Document Detail


Antiproliferative effects of lactic acid via the induction of apoptosis and cell cycle arrest in a human keratinocyte cell line (HaCaT).
MedLine Citation:
PMID:  19339159     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Alpha-hydroxy acids (AHAs) have been widely used in cosmetic industry. However, knowledge on cytotoxicity of AHAs in human keratinocytes is limited. OBJECTIVE: Lactic acid (LA) is one of the most commonly used AHAs in skin care and peeling formulations. We investigated the antiproliferative effects of LA in a human keratinocyte cell line (HaCaT). METHODS: HaCaT cells were treated with LA at 7.5 approximately 17.5mM for various time periods. The molecular mechanisms of anti-proliferation through cell cycle arrest and apoptosis were investigated by 4,6-diamidino-2-phenylindole dihydrochloride (DAPI) stain, flow cytometry, Western blot and confocal microscopy. RESULTS: Viability of HaCaT cells decreased on exposure to LA. Flow cytometry showed apoptosis was closely related to the increase of reactive oxygen species (ROS) and calcium release, and to the decline of mitochondrial membrane potential (MMP). Western blotting showed an increase in the levels of P21, P27 and a decrease in the levels of Cyclin E, Cyclin A, and CDK 2, indicating cell cycle arrest at G1/S. The occurrence of apoptosis was proved by the increased expressions of Fas, Bax, caspase-3, -8, and -9, apoptosis-inducing factor (AIF), and endonuclease G (EndoG), and the declined expressions of Bcl-2 and Bcl-xL. In addition, the intracytosolic release of AIF, EndoG, and cytochrome c contributing to the occurrence of apoptosis was demonstrated by confocal microscopy. CONCLUSION: We demonstrated that LA had antiproliferative effect in HaCaT cell through the inhibition of cell cycle progression at G1/S, and the induction of programmed cell death through caspase-dependent and caspase-independent pathways.
Authors:
Yu-Ping Hsiao; Hsin-Lien Huang; Wan-Wen Lai; Jing-Gung Chung; Jen-Hung Yang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-31
Journal Detail:
Title:  Journal of dermatological science     Volume:  54     ISSN:  1873-569X     ISO Abbreviation:  J. Dermatol. Sci.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-05-04     Completed Date:  2009-07-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9011485     Medline TA:  J Dermatol Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  175-84     Citation Subset:  IM    
Affiliation:
Department of Dermatology, Chung Shan Medical University Hospital, Taichung, Taiwan, ROC.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Chloromethyl Ketones / pharmacology
Apoptosis*
Apoptosis Regulatory Proteins / metabolism
Calcium / metabolism
Caspase 3 / drug effects,  metabolism
Cell Cycle / drug effects*,  physiology
Cell Line
Cell Proliferation / drug effects*
Cell Survival / drug effects,  physiology
Cysteine Proteinase Inhibitors / pharmacology
Cytochromes c / drug effects,  metabolism
Cytostatic Agents / pharmacology*
Endodeoxyribonucleases / drug effects,  metabolism
Humans
Keratinocytes / drug effects*,  metabolism
Lactic Acid / pharmacology*
Membrane Potential, Mitochondrial / drug effects,  physiology
Reactive Oxygen Species / metabolism
Chemical
Reg. No./Substance:
0/Amino Acid Chloromethyl Ketones; 0/Apoptosis Regulatory Proteins; 0/Cysteine Proteinase Inhibitors; 0/Cytostatic Agents; 0/Reactive Oxygen Species; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 50-21-5/Lactic Acid; 7440-70-2/Calcium; 9007-43-6/Cytochromes c; EC 3.1.-/Endodeoxyribonucleases; EC 3.1.21.-/endonuclease G; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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