Proteomic study of left ventricle and cortex in rats after myocardial infarction DOI Creative Commons
Mengli Chang, Huanhuan Wang,

Yuxin Lei

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: March 22, 2024

Myocardial infarction (MI) induces neuroinflammation indirectly, chronic may cause neurodegenerative diseases. Changes in the proteomics of heart and brain tissue after MI shed new light on mechanisms involved neuroinflammation. This study explored protein changes with a data-independent acquisition (DIA) mode approach. Permanent ligation left anterior descending coronary artery (LAD) was performed rats, immunofluorescence microglia cortex at 1d, 3d, 5d, 7d to detect Then accomplished obtain vital proteins post-MI. The results show that number significantly increased Model-1d group, Model-3d Model-5d Model-7d group compared Sham group. Various were obtained through DIA proteomics. Linking key targets disease, 14 cortex. Among them, elongation very long chain fatty acids 5 (ELOVL5) ATP-binding cassette subfamily G member 4 (ABCG4) verified western blotting (WB). WB consistent results. Therefore, these be related pathogenesis MI.

Language: Английский

Microglial Lyzl4 Facilitates β‐Amyloid Clearance in Alzheimer's Disease DOI Creative Commons
Jie Pan, Jie Zhong, Ji Geng

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: 12(2)

Published: Nov. 18, 2024

Abstract Alzheimer's Disease (AD) is a neurodegenerative condition characterized by the accumulation and deposition of amyloid‐β (Aβ) aggregates in brain. Despite wealth research on toxicity Aβ its role synaptic damage, mechanisms facilitating clearance are not yet fully understood. However, microglia, primary immune cells central nervous system, known to maintain homeostasis through phagocytic protein cellular debris. In this study, RNA sequencing analysis live cell functional screens employed uncover microglial genetic modifiers related AD. Lyzl4 identified, which encodes c‐type lysozyme‐like enzyme primarily localized lysosomes, as gene significantly upregulated AD microglia with aging propose that upregulation acts positive regulator clearance. Furthermore, it found overexpression boosts both vitro vivo, underscoring potential for mitigating burden. These novel insights position promising therapeutic target disease, paving way further exploration into treatments.

Language: Английский

Citations

1
Dual-probe fluorescence spectroscopy for sensitive quantitation of Alzheimer’s amyloid pathology DOI Creative Commons
Anastasiia A. Stepanchuk, Megan L. Morgan, Jeffrey T. Joseph

et al.

Acta Neuropathologica Communications, Journal Year: 2022, Volume and Issue: 10(1)

Published: Oct. 28, 2022

Protein misfolding is a prominent pathological hallmark of neurodegenerative disorders, including Alzheimer's disease (AD). Studies have shown that the diversity β sheet-rich protein deposits (such as amyloid plaques and neurofibrillary tangles), present across different brain regions, might underlie phenotypes only certain types aggregates be associated with cognitive decline. Conformationally sensitive fluorescent probes ability to report structures by virtue their shifting emission spectra. Here we defined binding affinity BSB MCAAD disease-relevant aggregates, combined two examine formalin-fixed paraffin-embedded mouse human samples. Coupled quantitative spectral phasor analysis, dual-probe staining approach revealed remarkable heterogeneity Distinct spectra were consistent in sections. The sensitivity this staining, imaging analysis outperformed conventional immunohistochemistry detected differences between greater parenchyma cognitively normal AD cases indicating subtle yet widespread proteopathy disease. Our method offers more sensitive, objective, examination pathology using tissue

Language: Английский

Citations

6
Feature-Based Molecular Networking Facilitates the Comprehensive Identification of Differential Metabolites in Diabetic Cognitive Dysfunction Rats DOI Creative Commons
Ke Du,

Chuanjia Zhai,

Xuejiao Li

et al.

Metabolites, Journal Year: 2023, Volume and Issue: 13(4), P. 538 - 538

Published: April 10, 2023

Cognitive dysfunction is a frequent complication of type 2 diabetes mellitus (T2DM), usually accompanied by metabolic disorders. However, the changes in diabetic cognitive (DCD) patients, especially compared to T2DM groups, are not fully understood. Due subtle differences alterations between DCD groups and comprehensive detection untargeted profiles hippocampus urine samples rats was conducted LC–MS, considering different ionization modes polarities examined compounds, feature-based molecular networking (FBMN) performed help identify differential metabolites from perspective this study. In addition, an association analysis O2PLS model. Finally, total 71 hippocampal tissue 179 were identified. The pathway enrichment results showed that glutamine glutamate metabolism, alanine, aspartate, glycerol phospholipid TCA cycle, arginine biosynthesis animals changed. Seven (AUC > 0.9) appeared as key might reflect target rats. This study FBMN facilitated identification may suggest underlying be considered potential biomarkers for DCD. Large clinical experiments needed subsequent elucidation possible mechanisms leading these verification biomarkers.

Language: Английский

Citations

3
Early life stress and the role of environmental and molecular moderators in the ontology of pathological and resilient behavioral phenotypes DOI
Nicholas J. Collins,

Taylor S. Campbell,

Katelyn M. Donoghue

et al.

Molecular Psychology Brain Behavior and Society, Journal Year: 2023, Volume and Issue: 1, P. 3 - 3

Published: Sept. 26, 2023

Early life stress (ELS) in the form of trauma or caregiver abuse and neglect is often associated with psychopathology. However, not everyone exposed to ELS develops a pathology; others display resilience, ability adapt persevere despite ongoing adversity. Several molecular moderator variables between behavioral phenotypes have been proposed, including single nucleotide polymorphisms (SNPs) epigenetic markers. Specifically, several SNPs aberrant methylation expression genes neurotransmitter systems brain-derived neurotrophic factor anxiety, depression schizophrenia. The present review seeks explore relationship SNPs, epigenomics disease, offer data suggest may also predict specific treatment efficacy psychological resilience. Due these different mental health outcomes as function ELS, it critical that environmental moderators be equally considered determining ontology resilient pathological phenotypes; this includes infant-caregiver relationship, degree control, magnitude, type stressor experienced. Finally, we will evidence intervention strategies, drug treatment, enrichment, exercise can ameliorate many psychological, biological, consequences exposure, help shift one toward phenotype.

Language: Английский

Citations

2
Proteomic study of left ventricle and cortex in rats after myocardial infarction DOI Creative Commons
Mengli Chang, Huanhuan Wang,

Yuxin Lei

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: March 22, 2024

Myocardial infarction (MI) induces neuroinflammation indirectly, chronic may cause neurodegenerative diseases. Changes in the proteomics of heart and brain tissue after MI shed new light on mechanisms involved neuroinflammation. This study explored protein changes with a data-independent acquisition (DIA) mode approach. Permanent ligation left anterior descending coronary artery (LAD) was performed rats, immunofluorescence microglia cortex at 1d, 3d, 5d, 7d to detect Then accomplished obtain vital proteins post-MI. The results show that number significantly increased Model-1d group, Model-3d Model-5d Model-7d group compared Sham group. Various were obtained through DIA proteomics. Linking key targets disease, 14 cortex. Among them, elongation very long chain fatty acids 5 (ELOVL5) ATP-binding cassette subfamily G member 4 (ABCG4) verified western blotting (WB). WB consistent results. Therefore, these be related pathogenesis MI.

Language: Английский

Citations

0