NDLI: Programmed cell death of stressed keratinocytes and its inhibition by vitamin D: The role of death and survival signaling pathways

Content Provider	Springer Nature Link
Author	Diker Cohen, T. Koren, R. Ravid, A.
Copyright Year	2006
Abstract	The epidermis is confronted with multiple environmental and pathophysiological stresses. This study shows that TNFα, oxidative stress, hyperosmotic and heat shock induced both caspase-dependent and independent cell death in human HaCaT keratinocytes. The hormonal form of vitamin D, 1,25(OH)2D3, which is an autocrine hormone in the epidermis, protected the cells from all the examined stresses and pathways leading to cell death. We aimed to define the signaling pathways that determine the life-death balance of stressed keratinocytes and participate in their protection by 1,25(OH)2D3. As assessed by employing specific inhibitors, the survival pathways mediated by the EGF receptor, ERK, PI-3K or Src kinase, or basal transcriptional activity are important for unstressed cell survival. However, only the EGF receptor, PI-3K and the Src kinase pathways mediate the survival of stressed cells in a stimulus-specific manner. Inhibition of the p38 and/or the JNK death pathways reduced caspase activation induced by oxidative stress, hyperosmotic shock and TNFα. The protective effect of 1,25(OH)2D3 was not mediated by the examined survival pathways. 1,25(OH)2D3 inhibited the stress-induced activation of p38 and JNK. Since mimicking this effect by pharmacological inhibition resulted in the attenuation of caspase activation, we infer that these pathways are involved in keratinocyte protection by 1,25(OH)2D3.
Starting Page	519
Ending Page	534
Page Count	16
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	11
Issue Number	4
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2006-03-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	apoptosis c-Jun N-terminal kinase keratinocytes p38 MAPK stress vitamin D Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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