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DJ-1 protects cell death from a mitochondrial oxidative stress due to GBA1 deficiency
Nam Younwoo,Na Jiyeon,Ma Shi-Xun,Park Ha-Eun,Park Hyeonwoo,Lee Eunmin,Kim Hyerynn,Jang Sang-Min,Ko Han Seok,Kim Sangjune 한국유전학회 2024 Genes & Genomics Vol.46 No.5
Background GBA1 mutations are the most common genetic risk factor for development of Parkinson’s disease (PD). The loss of catalytic activity in GBA1, as well as the reduction of the GBA1 protein in certain cellular compartment, may increase disease progression. However, the mechanisms underlying cellular dysfunction caused by GBA1 deficiency are still mostly unknown. Objective In this study, we focus on the genetic interaction between GBA1 deficiency and PD-causing genes, such as DJ-1, in mitochondrial dysfunction. Methods GBA1 knockout (KO) SH-SY5Y cells were used to assess DJ-1 functions against oxidative stress in vitro. The levels of cellular reactive oxygen species were monitored with MitoSOX reagent. The expression of the PARK7 gene was analyzed using the quantitative real-time PCR (qRT-PCR). To understand the mechanism underlying DJ-1 upregulation in GBA1 KO cells, we assess ROS levels, antioxidant protein, and cell viability in GBA1 KO cells with treatment of ROS inhibitor N-acetyl-cysteine or miglustat, which is an inhibitor of glucosylceramide synthase. Dopaminergic degeneration was assessed from Gba1 L444P heterozygous mice mated with Park7 knockout mice. Results We find that DJ-1 is significantly upregulated in GBA1 KO cells. Elevated levels of DJ-1 are attributed to the transcriptional expression of PARK7 mRNA, but not the inhibition of DJ-1 protein degradation. Because DJ-1 expression is highly linked to oxidative stress, we observe cellular reactive oxygen species (ROS) in GBA1 KO cells. Moreover, several antioxidant gene expressions and protein levels are increased in GBA1 KO cells. To this end, GBA1 KO cells are more susceptible to H2O2-induced cell death. Importantly, there is a significant reduction in dopaminergic neurons in the midbrain from Gba1 L444P heterozygous mice mated with Park7 knockout mice, followed by mild motor dysfunction. Conclusion Taken together, our results suggest that DJ-1 upregulation due to GBA1 deficiency has a protective role against oxidative stress. It may be supposed that mutations or malfunctions in the DJ-1 protein may have disadvantages in the survival of dopaminergic neurons in the brains of patients harboring GBA1 mutations. Background GBA1 mutations are the most common genetic risk factor for development of Parkinson’s disease (PD). The loss of catalytic activity in GBA1, as well as the reduction of the GBA1 protein in certain cellular compartment, may increase disease progression. However, the mechanisms underlying cellular dysfunction caused by GBA1 deficiency are still mostly unknown. Objective In this study, we focus on the genetic interaction between GBA1 deficiency and PD-causing genes, such as DJ-1, in mitochondrial dysfunction. Methods GBA1 knockout (KO) SH-SY5Y cells were used to assess DJ-1 functions against oxidative stress in vitro. The levels of cellular reactive oxygen species were monitored with MitoSOX reagent. The expression of the PARK7 gene was analyzed using the quantitative real-time PCR (qRT-PCR). To understand the mechanism underlying DJ-1 upregulation in GBA1 KO cells, we assess ROS levels, antioxidant protein, and cell viability in GBA1 KO cells with treatment of ROS inhibitor N-acetyl-cysteine or miglustat, which is an inhibitor of glucosylceramide synthase. Dopaminergic degeneration was assessed from Gba1 L444P heterozygous mice mated with Park7 knockout mice. Results We find that DJ-1 is significantly upregulated in GBA1 KO cells. Elevated levels of DJ-1 are attributed to the transcriptional expression of PARK7 mRNA, but not the inhibition of DJ-1 protein degradation. Because DJ-1 expression is highly linked to oxidative stress, we observe cellular reactive oxygen species (ROS) in GBA1 KO cells. Moreover, several antioxidant gene expressions and protein levels are increased in GBA1 KO cells. To this end, GBA1 KO cells are more susceptible to H2O2-induced cell death. Importantly, there is a significant reduction in dopaminergic neurons in the midbrain from Gba1 L444P heterozygous mice mated with Park7 knockout mice, followed by mild motor dysfunction. Conclusion Taken together, our results suggest that DJ-1 upregulation due to GBA1 deficiency has a protective role against oxidative stress. It may be supposed that mutations or malfunctions in the DJ-1 protein may have disadvantages in the survival of dopaminergic neurons in the brains of patients harboring GBA1 mutations.
빅벨리해마(Hippocampus abdominalis)에서의 Mitochondrial Heat Shock Protein 75 유전자의 특징과 발현 분석
고지연 ( Jiyeon Ko ),( Wan Qiang ),이숙경 ( Sukkyoung Lee ),( S. D. N. K. Bathige ),오민영 ( Minyoung Oh ),이제희 ( Jehee Lee ) 한국수산과학회 2015 한국수산과학회지 Vol.48 No.3
Mitochondrial heat shock protein 75 (mtHSP75) is a member of the HSP90 family and plays essential roles in re-folding proteins of the mitochondrial matrix. Mitochondria provide energy in the form of ATP and generate reactive oxygen species (ROS). Heat shock proteins (HSPs) are activated in response to stress, and protect cells. In this study, we characterized the mtHSP75 of the big-belly seahorse Hippocampus abdominalis. The protein (BsmtHSP75) is encoded by an open reading frame (ORF) of 2,157 nucleotides, has 719 amino acids (aa), and is of molecular mass 82 kDa. BsmtHSP75 has two functional domains, a histidine kinase-like ATPase (HATPase_c) domain (123-276 aa) and an HSP90 family domain (302-718 aa). BsmtHSP75 was expressed in all tested tissues of healthy seahorses. The ovary contained the highest transcription level, followed (in order) by the blood, brain, and muscle. Pouch tissue showed the lowest expression level. The expression of BsmtHSP75 was significantly (P<0.05) up-regulated on viral or bacterial challenge, suggesting that BsmtHSP75 plays a role in the immune defense against bacterial and viral pathogens.
