LINC00173 regulates polycystic ovarian syndrome progression by promoting apoptosis and repressing proliferation in ovarian granulosa cells via the microRNA-124-3p (miR-124-3p)/jagged canonical Notch ligand 1 (JAG1) pathway DOI Open Access
Lan Chen, Caixia Kong

Bioengineered, Journal Year: 2022, Volume and Issue: 13(4), P. 10373 - 10385

Published: April 1, 2022

As an endocrine and metabolic disorder, polycystic ovarian syndrome (PCOS) is common in females at childbearing age. Our work was intended to uncover the underlying role of LINC00173 its potential regulatory mechanism PCOS based on two cell lines (PCOS granulosa cells KGN cells) vivo model established from Sprague Dawley rats. It revealed that JAG1 expressions were upregulated, while miR-124-3p poorly expressed patients Functional assays showed overexpression repressed proliferation stimulated apoptosis cells, downregulation exhibited opposite effects. Besides, it verified upregulated expression via competitively binding miR-124-3p. Similarly, abundance inversely related level PCOS. Subsequently, rescue elucidated upregulation or eliminated effects mediated by knockdown. In addition, found adversely modulated positively LINC00173. Moreover, further demonstrated reduced vitality increased induced overexpressing could be relieved deletion. These findings suggested a latent regulating factor for progression modulating miR-124-3p/JAG1 cascade.

Language: Английский

Neuroinflammation in Alzheimer’s Disease: Current Progress in Molecular Signaling and Therapeutics DOI
Sujata Thakur,

Rishika Dhapola,

Phulen Sarma

et al.

Inflammation, Journal Year: 2022, Volume and Issue: 46(1), P. 1 - 17

Published: Aug. 20, 2022

Language: Английский

Citations

257

Lipopolysaccharide-Induced Model of Neuroinflammation: Mechanisms of Action, Research Application and Future Directions for Its Use DOI Creative Commons
Anna Skrzypczak-Wiercioch, Kinga Sałat

Molecules, Journal Year: 2022, Volume and Issue: 27(17), P. 5481 - 5481

Published: Aug. 26, 2022

Despite advances in antimicrobial and anti-inflammatory therapies, inflammation its consequences still remain a significant problem medicine. Acute inflammatory responses are responsible for directly life-threating conditions such as septic shock; on the other hand, chronic can cause degeneration of body tissues leading to severe impairment their function. Neuroinflammation is defined an response central nervous system involving microglia, astrocytes, cytokines including chemokines. It considered important neurodegerative diseases, Alzheimer's disease, Parkinson's disease amyotrophic lateral sclerosis. Lipopolysaccharide (LPS) strong immunogenic particle present outer membrane Gram-negative bacteria. major triggering factor cascade bacteria infection. The use LPS pro-inflammatory agent well-known model applied both vivo vitro studies. This review offers summary pathogenesis associated with exposure, especially field neuroinflammation. Moreover, we analyzed different models utilized area neuroscience. paper presents recent knowledge focused new insights experimental model.

Language: Английский

Citations

151

Ferroptosis as a mechanism of neurodegeneration in Alzheimer's disease DOI
Md. Jakaria, Abdel A. Belaidi, Ashley I. Bush

et al.

Journal of Neurochemistry, Journal Year: 2021, Volume and Issue: 159(5), P. 804 - 825

Published: Sept. 23, 2021

Alzheimer's disease (AD) is the most prevalent form of dementia, with complex pathophysiology that not fully understood. While β-amyloid plaque and neurofibrillary tangles define pathology disease, mechanism neurodegeneration uncertain. Ferroptosis an iron-mediated programmed cell death characterised by phospholipid peroxidation has been observed in clinical AD samples. This review will outline growing molecular evidence implicating ferroptosis pathogenesis AD, implications for disease-modifying therapies.

Language: Английский

Citations

141

Postoperative cognitive dysfunction—current research progress DOI Creative Commons
Qi Zhao, Hui Wan, Hui‐Lin Pan

et al.

