Subphysiological concentrations of extracellular calcium sensitize normal human keratinocytes to UVB-induced apoptosis

1999 ◽  
Vol 291 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Manish G. Kumar ◽  
Steven A. Hurwitz ◽  
Jenny Cotton ◽  
Dan F. Spandau
Keyword(s):  
Human Keratinocytes ◽  
Extracellular Calcium ◽  
Normal Human Keratinocytes ◽  
Normal Human ◽  
Induced Apoptosis

scholarly journals UVB-mediated activation of p38 mitogen-activated protein kinase enhances resistance of normal human keratinocytes to apoptosis by stabilizing cytoplasmic p53

2002 ◽  
Vol 365 (1) ◽  
pp. 133-145 ◽  
Author(s):  
Nadine CHOUINARD ◽  
Kristoffer VALERIE ◽  
Mahmoud ROUABHIA ◽  
Jacques HUOT
Keyword(s):  
Adaptive Response ◽  
Human Keratinocytes ◽  
Dominant Negative ◽  
Mitogen Activated Protein Kinase ◽  
Dominant Negative Mutant ◽  
Normal Human Keratinocytes ◽  
Mitogen Activated Protein ◽  
Normal Human ◽  
Induced Apoptosis ◽  
Negative Mutant

Human keratinocytes respond to UV rays by developing a fast adaptive response that contributes to maintaining their functions and survival. We investigated the role of the mitogen-activated protein kinase pathways in transducing the UV signals in normal human keratinocytes. We found that UVA, UVB or UVC induced a marked and persistent activation of p38, whereas c-Jun N-terminal kinase or extracellular signal-regulated kinase were less or not activated respectively. Inhibition of p38 activity by expression of a dominant-negative mutant of p38 or with SB203580 impaired cell viability and led to an increase in UVB-induced apoptosis. This sensitization to apoptosis was independent of caspase activities. Inhibition of p38 did not sensitize transformed HaCaT keratinocytes to UVB-induced apoptosis. In normal keratinocytes, expression of a dominant-negative mutant of p53 increased UVB-induced cell death, pointing to a role for p53. In these cells, UVB triggered a p38-dependent phosphorylation of p53 on Ser-15. This phosphorylation was associated with an SB203580-sensitive accumulation of p53, even in the presence of a serine phosphatase inhibitor. Accumulated p53 was localized mainly in the cytoplasm, independently of CRM1 nuclear export. In HaCaT cells, p53 was localized exclusively in the nucleus and its distribution and level were not affected by UVB or p38 inhibition. However, UVB induced an SB203580-insensitive phosphorylation on Ser-15 of mutated p53. Overall, our results suggest that, in normal human keratinocytes, protection against UVB depends on p38-mediated phosphorylation and stabilization of p53 and is tightly associated with the cytoplasmic sequestration of wild-type p53. We conclude that the p38/p53 pathway plays a key role in the adaptive response of normal human keratinocytes against UV stress.

Effects of extracellular calcium on the growth-differentiation switch in immortalized keratinocyte HaCaT cells compared with normal human keratinocytes

2009 ◽  
Vol 18 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Ludovic Micallef ◽  
Françoise Belaubre ◽  
Aline Pinon ◽  
Chantal Jayat-Vignoles ◽  
Christiane Delage ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Extracellular Calcium ◽  
Hacat Cells ◽  
Normal Human Keratinocytes ◽  
Normal Human

scholarly journals Resveratrol enhances apoptosis induced by the heterocyclic aromatic amines in p53-wt LoVo cells, but not in p53-deficient HaCaT cells

2020 ◽  
Author(s):  
Katarzyna Kuryłowicz ◽  
Agnieszka Cierniak ◽  
Ewelina Madej ◽  
Łukasz Skalniak ◽  
Agnieszka Wolnicka-Głubisz
Keyword(s):  
Human Keratinocytes ◽  
Human Colon ◽  
Cell Types ◽  
Heterocyclic Aromatic Amines ◽  
Hacat Cells ◽  
Human Colon Cancer ◽  
Normal Human Keratinocytes ◽  
Lovo Cells ◽  
Normal Human ◽  
Induced Apoptosis

In the present study, we investigated the influence of resveratrol on PhIP treated human colon cancer cells and compared the effect to HaCaT cells considered as normal, human keratinocytes. Our results show that resveratrol decreases DNA damage in both cell types, it increases the sensitivity of LoVo cells to apoptosis and has no effect on PhIP-treated HaCaT cells. We confirm that PhIP-induced apoptosis is p53 and caspase 3/7 dependent. Interestingly, normal cells such as HaCaT, which lack functional p53 are more resistant to PhIP treatment.

scholarly journals Protective Effects of Catalase Overexpression on UVB-induced Apoptosis in Normal Human Keratinocytes

2006 ◽  
Vol 281 (26) ◽  
pp. 17999-18007 ◽  
Author(s):  
Hamid Reza Rezvani ◽  
Frédéric Mazurier ◽  
Muriel Cario-André ◽  
Catherine Pain ◽  
Cécile Ged ◽  
...  
Keyword(s):  
Human Keratinocytes ◽  
Protective Effects ◽  
Normal Human Keratinocytes ◽  
Normal Human ◽  
Induced Apoptosis
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