Harnessing mIR-145 deficiency to modulate inflammation and prevent degeneration in a mouse model of multiple sclerosis DOI Creative Commons
Monique Marylin Alves de Almeida, Samantha F. Kornfeld, Yves De Repentigny

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 18, 2024

Abstract Multiple sclerosis (MS) is a progressive inflammatory disease of the central nervous system (CNS) marked by myelin loss, which impairs nerve function. Current therapies fail to halt progression or prevent and axonal degeneration. In this study, we explored impact miR-145 knockout in murine model experimental autoimmune encephalomyelitis (EAE), mimics MS pathology. Loss reduced clinical severity significantly decreased immune cell infiltration lumbar spinal cord during both onset chronic stages disease. Additionally, loss altered expression key genes modulated astrocytic activity throughout EAE. Of significant interest, acute treatment with an antisense oligonucleotide (ASO) targeting levels led severity, infiltration, increase regulatory T cells EAE mice. Moreover, deficiency mitigated axon Our findings suggest that ASOs may offer promising therapeutic strategy, addressing degenerative components MS.

Language: Английский

SARS-CoV-2 enhances complement-mediated endothelial injury via suppression of membrane complement regulatory proteins DOI Creative Commons
Jian Wu,

Sanpeng Xu,

Zhiqing Li

et al.

Emerging Microbes & Infections, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 13, 2025

Complement hyperactivation and thrombotic microangiopathy are closely associated with severe COVID-19. Endothelial dysfunction is a key mechanism underlying microangiopathy. To address the relationship between endothelial injury, complement activation of COVID-19, we wonder whether, if so, what how SARS-CoV-2 factors make cells (ECs) sensitive to complement-mediated cytotoxicity. We revealed that multiple proteins enhanced cytotoxicity ECs via inhibiting membrane regulatory (CRPs) enhancing deposition recognizing component FCN1. By screening CRISPR/Cas9-gRNA libraries, identified ADAMTS9, SYAP1 HIGD1A as intrinsic regulators CD59 on were inhibited by M, NSP16 ORF9b proteins. IFN-γ, GM-CSF IFN-α upregulated CD55 CD59, which IFN-γ antagonized inhibition three So, deficiency weakened protection CRPs against injury may be during infection. Our findings illustrated regulation attack self-cells infection immune responses, providing insights for potential targets treating

Language: Английский

Citations

0
Neurodegenerative diseases and neuroinflammation-induced apoptosis DOI Creative Commons

Shi Huang,

Yaxin Lu,

Wenjun Fang

et al.

Open Life Sciences, Journal Year: 2025, Volume and Issue: 20(1)

Published: Jan. 1, 2025

Abstract Neuroinflammation represents a critical pathway in the brain for clearance of foreign bodies and maintenance homeostasis. When neuroinflammatory process is dysregulate, such as over-activation microglia, which results excessive accumulation free oxygen inflammatory factors brain, among other factors, it can lead to an imbalance homeostasis development various diseases. Recent research has indicated that numerous neurodegenerative diseases closely associated with neuroinflammation. The pathogenesis neuroinflammation intricate, involving alterations genes proteins, well activation inhibition signaling pathways. Furthermore, inflammation result neuronal cell apoptosis, further exacerbate extent disease. This article presents summary recent studies on relationship between apoptosis caused by aim identify link two provide new ideas targets exploring pathogenesis, prevention treatment

Language: Английский

Citations

0
Rôle des lymphocytes T résidents mémoires dans les maladies inflammatoires du système nerveux central DOI
Roland Liblau

Bulletin de l Académie Nationale de Médecine, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Citations

0
NAVIGATING RHEUMATOID ARTHRITIS: INSIGHTS INTO LIGAND-ANCHORED NANOPARTICLE STRATEGIES FOR ANTI-INFLAMMATORY THERAPY AND RELIEF DOI Creative Commons

Shriya Karmarkar,

Trinette Fernandes,

Zainab Choonia

et al.

RSC Pharmaceutics, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 8, 2024

Ligand-based nanotechnology is promising in enhancing targeted drug delivery autoimmune disorders. This study explores molecular targets and new active targeting techniques. These technologies enhance specificity via precise targeting.

Language: Английский

Citations

1
Harnessing mIR-145 deficiency to modulate inflammation and prevent degeneration in a mouse model of multiple sclerosis DOI Creative Commons
Monique Marylin Alves de Almeida, Samantha F. Kornfeld, Yves De Repentigny

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 18, 2024

Abstract Multiple sclerosis (MS) is a progressive inflammatory disease of the central nervous system (CNS) marked by myelin loss, which impairs nerve function. Current therapies fail to halt progression or prevent and axonal degeneration. In this study, we explored impact miR-145 knockout in murine model experimental autoimmune encephalomyelitis (EAE), mimics MS pathology. Loss reduced clinical severity significantly decreased immune cell infiltration lumbar spinal cord during both onset chronic stages disease. Additionally, loss altered expression key genes modulated astrocytic activity throughout EAE. Of significant interest, acute treatment with an antisense oligonucleotide (ASO) targeting levels led severity, infiltration, increase regulatory T cells EAE mice. Moreover, deficiency mitigated axon Our findings suggest that ASOs may offer promising therapeutic strategy, addressing degenerative components MS.

Language: Английский

Citations

0