Frontiers in Behavioral Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Jan. 30, 2024

Postoperative cognitive dysfunction (POCD) commonly occurs after surgery, particularly in elderly individuals. It is characterized by a notable decline performance, encompassing memory, attention, coordination, orientation, verbal fluency, and executive function. This reduction abilities contributes to extended hospital stays heightened mortality. The prevalence of POCD can reach 40% within 1 week following cardiovascular surgery remains as high 17% 3 months post-surgery. Furthermore, exacerbates the long-term risk Alzheimer’s disease (AD). As result, numerous studies have been conducted investigate molecular mechanisms underlying potential preventive strategies. article provides review research progress on POCD.

Language: Английский

Citations

38

The Eminent Role of microRNAs in the Pathogenesis of Alzheimer's Disease DOI Creative Commons
Mohammad Samadian, Mahdi Gholipour, Mohammadreza Hajiesmaeili

et al.

Frontiers in Aging Neuroscience, Journal Year: 2021, Volume and Issue: 13

Published: March 15, 2021

Alzheimer's disease (AD) is an irrevocable neurodegenerative condition characterized by the presence of senile plaques comprising amassed β-amyloid peptides (Aβ) and neurofibrillary tangles mainly extremely phosphorylated Tau proteins. Recent studies have emphasized role microRNAs (miRNAs) in development AD. A number miRNAs, namely, miR-200a-3p, miR-195, miR-338-5p, miR-34a-5p, miR-125b-5p, miR-132, miR-384, miR-339-5p, miR-135b, miR-425-5p, been shown to participate AD through interacting with BACE1. Other miRNAs might affect inflammatory responses course Aberrant expression several plasma samples subjects has aptitude for differentiation from healthy subjects. Finally, a AD-modifying agents miRNA profile cell cultures or animal models. We performed comprehensive search summarized obtained data about function current review article.

Language: Английский

Citations

58

The potential role of dexmedetomidine on neuroprotection and its possible mechanisms: Evidence from in vitro and in vivo studies DOI
Kantarakorn Unchiti, Prangmalee Leurcharusmee, Artid Samerchua

et al.

European Journal of Neuroscience, Journal Year: 2021, Volume and Issue: 54(9), P. 7006 - 7047

Published: Sept. 25, 2021

Neurological disorders following brain injuries and neurodegeneration are on the rise worldwide cause disability suffering in patients. It is crucial to explore novel neuroprotectants. Dexmedetomidine, a selective α2-adrenoceptor agonist, commonly used for anxiolysis, sedation analgesia clinical anaesthesia critical care. Recent studies have shown that dexmedetomidine exerts protective effects multiple organs. This review summarized discussed current neuroprotective of dexmedetomidine, as well underlying mechanisms. In preclinical studies, reduced neuronal injury improved functional outcomes several models, including hypoxia-induced injury, ischaemic-reperfusion intracerebral haemorrhage, post-traumatic anaesthetic-induced substance-induced neuroinflammation, epilepsy neurodegeneration. Several mechanisms associated with function neurotransmitter regulation, inflammatory response, oxidative stress, apoptotic pathway, autophagy, mitochondrial other cell signalling pathways. summary, has potential be agent wide range neurological disorders.

Language: Английский

Citations

57

Proteostasis failure exacerbates neuronal circuit dysfunction and sleep impairments in Alzheimer’s disease DOI Creative Commons
Christopher D. Morrone, Radha Raghuraman, S. Abid Hussaini

et al.

Molecular Neurodegeneration, Journal Year: 2023, Volume and Issue: 18(1)

Published: April 21, 2023

Abstract Failed proteostasis is a well-documented feature of Alzheimer’s disease, particularly, reduced protein degradation and clearance. However, the contribution failed to neuronal circuit dysfunction an emerging concept in neurodegenerative research will prove critical understanding cognitive decline. Our objective convey disease progression with growing evidence for bidirectional relationship sleep disruption failure. Proteostasis tauopathy disrupts neurons that regulate sleep–wake cycle, which presents behavior as impaired slow wave rapid eye movement patterns. Subsequent loss further impairs Sleep defined seen early many disorders contributes memory impairments disease. Canonical pathological hallmarks, β-amyloid, tau, directly disrupt sleep, neurodegeneration locus coeruleus, hippocampal hypothalamic from tau proteinopathy causes circuitry sleep. Acting positive-feedback-loop, circadian rhythm then increase spread β-amyloid through proteasome, autophagy, unfolded response glymphatic This phenomenon extends beyond interactions impairment homeostasis TDP-43, α-synuclein, FUS, huntingtin proteins, implicating important consideration array diseases cases mixed neuropathology. Critically, dynamics this interaction environment are not fully elucidated deserving discussion research. Finally, we propose sleep-enhancing therapeutics potential interventions promoting healthy proteostasis, including clearance, mechanistically linking these processes. With clinical preclinical research, dynamic diagnostic therapeutic framework, informing precise single- combinatorial-treatments other brain disorders. Graphical

