Jump to ContentJump to Main Navigation
Show Summary Details
More options …

Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

12 Issues per year


IMPACT FACTOR 2016: 3.432

CiteScore 2016: 2.21

SCImago Journal Rank (SJR) 2016: 1.000
Source Normalized Impact per Paper (SNIP) 2016: 1.112

Online
ISSN
1437-4331
See all formats and pricing
More options …
Volume 45, Issue 4 (Apr 2007)

Issues

The c.–292C>T promoter polymorphism increases reticulocyte-type 15-lipoxygenase-1 activity and could be atheroprotective

Jonas Wittwer
  • 1Institute of Clinical Chemistry, Center for Integrative Human Physiology, University Hospital Zurich, Zurich, Switzerland
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Mathias Bayer / Armin Mosandl / Jörg Muntwyler
  • 4Cardiovascular Center Division of Cardiology, University Hospital Zurich, Zurich, Switzerland
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Martin Hersberger
  • 5Institute of Clinical Chemistry, Center for Integrative Human Physiology, University Hospital Zurich, Zurich, Switzerland
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2007-04-17 | DOI: https://doi.org/10.1515/CCLM.2007.103

Abstract

Background: Reticulocyte-type 15-lipoxygenase-1 (ALOX15) has anti-inflammatory and inflammatory effects and is implicated in the development of asthma, arthritis and atherosclerosis. Previously, we screened the human ALOX15 gene for variations because genetic variability in ALOX15 might influence these diseases. We found a C>T substitution at position c.–292 in the ALOX15 promoter that created a novel binding site for the transcription factor SPI1 and increased ALOX15 mRNA levels in monocytes from c.–292CT heterozygous volunteers.

Methods: To test whether the higher mRNA levels led to higher ALOX15 activity, we performed an activity assay and measured the arachidonic acid metabolite 15(S)-hydroxy-eicosatetraenoic acid [15(S)-HETE] by HPLC analysis. To test whether this polymorphism was associated with coronary artery disease (CAD), we investigated its association in a case-control study involving 498 Caucasians.

Results: The c.–292C>T polymorphism was associated with higher enzyme activity in heterozygous carriers. Intriguingly, this polymorphism also showed a tendency to be protective against atherosclerosis.

Conclusions: These results suggest that increased ALOX15 activity may attenuate inflammation, which could be caused by an increase in 15(S)-HETE and eventually by its metabolites, the lipoxins.

Clin Chem Lab Med 2007;45:487–92.

Keywords: inflammation; lipoxin; 15-lipoxygenase (15-LOX); polymorphism; PU.1; reticulocyte-type 15-lipoxygenase-1 (ALOX15); SFPI1; SPI1; transcription factor

About the article

Corresponding author: Martin Hersberger, Institute of Clinical Chemistry, University Hospital Zurich, Raemistraβe 100, 8091 Zurich, Switzerland Phone: +41-44-2553473, Fax: +41-44-2554590,


Received: 2006-10-13

Accepted: 2007-01-04

Published Online: 2007-04-17

Published in Print: 2007-04-01


Citation Information: Clinical Chemical Laboratory Medicine, ISSN (Online) 14346621, ISSN (Print) 14374331, DOI: https://doi.org/10.1515/CCLM.2007.103.

Export Citation

Citing Articles

Here you can find all Crossref-listed publications in which this article is cited. If you would like to receive automatic email messages as soon as this article is cited in other publications, simply activate the “Citation Alert” on the top of this page.

