Talk:Gastrointestinal Tract - Intestine Development: Difference between revisions
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==2012== | |||
===Bmp7 functions via a polarity mechanism to promote cloacal septation=== | |||
PLoS One. 2012;7(1):e29372. Epub 2012 Jan 13. | |||
Xu K, Wu X, Shapiro E, Huang H, Zhang L, Hickling D, Deng Y, Lee P, Li J, Lepor H, Grishina I. | |||
Source | |||
Department of Urology, School of Medicine, New York University, New York, New York, United States of America. | |||
Abstract | |||
BACKGROUND: | |||
During normal development in human and other placental mammals, the embryonic cloacal cavity separates along the axial longitudinal plane to give rise to the urethral system, ventrally, and the rectum, dorsally. Defects in cloacal development are very common and present clinically as a rectourethral fistula in about 1 in 5,000 live human births. Yet, the cellular mechanisms of cloacal septation remain poorly understood. | |||
METHODOLOGY/PRINCIPAL FINDINGS: | |||
We previously detected Bone morphogenetic protein 7 (Bmp7) expression in the urorectal mesenchyme (URM), and have shown that loss of Bmp7 function results in the arrest of cloacal septation. Here, we present evidence that cloacal partitioning is driven by Bmp7 signaling in the cloacal endoderm. We performed TUNEL and immunofluorescent analysis on cloacal sections from Bmp7 null and control littermate embryos. We found that loss of Bmp7 results in a dramatic decrease in the endoderm survival and a delay in differentiation. We used immunological methods to show that Bmp7 functions by activating the c-Jun N-terminal kinase (JNK) pathway. We carried out confocal and 3D imaging analysis of mitotic chromosome bundles to show that during normal septation cells in the cloacal endoderm divide predominantly in the apical-basal direction. Loss of Bmp7/JNK signaling results in randomization of mitotic angles in the cloacal endoderm. We also conducted immunohistochemical analysis of human fetal sections to show that BMP/phospho-SMAD and JNK pathways function in the human cloacal region similar as in the mouse. | |||
CONCLUSION/SIGNIFICANCE: | |||
Our results strongly indicate that Bmp7/JNK signaling regulates remodeling of the cloacal endoderm resulting in a topological separation of the urinary and digestive systems. Our study points to the importance of Bmp and JNK signaling in cloacal development and rectourethral malformations. | |||
PMID 22253716 | |||
==2011== | ==2011== | ||
Revision as of 00:34, 8 June 2012
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Cite this page: Hill, M.A. (2024, April 20) Embryology Gastrointestinal Tract - Intestine Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Gastrointestinal_Tract_-_Intestine_Development |
2012
Bmp7 functions via a polarity mechanism to promote cloacal septation
PLoS One. 2012;7(1):e29372. Epub 2012 Jan 13.
Xu K, Wu X, Shapiro E, Huang H, Zhang L, Hickling D, Deng Y, Lee P, Li J, Lepor H, Grishina I. Source Department of Urology, School of Medicine, New York University, New York, New York, United States of America. Abstract BACKGROUND: During normal development in human and other placental mammals, the embryonic cloacal cavity separates along the axial longitudinal plane to give rise to the urethral system, ventrally, and the rectum, dorsally. Defects in cloacal development are very common and present clinically as a rectourethral fistula in about 1 in 5,000 live human births. Yet, the cellular mechanisms of cloacal septation remain poorly understood. METHODOLOGY/PRINCIPAL FINDINGS: We previously detected Bone morphogenetic protein 7 (Bmp7) expression in the urorectal mesenchyme (URM), and have shown that loss of Bmp7 function results in the arrest of cloacal septation. Here, we present evidence that cloacal partitioning is driven by Bmp7 signaling in the cloacal endoderm. We performed TUNEL and immunofluorescent analysis on cloacal sections from Bmp7 null and control littermate embryos. We found that loss of Bmp7 results in a dramatic decrease in the endoderm survival and a delay in differentiation. We used immunological methods to show that Bmp7 functions by activating the c-Jun N-terminal kinase (JNK) pathway. We carried out confocal and 3D imaging analysis of mitotic chromosome bundles to show that during normal septation cells in the cloacal endoderm divide predominantly in the apical-basal direction. Loss of Bmp7/JNK signaling results in randomization of mitotic angles in the cloacal endoderm. We also conducted immunohistochemical analysis of human fetal sections to show that BMP/phospho-SMAD and JNK pathways function in the human cloacal region similar as in the mouse. CONCLUSION/SIGNIFICANCE: Our results strongly indicate that Bmp7/JNK signaling regulates remodeling of the cloacal endoderm resulting in a topological separation of the urinary and digestive systems. Our study points to the importance of Bmp and JNK signaling in cloacal development and rectourethral malformations.
