Transforming growth factor (TGF) - α in human milk

Okada, Masaki; Ohmura, Eiji; Kamiya, Y.; Murakami, H.; Onoda, Noritaka; Iwashita, Mitsutoshi; Wakai, Kae; Tsushima, Takahiro; Shizume, Kazuo

doi:10.1016/0024-3205(91)90452-h

Cited by 74 publications

(31 citation statements)

References 16 publications

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“…Further studies with a more sensitive antibody have shown higher molecular mass moieties in whole milk and its fractions, similar to those found in the media of human milk macrophages. This is consistent with the work of Okada et al [25] in their study of TGF-· in fractions of human milk, who found higher molecular weight bands immunoreactive for TGF-·. Several other investigators also have reported higher bands immunoreactive for TGF-· in multiple human tissue types and animal models [26][27][28][29][30][31][32][33][34][35][36][37].…”

Section: Methods Of Western Blot Analysis: Backgroundsupporting

confidence: 81%

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

Lessaris¹,

Forsythe²,

Wagner³

2000

Neonatology

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Objective: To determine if the addition of human milk fortifier (HMF) affects the distribution, immunoreactivity, or molecular mass profile of transforming growth factor-α (TGF-α) within the compartments of human milk. Methods: Fifteen milk samples were obtained. Each sample was divided into two aliquots; a powdered HMF was added to the first aliquot. TGF-α concentration was measured via radioimmunoassay in whole milk and its aqueous and fat fractions ± HMF. TGF-α molecular mass profiles of the samples (v/v) were measured via Western blotting. Results: TGF-α concentration (mean ± SD) in fortified whole milk (15.7 ± 7.1 pg/100 μl) vs. nonfortified whole milk (14.8 ± 8.0 pg/100 μl) and in the aqueous fraction of fortified (14.0 ± 2.7 pg/100 μl) vs. nonfortified (14.0 ± 3.5 pg/100 μl) did not differ statistically. There was, however, a marked decrease in the concentration of TGF-α in the fat fraction of fortified (30.6 ± 2.8 pg/100 μl) vs. nonfortified (98.0 ± 6.9 pg/100 μl) milk samples. Western blot for TGF-α in whole milk and its separated fractions revealed characteristic bands at 6.5, 12–16, 22, 26–30 and 46 kD. HMF alone and HMF with sodium taurocholate had a prominent band at 18 kD and fainter bands at 6.5, 26–30, and 46 kD. While whole and aqueous milk samples with HMF also consistently showed the 18-kD band, in 8/15 fat fraction samples with HMF the 18-kD band was nondetectable and was only faintly detectable in the remaining 7/15 samples. Conclusions: It appears that HMF differentially alters the biochemical profile of human milk with regard to TGF-α concentration and molecular mass profile. What effect this alteration in human milk biochemistry has on neonatal gut function remains unknown.

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Section: Methods Of Western Blot Analysis: Backgroundsupporting

confidence: 81%

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

Lessaris¹,

Forsythe²,

Wagner³

2000

Neonatology

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“…Defects in the JNK-deficient intestines were more severe in embryos than after birth, indic- ative of delayed development. Milk, especially colostrum, contains high levels of EGF and TGF-␣ that stimulate proliferation and maturation of the gastrointestinal tract of newborn infants (17). The presence of EGF in milk may account for the more normal intestinal morphology of JNK-deficient mice after birth.…”

Section: Jnk-and Egfr-deficient Mice Have Similar Defects In Epidermalmentioning

confidence: 99%

The c-Jun NH ₂ -terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis

Weston

Wong

Hall

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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The c-Jun NH2-terminal kinase (JNK) group of mitogen-activated protein kinases is activated in response to a wide array of cellular stresses and proinflammatory cytokines. Roles for JNK in the developing nervous system and T-cell-mediated immunity have been established by detailed studies of mice with compound mutations in the Jnk genes. However, little is known concerning the roles of JNK in other mammalian tissues. Mice lacking both of the ubiquitously expressed isoforms (JNK1 and -2) die during midgestation with neural tube closure defects and brain abnormalities. Here we show that JNK-deficient mice exhibit delayed epithelial development in the epidermis, intestines, and lungs. In addition, JNK-deficient mice exhibit an eyelid closure defect associated with markedly reduced epidermal growth factor (EGF) receptor function, and loss of expression of the ligand EGF. We further demonstrate that adult mice lacking either JNK1 or -2 display striking differences in epidermal proliferation and differentiation, indicative of distinct roles for these kinases in the skin. We conclude that JNK is necessary for epithelial morphogenesis and is an essential regulator of signal transduction by the EGF receptor in the epidermis.

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“…EGF is a peptide that exhibits trophic, maturational, and healing effects on intestinal mucosa (11,16,53). The major sources of EGF in the developing neonate are maternal colostrum, milk, and saliva (7,9,13,47,51,57). Diminished serum and saliva EGF levels were reported in neonates suffering NEC compared with healthy controls (28,62).…”

mentioning

confidence: 99%

Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis

Clark

Lane

MacLennan

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

131

105

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Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Although end-stage NEC is characterized histopathologically as extensive necrosis, apoptosis may account for the initial loss of epithelium before full development of disease. We have previously shown that epidermal growth factor (EGF) reduces the incidence of NEC in a rat model. Although EGF has been shown to protect intestinal enterocytes from apoptosis, the mechanism of EGF-mediated protection against NEC is not known. The aim of this study was to investigate if EGF treatment elicits changes in expression of apoptotic markers in the ileum during the development of NEC. With the use of a well-established neonatal rat model of NEC, rats were divided into the following three experimental groups: dam fed (DF), milk formula fed (NEC), or fed with formula supplemented with 500 ng/ml EGF (NEC+EGF). Changes in ileal morphology, gene and protein expression, and histological localization of apoptotic regulators were evaluated. Anti-apoptotic Bcl-2 mRNA levels were markedly reduced and pro-apoptotic Bax mRNA levels were markedly elevated in the NEC group compared with DF controls. Supplementation of EGF into formula significantly increased anti-apoptotic Bcl-2 mRNA, whereas pro-apoptotic Bax was significantly decreased. The Bax-to-Bcl-2 ratio for mRNA and protein was markedly decreased in NEC+EGF animals compared with the NEC group. The presence of caspase-3-positive epithelial cells was markedly reduced in EGF-treated rats. These data suggest that alteration of the balance between pro-and anti-apoptotic proteins in the site of injury is a possible mechanism by which EGF maintains intestinal integrity and protects intestinal epithelium against NEC injury.

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Transforming growth factor (TGF) - α in human milk

Cited by 74 publications

References 16 publications

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

The c-Jun NH ₂ -terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis

Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis

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Transforming growth factor (TGF) - α in human milk

Cited by 74 publications

References 16 publications

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

Effect of Human Milk Fortifier on the Immunodetection and Molecular Mass Profile of Transforming Growth Factor-Alpha

The c-Jun NH 2 -terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis

Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis

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The c-Jun NH ₂ -terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis