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Activin B, a homodimer of the inhibin βB subunit, acts as a regulator of gonadal function and as an adipokine. To clarify the role of activin B in dogs, we characterized the canine inhibin βB gene and signalling pathways regulated by the canine inhibin βB. Using 5′‐ and 3′‐rapid amplification of cDNA end (RACE) and RT‐PCR on RNA isolated from the ovary of dogs, we identified short and long forms of the inhibin βB gene. Immunoreactive inhibin βB molecules were detected at ~25 and ~14 kDa under nonreducing and reducing conditions, respectively, in culture supernatants from HEK293 cells transfected with a plasmid containing the long form of the inhibin βB gene, indicating activin B production and secretion. Similar to human and murine activin B, the canine activin B‐stimulated transcriptions of reporter genes, CAGA‐luc and Hepcidin‐luc, regulated by the canonical activin/transforming growth factor‐β (TGF‐β) and bone morphogenetic protein (BMP) pathway, respectively. Activin B‐induced CAGA‐luc transcription was not detected in ALK7‐deficient MDCK canine‐derived cells; however, the forced expression of ALK7 resulted in the activin B‐dependent expression in MDCK cells. Unexpectedly, the activin B‐induced activation of the BMP pathway was partially blocked by the inhibition of endogenous activin/TGF‐β receptor activity. The present study identified an experimentally isolated long form of the canine inhibin βB gene producing activin B that transactivates BMP‐ and activin/TGF‐β‐regulated gene expression. [ABSTRACT FROM AUTHOR]

The liver is the organ that responds to nutritional disturbances including magnesium deficiency. The present study evaluated cellular responses to magnesium deficiency using model cells of the liver, namely, HepG2 cells as hepatocytes, RAW264.7 cells as Kupffer cells and human umbilical vein endothelial cells (HUVECs) as vascular endothelial cells; we examined effects of culture with magnesium deficient medium on cell responses in individual types of cells as well as interactive responses among cells. Metabolomic analyses indicated that magnesium deficiency differentially affected the cellular content of metabolites among HepG2 cells, RAW264.7 cells and HUVECs. The cellular content of the metabolites in HepG2 cells and HUVECs was also affected by the conditioned medium from RAW264.7 cells cultured with the magnesium-deficient media. The changes in HUVECs partly resembled those of the livers of magnesium-deficient rats previously described. RNA-seq analyses indicated that magnesium deficiency modulated the expression levels of molecules related to the ubiquitin-proteasome pathway and oxidative stress/antioxidant response in HepG2 cells and RAW264.7 cells, respectively. Furthermore, when HUVECs were co-cultured with RAW264.7 cells, lipopolysaccharide-induced expression of interleukin (IL)-1β and IL-6 was enhanced by magnesium deficiency, depending on the presence of RAW264.7 cells. The present study reveals that magnesium deficiency affects cellular metabolism in HepG2 liver cells, RAW264.7 macrophages and HUVECs, and that the modulation of cellular responses to extracellular magnesium deficiency in HUVECs depends on the presence of RAW264.7 cells. The complex responses in individual cells and through cell interactions partly explain the regulatory reaction to magnesium deficiency in the liver. [ABSTRACT FROM AUTHOR]

• UCP1 is a transporter responsible for nonshivering thermogenesis in mammalian brown/beige fat. • We identified four alternative splice variants of bovine Ucp1 (variant 1–4). • Bovine Ucp1 comprises a substantial proportion of variant 1/3. • The gene products from Ucp1 variant 2–4 are efficiently degraded by the proteasome system. [ABSTRACT FROM AUTHOR]

Uncoupling protein 1 (UCP1) is responsible for non-shivering thermogenesis in brown/beige adipocytes in humans and rodents. Previously, we showed unexpected expression of UCP1 in bovine skeletal muscles. Here we evaluated Ucp1 mRNA levels in the muscle tissue of Japanese Black steers. Expression of Ucp1 was higher in 30-month-old cattle than in 26-month-old cattle. Levels of myosin heavy chain (Myh)1, an MYH predominantly expressed in fast-twitch muscles, were also significantly higher in cattle aged 30 months. A similar tendency was observed in the expression of other Myhs that are highly expressed in fast-twitch muscles, Myh2 and Myh4. Ucp1 expression was positively correlated with expression of Myh1, Myh2, and Myh4. Our results indicate the possibility of Ucp1 expression in fast-twitch muscle fibers.

This study reports the complete genome sequence of fowl aviadenovirus A strain JM1/1, which caused gizzard erosions in broilers occurring in Japan. The JM1/1 genome is 43,809 bp in length and most closely related to the strain chicken embryo lethal orphan (CELO); moreover, multiple site insertions and deletions were found., (Copyright © 2017 Thanasut et al.)