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Your search keyword '"Corrado, Marcella"' showing total 15 results
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15 results on '"Corrado, Marcella"'

14. RNA silencing of the mitochondrial ABCB7 transporter in HeLa cells causes an iron-deficient phenotype with mitochondrial iron overload

Author

Cavadini, Patrizia, Biasiotto, Giorgio, Poli, Maura, Levi, Sonia, Verardi, Rosanna, Zanella, Isabella, Derosas, Manuela, Ingrassia, Rosaria, Corrado, Marcella, and Arosio, Paolo

Abstract

X-linked sideroblastic anemia with ataxia (XLSA/A) is caused by defects of the transporter ABCB7 and is characterized by mitochondrial iron deposition and excess of protoporphyrin in erythroid cells. We describe ABCB7 silencing in HeLa cells by performing sequential transfections with siRNAs. The phenotype of the ABCB7-deficient cells was characterized by a strong reduction in proliferation rate that was not rescued by iron supplementation, by evident signs of iron deficiency, and by a large approximately 6-fold increase of iron accumulation in the mitochondria that was poorly available to mitochondrial ferritin. The cells showed an increase of protoporphyrin IX, a higher sensitivity to H2O2 toxicity, and a reduced activity of mitochondrial superoxide dismutase 2 (SOD2), while the activity of mitochondrial enzymes, such as citrate synthase or succinate dehydrogenase, and ATP content were not decreased. In contrast, aconitase activity, particularly that of the cytosolic, IRP1 form, was reduced. The results support the hypothesis that ABCB7 is involved in the transfer of iron from mitochondria to cytosol, and in the maturation of cytosolic Fe/S enzymes. In addition, the results indicate that anemia in XLSA/A is caused by the accumulation of iron in a form that is not readily usable for heme synthesis.

Published
2007
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15. Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21 Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis.

Author

Jian Wang, Devgan, Vikram, Corrado, Marcella, Prabhu, Nita S., El-Deiry, Wafik S., Riccardi, Carlo, Pandolfi, Pier Paolo, Missero, Caterina, and Dotto, G. Paolo

Subjects
*GLUCOCORTICOIDS, *TRIAMCINOLONE, *ADRENOCORTICAL hormones, *TUMOR necrosis factors, *GLYCOPROTEINS, *GROWTH factors, *MESSENGER RNA, *KERATINOCYTES, *APOPTOSIS
Abstract

Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21Cip1/WAF1, independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Published
2005
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