Characterization of the Oxidative Stress Initiated In Cultured Human Keratinocytes by Treatment with Peroxides

Vessey, Donald A.; Lee, Kyung-Hee.; Blacker, Kerry L.

doi:10.1111/1523-1747.ep12614831

Cited by 64 publications

(47 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Consequently, exposure of normal keratinocytes to 700 µM H 2 O 2 for more than one hour leads to irreversible toxicity. 32 We demonstrated the induction of psoriasin and calgranulin-B by 1 hour treatment with 75µM H 2 O 2 , but we have not observed any induction after longer treatment periods. This may indicate an association between psoriasin induction and apoptosis-inducing doses of H 2 O 2 , which is further supported by the increased survival of the psoriasin overexpressing MCF10A cells.…”

Section: Discussionmentioning

confidence: 50%

Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants

Carlsson¹,

Yhr²,

Petersson³

et al. 2005

Cancer Biology & Therapy

View full text Add to dashboard Cite

ABBREVIATIONSDCIS ductal carcinoma in situ ROS reactive oxygen species HEKn human epidermal keratinocytes neonatal NAC N-Acetyl-cysteine NFκB nuclear factor-κB PI3K phosphatidylinositol 3-kinase Research PaperPsoriasin (S100A7) and Calgranulin-B (S100A9) Induction is Dependent on Reactive Oxygen Species and is Downregulated by Bcl-2 and Antioxidants ABSTRACT S-100 proteins are calcium-binding proteins with important growth regulatory functions. Of these proteins, psoriasin and calgranulin-B have been shown to be highly upregulated in ductal carcinoma in situ (DCIS) of the breast and in psoriasis. The purpose of this study was to further elucidate the functional relevance of the overexpression of these two S-100 proteins in psoriasis and DCIS. We report the induction of both proteins by reactive oxygen species, phorbol ester TPA, and the induction of psoriasin in response to the PI3K inhibitor wortmannin. We also demonstrate that Bcl-2 overexpression represses the induction of psoriasin and calgranulin-B under these different conditions. The same effect was obtained with the antioxidant NAC, which indicates that the suppression of psoriasin and calgranulin-B induction is mediated by the antioxidant function of Bcl-2. Furthermore, we demonstrate that overexpression of a dominant negative IKKβ also inhibits the induction of psoriasin suggesting that the NFκB pathway is involved in the induction of this protein. Also, we found NFκB responsive DNA elements in the upstream promoter region of psoriasin. MCF10A cells with a stable retroviral overexpression of psoriasin were significantly more resistant to H 2 O 2 -induced cell death than control cells further supporting the hypothesis that these S-100 proteins may play a role in oxidative stress response.

show abstract

Section: Discussionmentioning

confidence: 50%

Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants

Carlsson¹,

Yhr²,

Petersson³

et al. 2005

Cancer Biology & Therapy

View full text Add to dashboard Cite

show abstract

“…For example, in cultured human keratinocytes, H 2 O 2 in the dose range of 200 to 700 μM was used to induce oxidative stress; as a result, half of the cells became permeable to trypan blue at 700 μM H 2 O 2 dose by 60 min [22]. In our studies with human neurons, we found that a significantly lower dose of H 2 O 2 (10 μM) caused 64% cell mortality.…”

Section: Discussionmentioning

confidence: 57%

Superoxide Dismutase-Loaded PLGA Nanoparticles Protect Cultured Human Neurons Under Oxidative Stress

Reddy

Kou

et al. 2008

Appl Biochem Biotechnol

129

View full text Add to dashboard Cite

The objective of the present study was to investigate the neuroprotective efficacy of superoxide dismutase (SOD), loaded in poly(D,L-lactide co-glycolide) (PLGA) nanoparticles (NPs), in cultured human neurons challenged with hydrogen peroxide (H 2 O 2 )-induced oxidative stress. We hypothesized that the protected and sustained intracellular delivery of SOD encapsulated in NPs would demonstrate better neuroprotection from oxidative stress than either with SOD or pegylated SOD (PEG-SOD) in solution. SOD-NPs (~81 ± 4 nm in diameter, 0.9% w/w SOD loading) released the encapsulated SOD in an active form in vitro, with 8.2% cumulative release during the first 24 hrs, followed by a slower release thereafter. The results demonstrated that PLGA-NPs are compatible with human neurons and the neuroprotective effect of SOD-NPs is dose-dependent, with efficacy seen at >100 U SOD, with less significant effects at lower doses. Neither SOD (25-200 U) nor PEG-SOD (100 U) in solution demonstrated the neuroprotective effect under similar conditions. The neuroprotective effect of SOD-NPs was seen up to 6 hrs following H 2 O 2 -induced oxidative stress, but the effect diminished thereafter. Confocal microscopic studies demonstrated better intracellular neuronal uptake of the encapsulated model protein (FITC-labeled BSA) than the protein in solution. Thus, the mechanism of efficacy of SOD-NPs appears to be due to the stability of the encapsulated enzyme and its better neuronal uptake following encapsulation.

