-type transcriptomic response wherein stress response- and glycolysis-related genes were upregulated, whereas genes involved in gluconeogenesis, amino acid metabolism, and nucleotide metabolism were suppressed. Notably, the pilus-specific adhesion genes, spaC, and spaF were significantly upregulated upon exposure to acid-stress. The transcriptomic results were further confirmed via quantitative polymerase chain reaction analysis. Moreover, acid-stressed LGG demonstrated an enhanced mucin-binding ability in vitro, with 1 log more LGG cells (p < 0.05) bound to a mucin layer in a 96-well culture plate as compared to the control. The enhanced intestinal binding ability of acid-stressed LGG was confirmed in an animal study, wherein significantly more viable LGG cells (≥ 2 log CFU/g) were observed in the ileum, caecum, and colon of acid-stressed LGG-treated mice as compared with a non-acid-stressed LGG-treated control group. To our knowledge, this is the first report showing that acid stress enhanced the intestine-binding ability of LGG through the induction of pili-related genes.
Miseon Park,Eun Jin Lim,Si-jeong Bea,Eunhye Kim,Young-eun Lee,Dong Ryul Lee,Youngsok Choi 한국동물생명공학회(구 한국동물번식학회) 2014 한국동물번식학회 한중일 심포지엄 Vol.2014 No.1
Aimp1 is known as a multifunctional cytokine in various cellular events. Recent study showed Aimp1 is localized in glandular epithelial, endothelial, and stromal cells in functionalis and basalis layers of the endometrium. However, the regulatory mechanism of Aimp1 in the uterus remains unknown. In the present study, we found that Aimp1 is expressed in the mouse uterus. Aimp1 transcripts were decreased at diestrus stage. However, the level of Aimp1 protein was significantly increased in the luminal epithelium in the uterine endometrium at the estrus stage during the estrous cycle. In addition, we found that the treatment of estrogen increased the expression of Aimp1 in the uterus. The treatment of estrogen increased Aimp1 expression in the uterus of ovarectomized mice. We identified one estrogen receptor binding element (ERE) on the mouse Aimp1 promoter. The activity of Aimp1 promoter was increased with estrogen treatment. Our findings indicate that Aimp1 might act as an important regulator to remodel the uterine endometrium and its expression might be regulated by estrogen during the estrous cycle. This will give us better understanding the dynamic change of uterine remodeling during the estrous cycle.
Kim, Miseon,Choi, Seo-Hyun,Jin, Yeung Bae,Lee, Hae-June,Ji, Young Hoon,Kim, Joon,Lee, Yun-Sil,Lee, Yoon-Jin Informa Healthcare 2013 International journal of radiation biology Vol.89 No.5
<P><I>Purpose</I>: Radiation-induced cardiovascular disease is a potentially severe side-effect of thoracic radiotherapy treatment. Clinically, this delayed side-effect presents as a form of accelerated atherosclerosis several years after irradiation. As general endothelial dysfunction is known to be an initiating event in radiation-induced vascular damage, we examined the effects of radiation on endothelial cells in radiation-induced atherosclerosis.</P><P><I>Materials and methods</I>: The effects of radiation on human aortic endothelial cells (HAoEC) were assessed by immunoblotting and immunofluorescence assays. Radiation-induced phenotypic changes of endothelial cells (ECs) were examined using atherosclerotic tissues of irradiated apoprotein E null (ApoE<SUP>−/−</SUP>) mice.</P><P><I>Results</I>: Radiation induced the HAoEC to undergo phenotypic conversion to form fibroblast-like cells, called the endothelial-to-mesenchymal transition (EndMT), which leads to the upregulation of mesenchymal cell markers such as alpha-smooth muscle actin (α-SMA), fibroblast specific protein-1 (FSP-1), and vimentin, and downregulation of endothelial cell-specific markers such as CD31 and vascular endothelial (VE)-cadherin. Furthermore, compared with low-density lipoprotein (LDL), oxidized low-density lipoprotein (ox-LDL) significantly augmented radiation-induced EndMT in HAoEC. These fibrotic phenotypes of ECs were found in atherosclerotic tissues of irradiated ApoE<SUP>−/−</SUP> mice with increased levels of ox-LDL.</P><P><I>Conclusions</I>: Taken together, these observations suggest that ox-LDL accelerates radiation-induced EndMT and subsequently contributes to radiation-induced atherosclerosis, providing a novel target for the prevention of radiation-induced atherosclerosis.</P>