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CD44-deficiency on hematopoietic cells limits T-cell number but does not protect against atherogenesis in LDL receptor-deficient mice
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Dept. of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
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2009 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 206, no 2, 369-374 p.Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Vascular and inflammatory cells express adhesion molecule CD44. We demonstrated previously that enhanced CD44 localizes in human atherosclerotic lesions. Apolipoprotein E/cd44 double-deficient mice and apolipoprotein E-deficient mice transplanted with CD44-deficient bone marrow (BM) exhibit reduced atherosclerosis. Since CD44 is a novel factor in atherogenesis, it is imperative that it is investigated in more than one animal model to conclusively determine its role in this particular disease pathology. To test the hypothesis that CD44 expressed by hematopoietic cells plays a critical role in atherogenesis in the low density lipoprotein (LDL) receptor-deficient mouse model, we performed BM reconstitution experiments.

METHODS: Lethally irradiated LDL receptor-deficient mice were transplanted with either CD44-deficient or wild-type BM. Beginning 10 weeks after successful reconstitution, mice consumed a cholesterol-enriched atherogenic diet for 6 or 11 weeks.

RESULTS: Surprisingly, CD44-deficiency on BM-derived inflammatory cells did not affect lesion size. Additionally, neither group displayed differences in smooth muscle cell, macrophage, collagen, or elastin content as well as lipoprotein levels. However, lesions in CD44-deficient BM-recipient mice contained fewer T-cells compared to wild-type BM mice. Interestingly, CD44-deficient T-cells expressed less chemokine receptor-5 mRNA. Furthermore, in vivo leukocyte adhesion decreased in CD44-deficient mice compared to wild-type mice.

CONCLUSION: This study surprisingly revealed that atherogenesis does not require CD44 expression on hematopoietic cells in the LDL receptor-deficient mouse model. However, CD44 promotes T-cell recruitment, downregulates chemokine receptor-5, and participates critically in leukocyte adhesion in vivo. Consequently, the anti-atherogenic role of CD44 may require CD44-deficiency on cell types other than inflammatory cells in the LDL receptor-deficient mouse model.

Place, publisher, year, edition, pages
Elsevier, 2009. Vol. 206, no 2, 369-374 p.
National Category
Other Basic Medicine
Research subject
Medical sciences
Identifiers
URN: urn:nbn:se:his:diva-11379DOI: 10.1016/j.atherosclerosis.2009.03.002ISI: 000271287000012PubMedID: 19345948ScopusID: 2-s2.0-70349429959OAI: oai:DiVA.org:his-11379DiVA: diva2:847228
Available from: 2015-08-19 Created: 2015-08-19 Last updated: 2016-04-12Bibliographically approved

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