The Latent Form of Transforming Growth Factor-ß Administered Orally Is Activated by Gastric Acid in Mice1,2  

Oleh:

Nakamura, Yuki ; Miyata, Masanori ; Ando, Takashi ; Shimokawa, Naomi

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 139 no. 08 (Aug. 2009), page 1463-1468.
Topik: Transforming growth factor-ß (TGFß); simulating the effects of gastric acid; Smad-responsive promoter activity in MFB-F11

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2009.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Transforming growth factor-ß (TGFß) is abundant in mammalian milk in a latent form. However, whether the latent form of TGFß in human milk is converted to the active form in vivo remains uncertain. To address this issue, we first investigated whether latent TGFß or human milk-borne latent TGFß was activated in an in vitro assay, simulating the effects of gastric acid. We then tested whether gastric acid was necessary for the activation of orally administered latent TGFß or human milk-borne latent TGFß in mice by inhibiting gastric acidity with cimetidine, an antagonist of H2-receptors. Latent TGFß or human milk-borne latent TGFß increased Smad-responsive promoter activity in MFB-F11 reporter cells at pH 1.2, but not at pH 7.0, regardless of the presence or absence of the gastric protease pepsin. In mice treated orally with latent TGFß (5 µg/mouse), the phosphorylation of Smad2 and TGFß target gene mRNA expression (TGFß and Smad7) was increased in the small intestine (P < 0.05) and this effect was inhibited by cimetidine (100 mg/kg, intraperitoneally). Similarly, mice treated orally with 1200 µL/d of human milk containing latent TGFß (3 µg/L) for 2 wk had increased TGFß and Smad7 mRNA expression in the small intestine (P < 0.05) and this was inhibited by the antiacid treatment. Therefore, the latent form of TGFß, such as TGFß in human milk, can be activated by gastric acid following oral administration in mice. This process may be involved in the conversion of human milk-borne latent TGFß to the active form in vivo.

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