[1]
Luiza Oliveira Perucci, Michelle Amantéa Sugimoto, Karina Braga Gomes, Luci Maria Dusse, Mauro Martins Teixeira, and Lirlândia Pires Sousa
Expert Opinion on Therapeutic Targets, 2017, Volume 21, Number 9, Page 879
[2]
Jochen A. Ackermann, Katharina Hofheinz, Mario M. Zaiss, and Gerhard Krönke
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, 2017, Volume 1862, Number 4, Page 371
[3]
Joana Viola and Oliver Soehnlein
Seminars in Immunology, 2015, Volume 27, Number 3, Page 184
[4]
M. Setkowicz, L. Mastalerz, A. Gielicz, A. Wojas-Pelc, and M. Sanak
British Journal of Dermatology, 2015, Volume 172, Number 2, Page 337
[5]
Thomas Horn, Susan Adel, Ralf Schumann, Saubashya Sur, Kumar Reddy Kakularam, Aparoy Polamarasetty, Pallu Redanna, Hartmut Kuhn, and Dagmar Heydeck
Progress in Lipid Research, 2015, Volume 57, Page 13
[6]
Magdalena Herová, Mattia Schmid, Claudio Gemperle, Christa Loretz, and Martin Hersberger
Atherosclerosis, 2014, Volume 235, Number 2, Page 256
[7]
Sophia J.A. Wuest, Thomas Horn, Jacqueline Marti-Jaun, Hartmut Kühn, and Martin Hersberger
Clinical Biochemistry, 2014, Volume 47, Number 6, Page 349
[8]
Huadan Ye, Xiaojing Li, Lingyan Wang, Qi Liao, Leiting Xu, Yi Huang, Liming Xu, Xuting Xu, Cheng Chen, Hangyu Wu, Yanping Le, Qiong Liu, Meng Ye, Changzheng Dong, and Shiwei Duan
Gene, 2013, Volume 531, Number 1, Page 71
[9]
Anna Planagumà, Shamsah Kazani, Gautham Marigowda, Oliver Haworth, Thomas J. Mariani, Elliot Israel, Eugene R. Bleecker, Douglas Curran-Everett, Serpil C. Erzurum, William J. Calhoun, Mario Castro, Kian Fan Chung, Benjamin Gaston, Nizar N. Jarjour, William W. Busse, Sally E. Wenzel, and Bruce D. Levy
American Journal of Respiratory and Critical Care Medicine, 2008, Volume 178, Number 6, Page 574
[10]
Sophia J.A. Wuest, Margot Crucet, Claudio Gemperle, Christa Loretz, and Martin Hersberger
Atherosclerosis, 2012, Volume 225, Number 1, Page 121
[11]
Michael J. Zhang and Matthew Spite
Annual Review of Nutrition, 2012, Volume 32, Number 1, Page 203
[12]
Valérie Capra, Magnus Bäck, Silvia S. Barbieri, Marina Camera, Elena Tremoli, and G. Enrico Rovati
Medicinal Research Reviews, 2013, Volume 33, Number 2, Page 364
[13]
Jie Zhao, Zhiyi He, Shanshan Ma, and Lei Li
Journal of Molecular Neuroscience, 2012, Volume 47, Number 3, Page 458
[14]
Rebecca Worsley-Hunt, Virginie Bernard, and Wyeth W Wasserman
Genome Medicine, 2011, Volume 3, Number 10, Page 65
[15]
Aksam J. Merched, Charles N. Serhan, and Lawrence Chan
Journal of Nutrigenetics and Nutrigenomics, 2011, Volume 4, Number 1, Page 12
[16]
Vanessa Waechter, Jacqueline Marti-Jaun, Angelika Weber, Zoltan Laszlo Madi, and Martin Hersberger
Clinical Chemistry and Laboratory Medicine, 2012, Volume 50, Number 1
[17]
Jonas Wittwer and Martin Hersberger
Prostaglandins, Leukotrienes and Essential Fatty Acids, 2007, Volume 77, Number 2, Page 67
[18]
Anca D. Dobrian, David C. Lieb, Banumathi K. Cole, David A. Taylor-Fishwick, Swarup K. Chakrabarti, and Jerry L. Nadler
Progress in Lipid Research, 2011, Volume 50, Number 1, Page 115
[19]
Martin Hersberger, Martina Müller, Jacqueline Marti-Jaun, Iris M. Heid, Stefan Coassin, Thomas F. Young, Vanessa Waechter, Christian Hengstenberg, Christine Meisinger, Annette Peters, Wolfgang König, Stephan Holmer, Heribert Schunkert, Norman Klopp, Florian Kronenberg, and Thomas Illig
Atherosclerosis, 2009, Volume 205, Number 1, Page 192
[20]
Martin Hersberger
Clinical Chemistry and Laboratory Medicine, 2010, Volume 48, Number 8
[21]
Anna Planaguma and Bruce D Levy
Future Lipidology, 2008, Volume 3, Number 6, Page 697
[22]
Kai Zhang, Yuan-yuan Wang, Qi-ji Liu, Hui Wang, Fang-fang Liu, Zhi-yong Ma, Yao-qin Gong, and Li Li
Heart and Vessels, 2010, Volume 25, Number 5, Page 368
[23]
Gregory J. Tranah, Brent C. Taylor, Li-Yung Lui, Joseph M. Zmuda, Jane A. Cauley, Kristine E. Ensrud, Teresa A. Hillier, Marc C. Hochberg, Jia Li, Brian K. Rhees, Henry A. Erlich, Mark D. Sternlicht, Gary Peltz, and Steven R. Cummings
Calcified Tissue International, 2008, Volume 83, Number 3, Page 155

Comments (0)

Please log in or register to comment.
Log in