Vascular endothelial growth factor (VEGF), tissue inhibitors of metalloproteinase-1 (TIMP-1) and nail fold capillaroscopy changes in children and adolescents with Gaucher disease; relation to residual disease severity

Salah, Nouran Yousef

doi:10.1016/j.cyto.2020.155120

Cited by 2 publications

(3 citation statements)

References 31 publications

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“…This elevation could be explained by neuroinflammation and oxidative stress which were the key secondary injury mechanisms triggered by TBI. A lot of studies on Gaucher disease and Fabry disease , have demonstrated that neuroinflammation and oxidative stress would cause glycosphingolipids storage disorders, resulting in the progressive accumulation of glucosylceramides in lysosomes of cells of the monocyte/macrophage lineage. Similarly, in other studies it was found that administration of CBs has been shown to reduce the inflammatory response in several mouse models of autoimmune disease, , which also proved the association of CBs with inflammation.…”

Section: Resultsmentioning

confidence: 99%

Quantitative Mass Spectrometry Imaging of Metabolomes and Lipidomes for Tracking Changes and Therapeutic Response in Traumatic Brain Injury Surrounding Injured Area at Chronic Phase

et al. 2021

ACS Chem. Neurosci.

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Traumatic brain injury (TBI) is a complex disease process that may contribute to temporary or permanent disability. Tracking spatial changes of lipids and metabolites in the brain helps unveil the underlying mechanisms of the disease procession and therapeutic response. Here, the liquid microjunction surface sampling technique was used for mass spectrometry imaging of both lipids and metabolites in rat models of controlled cortical impact with and without XueFu ZhuYu decoction treatment, and the work was focused on the diffuse changes outside the injured area at chronic phase (14 days after injury). Quantitative information was provided for phosphotidylcholines and cerebrosides by adding internal standards in the sampling solvent. With principal component analysis for the imaging data, the midbrain was found to be the region with the largest diffuse changes following TBI outside the injured area. In detail, several phosphatidylcholines, phosphatidylethanolamines, phosphatidic acids, and diacylglycerols were found to be significantly up-regulated particularly in midbrain and thalamus after TBI and XFZY treatment. It is associated with the reported "self-repair" mechanisms at the chronic phase of TBI activated by neuroinflammation. Several glycosphingolipids were found to be increased in most of brain regions after TBI, which was inferred to be associated with neuroinflammation and oxidative stress triggered by TBI. Moreover, different classes of small matabolites were significantly changed after TBI, including fatty acids, amino acids, and purines. All these compounds were involved in 10 metabolic pathway networks, and 6 target proteins of XFZY were found related to the impacted pathways. These results shed light on the molecular mechanisms of TBI pathologic processes and therapeutic response.

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Section: Resultsmentioning

confidence: 99%

Quantitative Mass Spectrometry Imaging of Metabolomes and Lipidomes for Tracking Changes and Therapeutic Response in Traumatic Brain Injury Surrounding Injured Area at Chronic Phase

et al. 2021

ACS Chem. Neurosci.

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“…The association with the biological activity of YKL-40 and the regulation of cell proliferation, activation, migration and adhesion was previously investigated [16]. Although increased serum YKL-40 and VEGF in many diseases have been demonstrated [17][18][19][20][21], very few studies have investigated YKL-40, especially with regard to the correlation of YKL-40 and VEGF in patients with wet AMD. Herein, serum YKL-40 levels were significantly elevated in patients with wet AMD and positively correlated with VEGF expression, implying the involvement of YKL-40 in the pathological process of wet AMD.…”

Section: Discussionmentioning

confidence: 99%

“…The association with the biological activity of YKL‐40 and the regulation of cell proliferation, activation, migration, and adhesion was previously investigated [ 16 ]. Although increased serum YKL‐40 and VEGF in many diseases have been demonstrated [ 17 , 18 , 19 , 20 , 21 ], very few studies have investigated YKL‐40, especially with regard to the correlation of YKL‐40 and VEGF in patients with wet AMD.…”

Section: Discussionmentioning

confidence: 99%

Elevated YKL‐40 serum levels may contribute to wet age‐related macular degeneration via the ERK1/2 pathway

et al. 2021

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Vascular endothelial growth factor (VEGF), tissue inhibitors of metalloproteinase-1 (TIMP-1) and nail fold capillaroscopy changes in children and adolescents with Gaucher disease; relation to residual disease severity

Cited by 2 publications

References 31 publications

Quantitative Mass Spectrometry Imaging of Metabolomes and Lipidomes for Tracking Changes and Therapeutic Response in Traumatic Brain Injury Surrounding Injured Area at Chronic Phase

Quantitative Mass Spectrometry Imaging of Metabolomes and Lipidomes for Tracking Changes and Therapeutic Response in Traumatic Brain Injury Surrounding Injured Area at Chronic Phase

Elevated YKL‐40 serum levels may contribute to wet age‐related macular degeneration via the ERK1/2 pathway

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