scholarly journals Protective effect and mechanism of rat recombinant S100 calcium‑binding protein A4 on oxidative stress injury of rat vascular endothelial cells

2018 ◽  
Author(s):  
Xiangyan Meng ◽  
Xiujie Gao ◽  
Zhiqing Zhang ◽  
Xuesi Zhou ◽  
Lei Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Calcium Binding ◽  
Vascular Endothelial Cells ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Vascular Endothelial ◽  
Stress Injury ◽  
S100 Calcium Binding Protein

scholarly journals Protective effect of Melissa officinalis extract against H2O2-induced oxidative stress in human vascular endothelial cells

2016 ◽  
Vol 11 (5) ◽  
pp. 383 ◽  
Author(s):  
Leila Safaeian ◽  
SeyyedEbrahim Sajjadi ◽  
ShaghayeghHaghjooy Javanmard ◽  
Hossein Montazeri ◽  
Fariba Samani
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Melissa Officinalis

Developmental Expression of Calcium-Binding Protein-Containing Neurons in Neocortical Transplants

1998 ◽  
Vol 7 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Jeffrey M. Rosenstein ◽  
Newton S. More ◽  
Nina Mani ◽  
Janette M. Krum
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Calcium Binding ◽  
Binding Protein ◽  
Substantial Reduction ◽  
Qualitative Change ◽  
Afferent Input ◽  
Calcium Binding Protein ◽  
Developmental Expression ◽  
Parvalbumin Neurons

The present study examined the development of calcium binding protein-containing neurons in a timed series of fetal neocortical transplants. The immunoexpression of parvalbumin and calbindin, which are subpopulations of GABAergic neurons, have been widely studied in normal development and in disease and injury states. Because of their purported resistance to oxidative injury by their ability to buffer Ca++ influx, these neurons have been particularly studied following ischemia. Because it is likely that oxidative stress is associated with the grafting procedure, we sought to determine if these neurons displayed enhanced survival characteristics. Normally, parvalbumin and calbindin represent about 5-10% of cortical neurons. Within 2-4 wk after grafting the expression of both proteins increased markedly in that a relatively larger number of neurons (27% for parvalbumin) were immunopositive. This increase was transitory, however, and by 4 mo and beyond, confocal microscopic data showed a reduction of over 50% of parvalbumin (+) neurons and processes. Calbindin (+) processes showed a qualitative change in that they were smaller with less terminal branching. Electron microscopy confirmed a substantial reduction in parvalbumin synaptic contacts. Interestingly, in older grafts, remaining parvalbumin neurons were those that were strongly NSE (+) suggesting a link between normal metabolism and Ca++ buffering in grafted neurons. It is possible that in early grafts certain neuronal populations transiently upregulated calcium binding proteins as a defensive mechanism against Ca++ influx associated with oxidative stress. Over time, however, following physiological normalization within grafts, the calcium binding protein (+) neurons are diminished, possibly due to lack of appropriate afferent input to the interneuronal pool.

scholarly journals Anterior Gradient Protein 3 and S100 Calcium-Binding Protein P Levels in Different Endometrial Epithelial Compartments May Play an Important Role in Recurrent Pregnancy Failure

2021 ◽  
Vol 22 (8) ◽  
pp. 3835
Author(s):  
Nicola Tempest ◽  
Elizabeth Batchelor ◽  
Christopher J. Hill ◽  
Hannan Al-Lamee ◽  
Josephine Drury ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Binding Protein ◽  
Embryo Implantation ◽  
Calcium Signalling ◽  
Premenopausal Women ◽  
Subcellular Location ◽  
Early Embryo ◽  
Calcium Binding Protein ◽  
Regulatory Function ◽  
S100 Calcium Binding Protein

Recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) are distressing conditions without effective treatments. The luminal epithelium (LE) is integral in determining receptivity of the endometrium, whereas functionalis glands and stroma aid in nurturing early embryo development. Calcium signalling pathways are known to be of vital importance to embryo implantation and pregnancy establishment, and anterior gradient protein 3 (AGR3) and S100 calcium-binding protein P (S100P) are involved with these pathways. We initially examined 20 full-thickness endometrial biopsies from premenopausal women across the menstrual cycle to characterize levels of AGR3 protein in each endometrial sub-region at the cellular level. A further 53 endometrial pipelle biopsies collected in the window of implantation were subsequently assessed to determine differential endometrial AGR3 and S100P levels relevant to RIF (n = 13) and RPL (n = 10) in comparison with parous women (n = 30) using immunohistochemistry. Significantly higher AGR3 and S100P immunostaining was observed in ciliated cells of the LE of women with recurrent reproductive failure compared with parous women, suggesting aberrant subcellular location-associated pathophysiology for these conditions. The nuclear localisation of S100P may allow transcriptional regulatory function, which is necessary for implantation of a viable pregnancy. Further work is thus warranted to assess their utility as diagnostic/therapeutic targets.

Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection

2006 ◽  
Vol 290 (5) ◽  
pp. C1399-C1410 ◽  
Author(s):  
Helena Parfenova ◽  
Shyamali Basuroy ◽  
Sujoy Bhattacharya ◽  
Dilyara Tcheranova ◽  
Yan Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Vascular Endothelium ◽  
Vascular Endothelial Cells ◽  
Glutamate Toxicity ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Apoptotic Effects ◽  
Cerebral Vascular

In cerebral circulation, epileptic seizures associated with excessive release of the excitatory neurotransmitter glutamate cause endothelial injury. Heme oxygenase (HO), which metabolizes heme to a vasodilator, carbon monoxide (CO), and antioxidants, biliverdin/bilirubin, is highly expressed in cerebral microvessels as a constitutive isoform, HO-2, whereas the inducible form, HO-1, is not detectable. Using cerebral vascular endothelial cells from newborn pigs and HO-2-knockout mice, we addressed the hypotheses that 1) glutamate induces oxidative stress-related endothelial death by apoptosis, and 2) HO-1 and HO-2 are protective against glutamate cytotoxicity. In cerebral endothelial cells, glutamate (0.1–2.0 mM) increased formation of reactive oxygen species, including superoxide radicals, and induced major keystone events of apoptosis, such as NF-κB nuclear translocation, caspase-3 activation, DNA fragmentation, and cell detachment. Glutamate-induced apoptosis was greatly exacerbated in HO-2 gene-deleted murine cerebrovascular endothelial cells and in porcine cells with pharmacologically inhibited HO-2 activity. Glutamate toxicity was prevented by superoxide dismutase, suggesting apoptotic changes are oxidative stress related. When HO-1 was pharmacologically upregulated by cobalt protoporphyrin, apoptotic effects of glutamate in cerebral endothelial cells were completely prevented. Glutamate-induced reactive oxygen species production and apoptosis were blocked by a CO-releasing compound, CORM-A1 (50 μM), and by bilirubin (1 μM), consistent with the antioxidant and cytoprotective roles of the end products of HO activity. We conclude that both HO-1 and HO-2 have anti-apoptotic effects against oxidative stress-related glutamate toxicity in cerebral vascular endothelium. Although HO-1, when induced, provides powerful protection, HO-2 is an essential endogenous anti-apoptotic factor against glutamate toxicity in the cerebral vascular endothelium.

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