The dynamic regulation of mitochondrial morphology is key for eukaryotic cells to manage physiological challenges. Therefore, it is important to understand the molecular basis of mitochondrial dynamic regulation. The aim of the present study was to explore the role of HIG1 hypoxia inducible domain family member 1B (HIGD-1B) in hypoxia-induced mitochondrial fragmentation. Protein expression was determined via western blotting. Immunofluorescence assays were performed to detect the subcellular location of HIGD-1B. Cell Counting Kit-8 assays and flow cytometry were carried out to measure cell viability and apoptosis, respectively. Protein interactions were evaluated by co-immunoprecipitation. In the present study, it was found that HIGD-1B serves a role in cell survival by maintaining the integrity of the mitochondria under hypoxic conditions. Knockdown of HIGD-1B promoted mitochondrial fragmentation, while overexpression of HIGD-1B increased survival by preventing activation of caspase-3 and -9. HIGD-1B expression was associated with cell viability and apoptosis in cardiomyocytes. Furthermore, HIGD-1B delayed the cleavage process of optic atrophy 1 (OPA1) and stabilized mitochondrial morphology by interacting with OPA1. Collectively, the results from the present study identified a role for HIGD-1B as an inhibitor of the mitochondrial fission in cardiomyocytes.
Diabetes with high blood glucose levels may damage the brain nerves and thus increase the risk of dementia. Previous studies have shown that dementia can be reflected in altered brain structure, facilitating computer-aided diagnosis of brain diseases based on structural magnetic resonance imaging (MRI). However, type 2 diabetes mellitus (T2DM)-mediated changes in the brain structures have not yet been studied, and only a few studies have focused on the use of brain MRI for automated diagnosis of T2DM. Hence, identifying MRI biomarkers is essential to evaluate the association between changes in brain structure and T2DM as well as cognitive impairment (CI). The present study aims to investigate four methods to extract features from MRI, characterize imaging biomarkers, as well as identify subjects with T2DM and CI.
Background Oxidative stress leads to an increase in reactive oxygen in the body. During heart failure (HF), when the body’s antioxidant defense system fails to remove excessive reactive oxygen species, myocardial cells will be damaged or even die. Over the past ten years, the number of research publications on oxidative stress related to HF has increased. Methods We searched publications published in 2012–2021 and the Web of Science Core Collection (WoSCC) recording information. Based on the VOSviewer and CiteSpace, we conducted a bibliometric analysis of the overall distribution of journals, keywords, authors, major countries, annual output, active institutions, and cocited literature. The Global Citation Score (GCS) was used to evaluate the impact and quality of highly cited papers. Results We retrieved 5,616 articles and reviews. Over the past ten years, the number of annual publications on oxidative stress related to HF has increased. USA has published the largest number of articles and obtained the highest number of citations (NC) and H-index. The University of California and PLoS One are the most productive affiliations and journals in terms of publications on oxidative stress related to HF. The GCS of articles written by Paulus WJ in 2013 was 1,632, which was the top ranking. The most frequent keywords are “oxidative stress”, “heart failure”, “inflammation”, “dysfunction” and “apoptosis”. The top three authors are Kang Yuming, Ren Jun and Okoshi Katashi. “Impact“, “induced myocardial infarction”, “cardiovascular outcome”, “empagliflozin”, “sglt2 inhibitor”, “protect”, and “Na + /H + exchanger” have become popular research topics. Conclusions Our research shows the research focus and development trends of oxidative stress related to HF in the past decade. Understanding the most important indicators of oxidative stress related to HF and the hot spots in the field of oxidative stress research related to HF can assist scholars, countries and policy-makers in the field in better understanding oxidative stress related to HF and can also lead to better decisions in oxidative stress treatment.
OBJECTIVE: To study the effect of K‐ras antisense oligodeoxynucleotides (ASODN) on human pancreatic cancer cell line PaTu 8988s at different times after treatment. METHODS: Human pancreatic cancer cells (PaTu 8988s) in exponential growth stage were used at a cell concentration of 1 × 105/mL; 0.5 mL of the cell suspension was placed in each well of replicate 24‐well culture plates in the presence of different concentrations (50 and 100 μg/mL) of ASODN and sense oligodeoxynucleotides (SODN). Cell counts and 3‐[4,5‐dimethylthiazolzyl]‐2,5‐diphenyl tetrazolium bromide (MTT) assays were carried out 24, 48 and 72 h after treatment. RESULTS: At 12, 24, 48 and 72 h after ASODN treatment, the following rates of inhibition were observed: for 50 μg/mL, 42.3, 66.6, 69.6 and 74.6%, respectively; for 100 μg/mL, 66.2, 91.4, 98.2 and 98.3%, respectively. CONCLUSION: The inhibitory effect of ASODN began at 12 h post‐treatment and became more marked at 48–72 h. The higher the concentration of ASODN, the earlier the peak of inhibitory rate appears.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.