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Latexin regulates the abundance of multiple cellular proteins in hematopoietic stem cells

✍ Scribed by Kanae Mitsunaga; Jiro Kikuchi; Taeko Wada; Yusuke Furukawa

Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
921 KB
Volume
227
Category
Article
ISSN
0021-9541

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✦ Synopsis

Abstract

Latexin is the only known carboxypeptidase A inhibitor in mammals and shares structural similarity with cystatin C, suggesting that latexin regulates the abundance of as yet unidentified target proteins. A forward genetic approach revealed that latexin is involved in homeostasis of hematopoietic stem cells (HSCs) in mice; however, little is known about the mechanisms by which latexin negatively affects the numbers of HSCs. In this study, we found that latexin is preferentially expressed in hematopoietic stem/progenitor cells, and is co‐localized with the molecules responsible for the interaction of HSCs with a bone marrow niche, such as N‐cadherin, Tie2, and Roundabout 4. Latexin‐knockout young female mice showed an increase in the numbers of KSL (c‐Kit^+^/Sca‐1^+^/linegae marker‐negative) cells, which may be attributable to enhanced self‐renewal because latexin‐deficient KSL cells formed more colonies than their wild‐type counterparts in methylcellulose culture. Proteomic analysis of Sca‐1^+^ bone marrow cells demonstrated that latexin ablation reduced the abundance of multiple cellular proteins, including N‐cadherin, Tie2, and Roundabout 4. Finally, we found that latexin expression was lost or greatly reduced in approximately 50% of human leukemia/lymphoma cell lines. These results imply that latexin inhibits the self‐renewal of HSCs by facilitating the lodgment of HSCs within a bone marrow niche to maintain HSC homeostasis. J. Cell. Physiol. 227: 1138–1147, 2012. © 2011 Wiley Periodicals, Inc.

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