Language: Английский

Citations

28

The role of microRNAs in neurobiology and pathophysiology of the hippocampus DOI Creative Commons

Seyed Khalil Rashidi,

Ata Kalirad, Shahram Rafie

et al.

Frontiers in Molecular Neuroscience, Journal Year: 2023, Volume and Issue: 16

Published: Sept. 4, 2023

MicroRNAs (miRNAs) are short non-coding and well-conserved RNAs that linked to many aspects of development disorders. control the expression genes related different biological processes play a prominent role in harmonious genes. During neural central nervous system, miRNAs regulated time space. In mature brain, dynamic continues, highlighting their functional importance neurons. The hippocampus, as one crucial brain structures, is key component major connections brain. Gene abnormalities hippocampus lead disturbance neurogenesis, maturation synaptic formation. These disturbances at root several neurological disorders behavioral deficits, including Alzheimer's disease, epilepsy schizophrenia. There strong evidence contributed neurodegenerative mechanisms through imbalanced activity ion channels, neuronal excitability, plasticity apoptosis. Some affect oxidative stress, inflammation, differentiation, migration neurogenesis hippocampus. Furthermore, signaling cascades neurodegeneration, such NF-Kβ signaling, PI3/Akt Notch pathway, closely modulated by miRNAs. observations, suggest microRNAs significant regulators complicated network gene regulation current review, we focus on miRNA progression normal We also consider how for pathophysiological pathways.

Language: Английский

Citations

24

miR-129-5p as a biomarker for pathology and cognitive decline in Alzheimer’s disease DOI Creative Commons
Sang‐Won Han, Jung‐Min Pyun, Paula J. Bice

et al.

Alzheimer s Research & Therapy, Journal Year: 2024, Volume and Issue: 16(1)

Published: Jan. 9, 2024

Abstract Background Alzheimer’s dementia (AD) pathogenesis involves complex mechanisms, including microRNA (miRNA) dysregulation. Integrative network and machine learning analysis of miRNA can provide insights into AD pathology prognostic/diagnostic biomarkers. Methods We performed co-expression to identify modules associated with AD, its neuropathology markers, cognition using brain tissue profiles from the Religious Orders Study Rush Memory Aging Project (ROS/MAP) ( N = 702) as a discovery dataset. association hub miRNAs cognition. After selecting target genes miRNAs, we their then pathway-based enrichment analysis. For replication, consensus ROS/MAP dataset an independent 16) Gene Expression Omnibus (GEO). Furthermore, approach assess performance for classification. Results Network identified glucose metabolism pathway-enriched module (M3) significantly Five (miR-129-5p, miR-433, miR-1260, miR-200a, miR-221) M3 had significant associations clinical and/or pathologic traits, miR129-5p by far strongest across all phenotypes. Gene-set corresponding enriched biological pathways ErbB, AMPK, MAPK, mTOR signaling pathways. Consensus two AD-associated (miR-129-5p miR-221). Machine showed that classification (area under curve (AUC) 0.807) age, sex, APOE ε4 carrier status was improved 6.3% inclusion five miRNAs. Conclusions signatures, especially miR-129-5p, cognition, enhancing our understanding leading better potential diagnostic/prognostic

Language: Английский

Citations

10

A review on the lncRNA-miRNA-mRNA regulatory networks involved in inflammatory processes in Alzheimer’s disease DOI
Masoumeh Kazemi,

Mahla Sanati,

Mahmoud Shekari Khaniani

et al.

Brain Research, Journal Year: 2025, Volume and Issue: unknown, P. 149595 - 149595

Published: March 1, 2025

Language: Английский

Citations

1