Synaptotagmins in Neurodegeneration

Glavan, Gordana; Schliebs, Reinhard; Živin, Marko

doi:10.1002/ar.21026

Cited by 45 publications

(40 citation statements)

References 103 publications

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“…Synaptotagmins are transmembrane proteins with two Ca 2+ -binding C(2) domains in their cytosolic region. Syt7 regulates the exocytosis of lysosomes and thereby plays a role in bone resorption [39], cell migration [40], CTL responses [41], and neurodegeneration [42]. ITPKA phosphorylates inositol 1,4,5-trisphosphate, thereby modulating the calcium (Ca 2+ ) level within the cell and the levels of a large number of inositol polyphosphates [43].…”

Section: Discussionmentioning

confidence: 99%

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Nokhbehsaim

Eick

Nogueira

et al. 2013

Mediators of Inflammation

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Periodontitis is an inflammatory disease caused by pathogenic microorganisms and characterized by the destruction of the periodontium. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), may be a pathomechanistic link between both diseases. The aim of this in vitro study was to examine the regulation of periodontal ligament (PDL) cells by NAMPT and its production under inflammatory and infectious conditions. NAMPT caused a significant upregulation of 9 genes and downregulation of 3 genes, as analyzed by microarray analysis. Eight of these genes could be confirmed by real-time PCR: NAMPT induced a significant upregulation of EGR1, MMP-1, SYT7, ITPKA, CCL2, NTM, IGF2BP3, and NRP1. NAMPT also increased significantly the MMP-1 and CCL2 protein synthesis. NAMPT was significantly induced by interleukin-1β and the periodontal microorganism P. gingivalis. NAMPT may contribute to periodontitis through upregulation of MMP-1 and CCL2 in PDL cells. Increased NAMPT levels, as found in obesity, may therefore represent a mechanism whereby obesity could confer an increased risk of periodontitis. Furthermore, microbial and inflammatory signals may enhance the NAMPT synthesis in PDL cells and thereby contribute to the increased gingival and serum levels of this adipokine, as found in periodontitis.

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Section: Discussionmentioning

confidence: 99%

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Nokhbehsaim

Eick

Nogueira

et al. 2013

Mediators of Inflammation

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“…Synaptotagmins are involved in neuronal processes and play a role in neurodegeneration. 1 Because of the special localization of Syt1 in mouse oocytes, we analyzed the oocyte maturation process after Syt1-MO knockdown. Interestingly, compared with the control oocytes, Syt1-knockdown oocytes were arrested at the Pro-MI/ MI stage, and the PB1 failed to extrude.…”

Section: Discussionmentioning

confidence: 99%

Synaptotagmin1 is required for spindle stability and metaphase-to-anaphase transition in mouse oocytes

Zhu

Qi²,

Li³

et al. 2012

Cell Cycle

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“…We previously showed dopamine dependent plasticity of Syt 7 expression in hypersensitive striatum in animal models of Parkinson's disease [9]–[11]. Specifically, antiparkinsonian drugs induced a robust increase in striatal Syt 7 mRNA levels in 6-OHDA and reserpinized rats, two established models for Parkinson's disease, via a dopamine D1 receptor-linked mechanism [9], [10].…”

Section: Introductionmentioning

confidence: 98%

Differential Patterns of Synaptotagmin7 mRNA Expression in Rats with Kainate- and Pilocarpine-Induced Seizures

2012

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Previous studies in rat models of neurodegenerative disorders have shown disregulation of striatal synaptotagmin7 mRNA. Here we explored the expression of synaptotagmin7 mRNA in the brains of rats with seizures triggered by the glutamatergic agonist kainate (10 mg/kg) or by the muscarinic agonist pilocarpine (30 mg/kg) in LiCl (3 mEq/kg) pre-treated (24 h) rats, in a time-course experiment (30 min - 1 day). After kainate-induced seizures, synaptotagmin7 mRNA levels were transiently and uniformly increased throughout the dorsal and ventral striatum (accumbens) at 8 and 12 h, but not at 24 h, followed at 24 h by somewhat variable upregulation within different parts of the cerebral cortex, amigdala and thalamic nuclei, the hippocampus and the lateral septum. By contrast, after LiCl/pilocarpine-induced seizures, there was a more prolonged increase of striatal Synaptotagmin7 mRNA levels (at 8, 12 and 24 h), but only in the ventromedial striatum, while in some other of the aforementioned brain regions there was a decline to below the basal levels. After systemic post-treatment with muscarinic antagonist scopolamine in a dose of 2 mg/kg the seizures were either extinguished or attenuated. In scopolamine post-treated animals with extinguished seizures the striatal synaptotagmin7 mRNA levels (at 12 h after the onset of seizures) were not different from the levels in control animals without seizures, while in rats with attenuated seizures, the upregulation closely resembled kainate seizures-like pattern of striatal upregulation. In the dose of 1 mg/kg, scopolamine did not significantly affect the progression of pilocarpine-induced seizures or pilocarpine seizures-like pattern of striatal upregulation of synaptotagmin7 mRNA. In control experiments, equivalent doses of scopolamine per se did not affect the expression of synaptotagmin7 mRNA. We conclude that here described differential time course and pattern of synaptotagmin7 mRNA expression imply regional differences of pathophysiological brain activation and plasticity in these two models of seizures.

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Synaptotagmins in Neurodegeneration

Cited by 45 publications

References 103 publications

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Stimulation of MMP-1 and CCL2 by NAMPT in PDL Cells

Synaptotagmin1 is required for spindle stability and metaphase-to-anaphase transition in mouse oocytes

Differential Patterns of Synaptotagmin7 mRNA Expression in Rats with Kainate- and Pilocarpine-Induced Seizures

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