Author Correction: Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease

Krashia, Paraskevi; Cordella, Alberto; Nobili, Annalisa; Barbera, Livia La; Federici, Mauro; Leuti, Alessandro; Campanelli, Federica; Natale, Giuseppina; Marino, Gioia; Calabrese, Valeria; Vedele, Francescangelo; Ghiglieri, Veronica; Picconi, Barbara; Lazzaro, Giulia Di; Schirinzi, Tommaso; Sancesario, Giulia Maria; Casadei, Nicolas; Rieß, Olaf; Bernardini, Sergio; Pisani, Antonio; Calabresi, Paolo; Viscomi, Maria Teresa; Serhan, Charles N.; Chiurchiù, Valerio; D’Amelio, Marcello; Mercuri, Nicola Biagio

doi:10.1038/s41467-019-12538-2

Cited by 11 publications

(13 citation statements)

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“…Next, we sought to determine the levels of oligomeric species of secreted αSyn by using an antibody that specifically recognizes αSyn oligomers. To test the specificity of this antibody, we conducted a dot blot with purified αSyn monomer and pre-formed fibrils and observed that the antibody is unable to detect monomeric αSyn while it robustly recognized fibrillar αSyn, consistent with prior efforts validating this reagent (Lassen et al, 2018;Krashia et al, 2019;Matsui et al, 2019). Finally, we analyzed the conditioned media from WT and GBA1 heterozygous-null iNs and found that secreted αSyn from GBA1 heterozygous-null iNs contain more oligomeric αSyn than that from WT cells ( Figure 3D).…”

Section: Gba1 Heterozygous-null Neurons Accumulate Soluble and Insolusupporting

confidence: 73%

LRRK2 Kinase Inhibition Rescues Deficits in Lysosome Function Due to Heterozygous GBA1 Expression in Human iPSC-Derived Neurons

et al. 2020

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Section: Gba1 Heterozygous-null Neurons Accumulate Soluble and Insolusupporting

confidence: 73%

LRRK2 Kinase Inhibition Rescues Deficits in Lysosome Function Due to Heterozygous GBA1 Expression in Human iPSC-Derived Neurons

et al. 2020

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“…Neuroinflammation has been shown to commence early in PD, peaking in moderately affected individuals, this fits with our data on PD Braak 3-4 subjects [40]. CSF and plasma DHA derived resolvin D1 (RvD1) are reduced in patients with earlyonset PD [41], suggesting that inflammation resolution processes could be dysfunctional. We find the picture is complex, as should be expected, with both anti-and pro-inflammatory processes activated simultaneously to tune a potentially compensatory response to disease.…”

Section: Discussionsupporting

confidence: 89%

Sex specific inflammatory profiles of cerebellar mitochondria are attenuated in Parkinson’s disease

Ingram

Shephard

Sarmad

et al. 2020

Aging

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Response to inflammation is a key determinant in many diseases and their outcomes. Diseases that commonly affect older people are frequently associated with altered inflammatory processes. Neuroinflammation has been described in Parkinson's disease (PD) brain. PD is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and at the sub-cellular level, mitochondrial dysfunction is a key feature. However, there is evidence that a different region of the brain, the cerebellum, is involved in the pathophysiology of PD. We report relative levels of 40 pro-and anti-inflammatory cytokines measured in PD and control cerebellar mitochondria. These data were obtained by screening cytokine antibody arrays. In parallel, we present concentrations of 29 oxylipins and 4 endocannabinoids measured in mitochondrial fractions isolated from post-mortem PD cerebellum with age and sex matched controls. Our oxylipin and endocannabinoid data were acquired via quantitation by LC-ESI-MS/MS. The separate sample sets both show there are clearly different inflammatory profiles between the sexes in control samples. Sex specific profiles were not maintained in cerebellar mitochondria isolated from PD brains.

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“…In addition, SPMs enhance the macrophage efferocytosis of apoptotic neutrophils and cellular debris, which is the hallmark of the resolution of inflammation [ 9 ]. SPMs have shown their therapeutic effectiveness in pre-clinical models of acute and chronic inflammation, including atherosclerosis [ 8 , 10 ], neuroinflammatory diseases [ 11 , 12 , 13 ], cystic fibrosis [ 14 ], arthritis [ 15 ], ocular disease [ 16 ], liver disease [ 17 , 18 ], ischemia ( Figure 1 A) [ 19 , 20 , 21 , 22 ], asthma ( Figure 1 B) [ 23 , 24 , 25 ], infections ( Figure 1 C,D) [ 26 , 27 , 28 ], and cancer [ 29 , 30 , 31 ]. SPMs also regulate mechanisms involved in organ protection, wound healing, and tissue repair and regeneration, and they increase the host’s defense [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Is Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer

Babar,

Nassar,

Nie

et al. 2024

Metabolites

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Acute inflammation is the body’s first defense in response to pathogens or injury that is partially governed by a novel genus of endogenous lipid mediators that orchestrate the resolution of inflammation, coined specialized pro-resolving mediators (SPMs). SPMs, derived from omega-3-polyunstaturated fatty acids (PUFAs), include the eicosapentaenoic acid-derived and docosahexaenoic acid-derived Resolvins, Protectins, and Maresins. Herein, we review their biosynthesis, structural characteristics, and therapeutic effectiveness in various diseases such as ischemia, viral infections, periodontitis, neuroinflammatory diseases, cystic fibrosis, lung inflammation, herpes virus, and cancer, especially focusing on therapeutic effectiveness in respiratory inflammation and ischemia-related injuries. Resolvins are sub-nanomolar potent agonists that accelerate the resolution of inflammation by reducing excessive neutrophil infiltration, stimulating macrophage functions including phagocytosis, efferocytosis, and tissue repair. In addition to regulating neutrophils and macrophages, Resolvins control dendritic cell migration and T cell responses, and they also reduce the pro-inflammatory cytokines, proliferation, and metastasis of cancer cells. Importantly, several lines of evidence have demonstrated that Resolvins reduce tumor progression in melanoma, oral squamous cell carcinoma, lung cancer, and liver cancer. In addition, Resolvins enhance tumor cell debris clearance by macrophages in the tumor’s microenvironment. Resolvins, with their unique stereochemical structure, receptors, and biosynthetic pathways, provide a novel therapeutical approach to activating resolution mechanisms during cancer progression.

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Author Correction: Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 11 publications

References 0 publications

LRRK2 Kinase Inhibition Rescues Deficits in Lysosome Function Due to Heterozygous GBA1 Expression in Human iPSC-Derived Neurons

LRRK2 Kinase Inhibition Rescues Deficits in Lysosome Function Due to Heterozygous GBA1 Expression in Human iPSC-Derived Neurons

Sex specific inflammatory profiles of cerebellar mitochondria are attenuated in Parkinson’s disease

Is Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer

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