Regulation of lactoferrin gene expression by estrogen and epidermal growth factor

Teng, Christina T.

doi:10.1007/bf02738154

Cited by 33 publications

(18 citation statements)

References 56 publications

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“…Therefore, increased recruitment of neutrophils and compliment with an increase of lactoferrin production by epithelial cells occurs in the initial phase of infection. Although there has been extensive research efforts on the structure-function relationship of LF and its application in nutritional supplement and prevention of infections and cancers [8][9][10][11][12], studies on the regulation of LF expression by physiological stimuli has been limited [13,14].…”

Section: Introductionmentioning

confidence: 99%

Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Limmon

Imani

et al. 2009

Biochimie

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Lactoferrin (LF) is a multifunctional protein. While its functions and mechanism of actions are actively being investigated, the cellular signals that regulate LF expression have not been as explored. We have previously demonstrated that LF is upregulated by estrogen in reproductive system. In this study, we show that the expression of LF was stimulated by bacterial lipopolysaccharide (LPS) and double-stranded RNA (dsRNA) in normal mouse mammalian HC-11 cells. When cells were exposed to either LPS or dsRNA, the mRNA and protein of LF were increased in a dose-and time-dependent manner, yet the kinetics of LF induction by dsRNA or LPS was different. The LPS and dsRNAinduced LF was mainly released into the culture medium where it blocked TNF-α production in exposed cells. We explored the mechanisms of LF induction by LPS and dsRNA using specific inhibitors and found that the induction could be attenuated by inhibitors to PKC, NF-kB, p38 and JNK, but not by an inhibitor to PKA. Interestingly, ERK inhibitor was effective against dsRNA but not against LPS induction of LF. These data suggest that LF was induced by LPS and dsRNA through PKC, NF-kB and MAPK pathways which in turn plays an inhibitory role in the continuation of innate inflammation.

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Section: Introductionmentioning

confidence: 99%

Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Limmon

Imani

et al. 2009

Biochimie

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“…In addition, high levels of lactoferrin in the colostrum and milk suggest a nutritional value for the infant (4). Lactoferrin may also be involved in normal reproduction function, and its expression in the endometrium and uterus is under the influence of estrogen and epidermal growth factor (5). Together, the expression and regulation of lactoferrin in various tissues and under a wide variety of physiological conditions imply that the protein is needed for protection and nutrition.…”

mentioning

confidence: 99%

“…Together, the expression and regulation of lactoferrin in various tissues and under a wide variety of physiological conditions imply that the protein is needed for protection and nutrition. We have extensively studied lactoferrin expression under the influence of estrogen in the reproductive tract (5)(6)(7)(8)(9). To understand the molecular mechanisms that are involved in estrogen regulation of the lactoferrin gene in the uterus, we have isolated and characterized a compounded estrogen response element (ERE) 1 of the lactoferrin gene promoter from both human and mouse (7)(8)(9).…”

mentioning

confidence: 99%

Estrogen Receptor-related Receptor α1 Interacts with Coactivator and Constitutively Activates the Estrogen Response Elements of the Human Lactoferrin Gene

Zhang

Teng

2000

Journal of Biological Chemistry

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130

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The human estrogen receptor-related receptor (ERR␣1, NR3B1a) was shown to bind a steroidogenic factor binding element (SFRE), TCAAGGTCATC, 26 base pairs upstream from the estrogen response element (ERE) of the human lactoferrin gene promoter. A mutation made at SFRE significantly reduced estrogen-dependent transcription from the lactoferrin ERE in human endometrial cells. In this study, we demonstrated that ERR␣1 binds both SFRE and ERE elements and constitutively transactivates the lactoferrin gene promoter. In DNase I footprinting protection analysis, both SFRE and ERE regions were protected by glutathione S-transferase-ERR␣1 fusion protein. The receptor formed two protein-DNA complexes with either SFRE or ERE in electrophoresis mobility shift assay. Homodimerization of ERR␣1 was confirmed with the mammalian two-hybrid system. ERR␣1 activates reporter constructs containing various types of estrogen response elements in endometrial and non-endometrial cells in transient transfection experiments. Overexpressing the coactivator, SRC1a or GRIP1, further enhances ERR␣1-induced transcriptional activity. We demonstrated that the AF2 domain of ERR␣1 is essential for the transactivation function and that deletion or mutation at this region abrogates the activation capability. Protein-protein interaction between the SRC1a and ERR␣1 C terminus was confirmed with a GST glutathione S-transferase "pull-down" assay. When comparing ERR␣1 and the estrogen receptor ␣ (ER␣) in many of the experiments, we found that ER␣ can also bind SFRE of the lactoferrin gene and transactivate the promoter activity in a ligand-dependent manner. The present study demonstrated that ERR␣1 binds similar DNA elements as ER␣ and confers its transactivation function constitutively. Therefore, ERR␣1 may actively modulate the estrogen response of lactoferrin gene as well as other estrogen-responsive genes.

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“…The levels of lactoferrin, EGF, and TGF-␤2 in colostrum could be influenced by each other. The expression of lactoferrin in mouse uterus was regulated by EGF [34], and TGF-␤1 stimulated lactoferrin release from human neutrophils [35]. Whereas the mechanisms for increased lactoferrin, EGF, and TGF-␤2 by chicken extract are not clearly known.…”

Section: Controlmentioning

confidence: 96%

Chicken extract affects colostrum protein compositions in lactating women

Chao¹,

Tseng²,

Chang³

et al. 2004

The Journal of Nutritional Biochemistry

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Regulation of lactoferrin gene expression by estrogen and epidermal growth factor

Cited by 33 publications

References 56 publications

Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Induction of lactoferrin gene expression by innate immune stimuli in mouse mammary epithelial HC-11 cells

Estrogen Receptor-related Receptor α1 Interacts with Coactivator and Constitutively Activates the Estrogen Response Elements of the Human Lactoferrin Gene

Chicken extract affects colostrum protein compositions in lactating women

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