Vitamin D protects keratinocytes from deleterious effects of ionizing radiation

The British Journal of Dermatology
M LangbergA Ravid

Abstract

Radiotherapy can induce severe skin responses that may limit the clinically acceptable radiation dose. The responses include erythema, dry and moist desquamation, erosions and dermal-epidermal blister formation. These effects reflect injury to, and reproductive failure of, epidermal cells and may also be due to dysregulation of the tissue remodelling process caused by excessive proteolytic activity. Calcitriol, the hormonally active vitamin D metabolite, protects keratinocytes from programmed cell death induced by various noxious stimuli. To examine whether calcitriol protects proliferating keratinocytes from the damage inflicted by ionizing radiation under conditions similar to those employed during radiotherapy. Autonomously proliferating HaCaT keratinocytes, used as a model for basal layer keratinocytes, were irradiated using a linear accelerator. Cell death was monitored by vital staining, executioner caspase activation, lactic dehydrogenase release and colony formation assay. Induction of matrix metalloproteinase-9 was assessed by gelatinase activity assay and mRNA determination. Levels of specific proteins were determined by immunoblotting. Treatment with calcitriol inhibited both caspase-dependent and -independent progra...Continue Reading

References

May 1, 1993·Carcinogenesis·T A LehmanE M Rogan
Oct 9, 1998·The Journal of Investigative Dermatology·M B SchilliA Menrad
Feb 17, 1999·The British Journal of Dermatology·O Garach-JehoshuaR Koren
May 18, 1999·The New England Journal of Medicine·M S Blumberg
Nov 10, 2000·International Journal of Cancer. Journal International Du Cancer·V PatelW A Yeudall
Dec 15, 2000·International Journal of Molecular Medicine·Y Herouy
Oct 12, 2001·Apoptosis : an International Journal on Programmed Cell Death·T Stiewe, B M Pützer
Jan 24, 2003·Critical Reviews in Biochemistry and Molecular Biology·Philippe E Van den SteenGhislain Opdenakker
Jun 12, 2003·International Journal of Cancer. Journal International Du Cancer·Gregory E WeitsmanRuth Koren
Mar 23, 2004·Annals of the New York Academy of Sciences·Talia Diker-CohenAmiram Ravid
Oct 28, 2004·Experimental Dermatology·Bodo LehmannJörg Reichrath
Jun 10, 2005·The EMBO Journal·Olav GressnerMartina Müller
Dec 1, 2005·Life Sciences·Bahar BaltalarliGülçin Abban
Mar 15, 2006·Apoptosis : an International Journal on Programmed Cell Death·T Diker-CohenA Ravid
Apr 8, 2006·Cell Death and Differentiation·F Murray-ZmijewskiJ-C Bourdon
Apr 19, 2006·Cancer Research·Golnar AfsharDaphne A Haas-Kogan
Jul 26, 2006·International Journal of Oncology·Jer-Yen YangMickey C-T Hu
Aug 8, 2006·The Journal of Steroid Biochemistry and Molecular Biology·Ruth KorenAmiram Ravid

❮ Previous
Next ❯

Citations

Aug 19, 2015·Journal of Cellular Physiology·Amiram RavidRuth Koren
Sep 18, 2010·The British Journal of Dermatology·T ZeeliA Ravid
Feb 9, 2010·Dermatologic Therapy·Jeremiah Miller, Richard L Gallo
Jul 12, 2011·Toxicology in Vitro : an International Journal Published in Association with BIBRA·Haijun YangYuxin Zheng
Jul 7, 2015·Indian Journal of Dermatology, Venereology and Leprology·Bhawna WadhwaVijay Kumar Garg
Jun 5, 2012·Peptides·Fabiano Pinheiro da Silva, Marcel Cerqueira César Machado
May 19, 2012·Expert Review of Anticancer Therapy·Paulina SzyszkaAndrzej T Slominski
Apr 26, 2020·International Journal of Environmental Research and Public Health·W S KwanK N Yu
Dec 8, 2010·Expert Review of Anti-infective Therapy·Jim Bartley
Jun 27, 2017·NPJ Breast Cancer·Nicola J NasserEyal Fenig
Aug 23, 2020·International Journal of Molecular Sciences·Jarosław NuszkiewiczKarolina Szewczyk-Golec
Sep 11, 2020·International Journal of Radiation Biology·Andrea L DiCarloDavid R Cassatt

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptotic Caspases

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis