NDLI: The bone morphogenetic protein signaling pathway is upregulated in a mouse model of total parenteral nutrition.

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The bone morphogenetic protein signaling pathway is upregulated in a mouse model of total parenteral nutrition.

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The bone morphogenetic protein signaling pathway is upregulated in a mouse model of total parenteral nutrition.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Chaojun Feng, Yongjia Yang, Hua Koga, Hiroyuki Teitelbaum, Daniel H.
Description	Country affiliation: United States Author Affiliation: Zhang C ( Section of Pediatric Surgery, Department of Surgery, University of Michigan Medical School and C. S. Mott Children's Hospital, Ann Arbor, MI 48109, USA.)
Abstract	Total parenteral nutrition (TPN) results in intestinal mucosal atrophic changes due to an absence of enteral nutrition; however, the mechanisms responsible for this are not fully understood. It has been shown that bone morphogenetic protein (BMP) activation inhibits intestinal epithelial cell (EC) proliferation. Therefore, we hypothesized that the BMP pathway could be upregulated by TPN. To address this, we randomly assigned mice to receive TPN or to be enterally fed (control) for 7 d. Mucosal EC isolates were harvested from the entire length of small intestine for RNA and protein measurements. Full-thickness, mid-small bowel was processed for histological examination. TPN increased the abundance of BMP2, BMP4, and BMP type II receptor at the RNA and protein levels. Phosphorylation of Smad1, Smad5, and Smad8 also was greater in the TPN group than in the control, which helped to confirm activation of this pathway. Interestingly, the TPN and control groups did not differ in the mRNA expression of the extracellular soluble bmp antagonists, noggin, gremlin, chordin, or follistatin. Compared to the control group, the expression of c-Myc (cellular myelocytomatosis) mRNA was lower, whereas the level of p21(WAF1/CIP1) was greater, in the TPN group. Because the BMP family may function through suppression of Wnt-beta-catenin signaling, this pathway was also examined. mRNA expression of Wnt 3, Wnt5a, and the Wnt receptor Lrp5 were lower in the TPN group compared to controls. The results suggest that the BMP signaling pathway may be involved in the development of intestinal mucosal atrophy due to TPN administration.
File Format	HTM / HTML
ISSN	00223166
e-ISSN	15416100
DOI	10.3945/jn.108.096669
Journal	Journal of Nutrition
Issue Number	7
Volume Number	139
Language	English
Publisher	American Society for Nutrition
Publisher Date	2009-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Bone Morphogenetic Protein 4 Intestine, Small Signal Transduction Bone Morphogenetic Protein 2 Parenteral Nutrition, Total Mice, Inbred C57bl Gene Expression Regulation Reference Values Pharmacology Bone Morphogenetic Protein Receptors, Type Ii Animals Polymerase Chain Reaction Dipeptides Genetics Models, Animal Physiology Mice Discipline Nutrition Bone Morphogenetic Proteins Glutamine
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Medicine

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