( Yousang Ko ),( Hyung Woo Kim ),( Jinsoo Min ),( Jee Youn Oh ),( Ji Young Kang ),( Hyeon-kyoung Koo ),( Yunhyung Kwon ),( Jiyeon Yang ),( Jiyeon Han ),( You Jin Jang ),( Sung-soon Lee ),( Jae Seuk Pa 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Background Early diagnosis and subsequent treatment for pulmonary tuberculosis (PTB) is essential for Tuberculosis prevention and control. Despite South Korea is an area of intermediate TB burden with a prevalence rate of 101/100,000 persons in 2014, there has been no investigation for determining factors associated with delays. It is necessary to guide public health action. Methods A nationwide, prospective, and observational cohort study for tuberculosis patients has been ongoing in Korea since September 2018. We described the distribution of delays from symptom onset to first visit of medical facility (patient-related delay) and from presentation to treatment (healthcare-related delay). Factors associated with patient-related delay and healthcare-related delay was identified using a multivariable analysis model. Results A total of 6,715 patients were diagnosed with PTB in 2019. For patient-related delay and healthcare-related delay were included as 3,783 and 5,660 cases, respectively. Mean patient-related delay was 49.4 (± 110.8). In multivariate regression analysis, Neuro-psychiatric disease was an independent risk factor for patient-related delay (HR 1.444; 95% confidence interval 1.191 to 1.750, p<0.001), malignancy (HR 1.313; 95% confidence interval 1.172 to 1.471, p<0.001), extra-PTB (HR 1.283; 95% confidence interval 1.150 to 1.431, p<0.001) and poor economic status (HR 1.090; 95% confidence interval 1.005 to 1.182, p=0.037). Mean healthcare-related delay was 13.3 (± 34.9). In multivariate regression analysis, Age over 65 years was an independent risk factor for healthcare-related delay (HR 1.120; 95% confidence interval 1.048 to 1.198, p=0.001) and early PTB defined as low microbiologic burden (HR 1.313; 95% confidence interval 1.206 to 1.429, p<0.001). Conclusions Our findings support continued initiatives to enable access to care for patients with neuro-psychiatric disease, malignancy, extra-PTB and poor economic status to reduce patient-related delayiagnosis of PTB. Moreover, clinician should pay attention in elderly and have awareness of TB clinical characteristics to find early PTB case.
Bioinformatics services for analyzing massive genomic datasets
Ko, Gunhwan,Kim, Pan-Gyu,Cho, Youngbum,Jeong, Seongmun,Kim, Jae-Yoon,Kim, Kyoung Hyoun,Lee, Ho-Yeon,Han, Jiyeon,Yu, Namhee,Ham, Seokjin,Jang, Insoon,Kang, Byunghee,Shin, Sunguk,Kim, Lian,Lee, Seung-Wo Korea Genome Organization 2020 Genomics & informatics Vol.18 No.1
The explosive growth of next-generation sequencing data has resulted in ultra-large-scale datasets and ensuing computational problems. In Korea, the amount of genomic data has been increasing rapidly in the recent years. Leveraging these big data requires researchers to use large-scale computational resources and analysis pipelines. A promising solution for addressing this computational challenge is cloud computing, where CPUs, memory, storage, and programs are accessible in the form of virtual machines. Here, we present a cloud computing-based system, Bio-Express, that provides user-friendly, cost-effective analysis of massive genomic datasets. Bio-Express is loaded with predefined multi-omics data analysis pipelines, which are divided into genome, transcriptome, epigenome, and metagenome pipelines. Users can employ predefined pipelines or create a new pipeline for analyzing their own omics data. We also developed several web-based services for facilitating downstream analysis of genome data. Bio-Express web service is freely available at https://www. bioexpress.re.kr/.
Ko, Kuk Won,Lee, Jiyeon,Moon, Hongsuk,Lee, Sangjoon The Institute of Internet 2015 International Journal of Internet, Broadcasting an Vol.7 No.2
Biometric techniques for authentication using body parts such as a fingerprint, face, iris, voice, finger-vein and also photoplethysmography have become increasingly important in the personal security field, including door access control, finance security, electronic passport, and mobile device. Finger-vein images are now used to human identification, however, difficulties in recognizing finger-vein images are caused by capturing under various conditions, such as different temperatures and illumination, and noise in the acquisition camera. The human photoplethysmography is also important signal for human identification. In this paper To increase the recognition rate, we develop camera based identification method by combining finger vein image and photoplethysmography signal. We use a compact CMOS camera with a penetrating infrared LED light source to acquire images of finger vein and photoplethysmography signal. In addition, we suggest a simple pattern matching method to reduce the calculation time for embedded environments. The experimental results show that our simple system has good results in terms of speed and accuracy for personal identification compared to the result of only finger vein images.