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Molecular and Cellular Biology, January 2003, p. 178-185, Vol. 23, No. 1
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.1.178-185.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Iron Status in Mice Carrying a Targeted Disruption of Lactoferrin

Pauline P. Ward, Marisela Mendoza-Meneses, Grainne A. Cunningham, and Orla M. Conneely*

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030

Received 20 May 2002/ Returned for modification 11 July 2002/ Accepted 19 September 2002

Lactoferrin is a member of the transferrin family of iron-binding glycoproteins present in milk, mucosal secretions, and the secondary granules of neutrophils. While several physiological functions have been proposed for lactoferrin, including the regulation of intestinal iron uptake, the exact function of this protein in vivo remains to be established. To directly assess the physiological functions of lactoferrin, we have generated lactoferrin knockout (LFKO-/-) mice by homologous gene targeting. LFKO-/- mice are viable and fertile, develop normally, and display no overt abnormalities. A comparison of the iron status of suckling offspring from LFKO-/- intercrosses and from wild-type (WT) intercrosses showed that lactoferrin is not essential for iron delivery during the postnatal period. Further, analysis of adult mice on a basal or a high-iron diet revealed no differences in transferrin saturation or tissue iron stores between WT and LFKO-/- mice on either diet, although the serum iron levels were slightly elevated in LFKO-/- mice on the basal diet. Consistent with the relatively normal iron status, in situ hybridization analysis demonstrated that lactoferrin is not expressed in the postnatal or adult intestine. Collectively, these results support the conclusion that lactoferrin does not play a major role in the regulation of iron homeostasis.


* Corresponding author. Mailing address: Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030. Phone: (713) 798 6233. Fax: (713) 798-7583. E-mail: orlac{at}bcm.tmc.edu.


Molecular and Cellular Biology, January 2003, p. 178-185, Vol. 23, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.1.178-185.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




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