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3. S-Nitrosylation of cathepsin B affects autophagic flux and accumulation of protein aggregates in neurodegenerative disorders

Author

Kim, Ki-Ryeong, Cho, Eun-Jung, Eom, Jae-Won, Oh, Sang-Seok, Nakamura, Tomohiro, Oh, Chang-ki, Lipton, Stuart A, and Kim, Yang-Hee

Subjects
Biochemistry and Cell Biology, Biological Sciences, Neurodegenerative, Neurosciences, Dementia, Aging, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Acquired Cognitive Impairment, 2.1 Biological and endogenous factors, Neurological, Animals, Humans, Mice, Cathepsin B, Protein Aggregates, Neurodegenerative Diseases, Proteins, Alzheimer Disease, Cysteine, Nitric Oxide, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Protein S-nitrosylation is known to regulate enzymatic function. Here, we report that nitric oxide (NO)-related species can contribute to Alzheimer's disease (AD) by S-nitrosylating the lysosomal protease cathepsin B (forming SNO-CTSB), thereby inhibiting CTSB activity. This posttranslational modification inhibited autophagic flux, increased autolysosomal vesicles, and led to accumulation of protein aggregates. CA-074Me, a CTSB chemical inhibitor, also inhibited autophagic flux and resulted in accumulation of protein aggregates similar to the effect of SNO-CTSB. Inhibition of CTSB activity also induced caspase-dependent neuronal apoptosis in mouse cerebrocortical cultures. To examine which cysteine residue(s) in CTSB are S-nitrosylated, we mutated candidate cysteines and found that three cysteines were susceptible to S-nitrosylation. Finally, we observed an increase in SNO-CTSB in both 5XFAD transgenic mouse and flash-frozen postmortem human AD brains. These results suggest that S-nitrosylation of CTSB inhibits enzymatic activity, blocks autophagic flux, and thus contributes to AD pathogenesis.

Published
2022

18. Impact of Academia-Government Collaboration on Laboratory Medicine Standardization in South Korea: analysis of eight years creatinine proficiency testing experience.

Author

Lee, Seunghoo, Yu, Joonsang, Cho, Chan-Ik, Cho, Eun-Jung, Jeong, Tae-Dong, Kim, Sollip, Lee, Woochang, Chun, Sail, and Min, Won-Ki

Subjects
CREATININE, CLINICAL pathology, STANDARDIZATION, REFERENCE sources, TEST methods
Abstract

To evaluate the performance of the Academia-Government Collaboration for Laboratory Medicine Standardization in Korea (KR-STDZN) based on data from KR-STDZN proficiency testing (KR-STDZN-PT) for creatinine over eight years (2015–2022). We used KR-STDZN-PT data of creatinine tests from 2015 to 2022. Acceptance of the participating institutions' test results was assessed by calculating the acceptance performance as absolute bias (absBias%), total coefficient of variance (tCV%), and total error (TE%) for each sample using six measurements from each institution and true values of each reference material. The test result was considered acceptable when absBias%, tCV%, and TE% were <5.10, <3.20, and <11.40 %, respectively. The proportion of acceptable institutions among all participating institutions in each round was defined as the acceptance rate. Improvements in absBias%, tCV%, and TE% were analyzed using creatinine concentration ranges in samples. The number of participating institutions increased from 2015 to 2017 but remained consistent since 2018. The acceptance rates for absBias% and TE% increased from 52.2 and 77.6 %, in 2015 and to 90.7 and 96.3 %, in 2022, respectively. The acceptance rate for tCV% remained in the 90 % range for eight years. When creatinine <3 mg/dL, mean absBias%, and mean TE% improved significantly in 2021–2022 compared to 2015–2016 (p<0.05). When creatinine >3 mg/dL, acceptance performance did not improve. Mean tCV% remained consistent annually regardless of creatinine concentration. No significant variations in test methods were observed. The collaboration between academia and the government improved creatinine testing quality. Nevertheless, KR-STDZN must be expanded and refined. [ABSTRACT FROM AUTHOR]

Published
2024
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