show abstract

“…The observations, in the large NHS type 1 diabetic cohort, that plasma methylglyoxal levels rise as GAPDH declines, support a role for this enzyme in determining methylglyoxal levels. The reasons for the decrease in GAPDH activity is less clear, but it is well known that the activity of this enzyme is susceptible to a number of metabolic perturbations associated with diabetes, including oxidative stress (30), direct glycation (31,32), and altered redox state with reduced levels of NAD ϩ (33,34). Not precluded is the possibility that variable susceptibility of GAPDH to such modifications or inherent differences in GAPDH per se could be secondary to genetic factors linked to nephropathy risk (35).…”

Section: Discussionmentioning

confidence: 99%

“…The relationship between increased oxidative stress and increased methylglyoxal production is not clear. One possibility is that increased oxidative stress leads to a direct alteration of GAPDH, resulting in decreased GAPDH activity and increased methylglyoxal production (30,42). Concurrent increases in dicarbonyl and oxidative stress, associated with decreased GAPDH activity in the NHS cohort, is also consistent with Brownlee's (43) proposed unifying hypothesis of diabetes complications, although our observations more specifically support a role for these mechanisms in the pathogenesis of diabetic nephropathy in human diabetic populations.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to Diabetic Nephropathy Is Related to Dicarbonyl and Oxidative Stress

et al. 2005

View full text Add to dashboard Cite

Dicarbonyl and oxidative stress may play important roles in the development of diabetes complications, and their response to hyperglycemia could determine individual susceptibility to diabetic nephropathy. This study examines the relationship of methylglyoxal, 3-deoxyglucosone (3DG), and oxidative stress levels to diabetic nephropathy risk in three populations with diabetes. All subjects in the Overt Nephropathy Progressor/Nonprogressor (ONPN) cohort (n ‫؍‬ 14), the Natural History of Diabetic Nephropathy study (NHS) cohort (n ‫؍‬ 110), and the Pima Indian cohort (n ‫؍‬ 45) were evaluated for clinical nephropathy, while renal structural measures of fractional mesangial volume [Vv(Mes/glom)] and glomerular basement membrane (GBM) width were determined by electron microscopy morphometry in the NHS and Pima Indian cohorts. Methylglyoxal and 3DG levels reflected dicarbonyl stress, while reduced glutathione (GSH) and urine 8-isoprostane (8-IP) measured oxidative stress. Cross-sectional measures of methylglyoxal production by red blood cells incubated in 30 mmol/l glucose were increased in nephropathy progressors relative to nonprogressors in the ONPN (P ‫؍‬ 0.027) and also reflected 5-year GBM thickening in the NHS cohort (P ‫؍‬ 0.04). As nephropathy progressed in the NHS cohort, in vivo levels of methylglyoxal (P ‫؍‬ 0.036), 3DG (P ‫؍‬ 0.004), and oxidative stress (8-IP, P ‫؍‬ 0.007 and GSH, P ‫؍‬ 0.005) were seen, while increased methylglyoxal levels occurred as nephropathy progressed (P ‫؍‬ 0.0016) in the type 2 Pima Indian cohort. Decreased glyceraldehyde-3-phosphate dehydrogenase activity also correlated with increased methylglyoxal levels (P ‫؍‬ 0.003) in the NHS cohort. In conclusion, progression of diabetic nephropathy is significantly related to elevated dicarbonyl stress and possibly related to oxidative stress in three separate populations, suggesting that these factors play a role in determining individual susceptibility. Diabetes 54:3274 -3281, 2005

show abstract

Characterization of the Oxidative Stress Initiated In Cultured Human Keratinocytes by Treatment with Peroxides

Cited by 64 publications

References 23 publications

Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants

Psoriasin (S100A7) and calgranulin-B (S100A9) induction is dependent on reactive oxygen species and is downregulated by Bcl-2 and antioxidants

Superoxide Dismutase-Loaded PLGA Nanoparticles Protect Cultured Human Neurons Under Oxidative Stress

Susceptibility to Diabetic Nephropathy Is Related to Dicarbonyl and Oxidative Stress

Contact Info

Product

Resources

About