scholarly journals Immobilization of Glycogen Synthase Kinase-3β Inhibitor on 316L Stainless Steel via Polydopamine to Accelerate Endothelialization

2021 ◽  
Vol 9 ◽  
Author(s):  
Ming Zhang ◽  
Xudong Shi ◽  
Hai Sun ◽  
Donghua Xu ◽  
Yang Gao ◽  
...  
Keyword(s):  
Stainless Steel ◽  
316L Stainless Steel ◽  
Glycogen Synthase ◽  
Bioactive Molecules ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3Β ◽  
Human Coronary Artery ◽  
Water Contact ◽  
Widespread Application ◽  
Vascular Stents

The coverage of stents with healthy endothelium is crucial to the success of cardiovascular stent implantation. Immobilizing bioactive molecules on stents is an effective strategy to generate such stents. Glycogen synthase kinase-3β inhibitor (GSKi) is a bioactive molecule that can effectively accelerate vascular endothelialization. In this work, GSKi was covalently conjugated on 316L stainless steel through polydopamine to develop a stable bioactive surface. Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) and water contact angle results revealed the successful introduction of GSKi onto 316L stainless steel. The GSKi coating did not obviously affect the hemocompatibility of plates. The adhesion and proliferation of human coronary artery endothelial cells (HCAECs) on stainless steel was significantly promoted by the addition of GSKi. In summary, this work provides a universal and stable strategy of immobilizing GSKi on the stent surface. This method has the potential for widespread application in the modification of vascular stents.

Is Going for Cure in CML Targeting Aberrant Glycogen Synthase Kinase 3β?

2017 ◽  
Vol 18 (4) ◽  
pp. 396-404
Author(s):  
Concetta Saponaro ◽  
Michele Maffia ◽  
Nicola Renzo ◽  
Addolorata Coluccia
Keyword(s):  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3Β

scholarly journals Association of glycogen synthase kinase-3β with Parkinson’s disease (Review)

2014 ◽  
Vol 9 (6) ◽  
pp. 2043-2050 ◽  
Author(s):  
DA-WEI LI ◽  
ZHI-QIANG LIU ◽  
WEI-CHEN ◽  
MIN-YAO ◽  
GUANG-REN LI
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3Β

scholarly journals Melatonin Induces Melanogenesis in Human SK-MEL-1 Melanoma Cells Involving Glycogen Synthase Kinase-3 and Reactive Oxygen Species

2020 ◽  
Vol 21 (14) ◽  
pp. 4970
Author(s):  
Juan Perdomo ◽  
Carlos Quintana ◽  
Ignacio González ◽  
Inmaculada Hernández ◽  
Sara Rubio ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Glycogen Synthase ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Glycogen Synthase Kinase ◽  
Oxygen Species ◽  
Glycogen Synthase Kinase 3Β ◽  
Human Melanoma Cells

Melatonin is present in all living organisms where it displays a diversity of physiological functions. Attenuation of melanogenesis by melatonin has been reported in some mammals and also in rodent melanoma cells. However, melatonin may also stimulate melanogenesis in human melanoma cells through mechanisms that have not yet been revealed. Using the human melanoma cells SK-MEL-1 as a model, an increase in both tyrosinase activity and melanin was already observed at 24 h after melatonin treatment with maximal levels of both being detected at 72 h. This effect was associated with the induction in the expression of the enzymes involved in the synthesis of melanin. In this scenario, glycogen synthase kinase-3β seems to play a significant function since melatonin decreased its phosphorylation and preincubation with specific inhibitors of this protein kinase (lithium or BIO) reduced the expression and activity of tyrosinase. Blocking of PI3K/AKT pathway stimulated melanogenesis and the effect was suppressed by the inhibitors of glycogen synthase kinase-3β. Although melatonin is a recognized antioxidant, we found that it stimulates reactive oxygen species generation in SK-MEL-1 cells. These chemical species seem to be an important signal in activating the melanogenic process since the antioxidants N-acetyl-l-cysteine and glutathione decreased both the level and activity of tyrosinase stimulated by melatonin. Our results support the view that regulation of melanogenesis involves a cross-talk between several signaling pathways.

Lithium Pharmacology and a Potential Role of Lithium on Methamphetamine Abuse and Dependence

2019 ◽  
Vol 11 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Nobue Kitanaka ◽  
Frank Scott Hall ◽  
George Richard Uhl ◽  
Junichi Kitanaka
Keyword(s):  
Molecular Mechanisms ◽  
Behavioral Sensitization ◽  
Tryptophan Hydroxylase ◽  
Glycogen Synthase ◽  
Lithium Treatment ◽  
Glycogen Synthase Kinase ◽  
Therapeutic Effects ◽  
Potential Candidate ◽  
Glycogen Synthase Kinase 3Β ◽  
Methamphetamine Abuse

Background:The effectiveness of lithium salts in neuropsychiatric disorders such as bipolar disorder, Alzheimer’s disease, and treatment-resistant depression has been documented in an extensive scientific literature. Lithium inhibits inositol monophosphatase, inositol polyphosphate 1- phosphatase, and glycogen synthase kinase-3 and decreases expression level of tryptophan hydroxylase 2, conceivably underlying the mood stabilizing effects of lithium, as well as procognitive and neuroprotective effects. However, the exact molecular mechanisms of action of lithium on mood stabilizing and pro-cognitive effects in humans are still largely unknown.Objective:On the basis of the known aspects of lithium pharmacology, this review will discuss the possible mechanisms underlying the therapeutic effects of lithium on positive symptoms of methamphetamine abuse and dependence.Conclusion:It is possible that lithium treatment reduces the amount of newly synthesized phosphatidylinositol, potentially preventing or reversing neuroadaptations contributing to behavioral sensitization induced by methamphetamine. In addition, it is suggested that exposure to repeated doses of methamphetamine induces hyperactivation of glycogen synthase kinase-3β in the nucleus accumbens and in dorsal hippocampus, resulting in a long-term alterations in synaptic plasticity underlying behavioral sensitization as well as other behavioral deficits in memory-related behavior. Therefore it is clear that glycogen synthase kinase-3β inhibitors can be considered as a potential candidate for the treatment of methamphetamine abuse and dependence.

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