PMID 22253716
2011
Intestinal development and differentiation
Exp Cell Res. 2011 Nov 15;317(19):2702-10. Epub 2011 Sep 24.
Noah TK, Donahue B, Shroyer NF. Source Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Abstract
In this review, we present an overview of intestinal development and cellular differentiation of the intestinal epithelium. The review is separated into two sections: Section one summarizes organogenesis of the small and large intestines, including endoderm and gut tube formation in early embryogenesis, villus morphogenesis, and crypt formation. Section two reviews cell fate specification and differentiation of each cell type within the intestinal epithelium. Growth factor and transcriptional networks that regulate these developmental processes are summarized.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID 21978911
TWO PATTERNS OF DEVELOPMENT OF INTERSTITIAL CELLS OF CAJAL IN THE HUMAN DUODENUM
J Cell Mol Med. 2011 Feb 25. doi: 10.1111/j.1582-4934.2011.01287.x. [Epub ahead of print]
Radenkovic G. Source Department of Histology and Embryology, Faculty of Medicine, University of Nis, Nis, Serbia.
Abstract
At the end of the embryonic period of human development, c-kit immunoreactive (c-kit IR) cells identifiable as interstitial cells of Cajal (ICC) are present in the oesophagus and stomach wall. In the small and large bowel, c-kit-IR cells appear later (in the small bowel at 9 weeks, and in the colon at 10-12 weeks), also in the MP region. The object of the present study was to determine the timing of appearance and distribution of c-kit IR cells in the human embryonic and fetal duodenum. I used immunohistochemistry to examine the embryonic and fetal duodenum for cells expressing CD117 (Kit), expressed by mature ICC and ICC progenitor cells and CD34 to identify presumed ICC progenitors. Enteric plexuses were examined by way of anti-neuron specific enolase and the differentiation of smooth muscle cells was studied using anti-desmin antibodies. At the end of the embryonic period of development, c-kit IR cells were solely present in the proximal duodenum in the form of a wide belt of densely packed cells around the inception of the MP ganglia. In the distal duodenum, c-kit IR cells emerged at the beginning of the fetal period in the form of thin rows of pleomorphic cells at the level of the MP. From the beginning of the 4(th) month, the differences in the distribution of ICC in the different portions of the duodenum were established, and this relationship was still present in later developmental stages. In fact, in the proximal duodenum, ICC of the myenteric plexus (ICC-MP), ICC of the circular muscle (ICC-CM), and ICC of the septa (ICC-SEP) were present, and in the distal duodenum ICC-MP and ICC-SEP only. In conclusion, in the humans there is a difference in the timing and patterns of development of ICC in the proximal duodenum compared to the distal duodenum.
2011.
PMID: 21352475
2008
Fgf9 signaling regulates small intestinal elongation and mesenchymal development
Development. 2008 Sep;135(17):2959-68. Epub 2008 Jul 24.
Geske MJ, Zhang X, Patel KK, Ornitz DM, Stappenbeck TS. Source Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA.
Abstract
Short bowel syndrome is an acquired condition in which the length of the small intestine is insufficient to perform its normal absorptive function. Current therapies are limited as the developmental mechanisms that normally regulate elongation of the small intestine are poorly understood. Here, we identify Fgf9 as an important epithelial-to-mesenchymal signal required for proper small intestinal morphogenesis. Mouse embryos that lack either Fgf9 or the mesenchymal receptors for Fgf9 contained a disproportionately shortened small intestine, decreased mesenchymal proliferation, premature differentiation of fibroblasts into myofibroblasts and significantly elevated Tgfbeta signaling. These findings suggest that Fgf9 normally functions to repress Tgfbeta signaling in these cells. In vivo, a small subset of mesenchymal cells expressed phospho-Erk and the secreted Tgfbeta inhibitors Fst and Fstl1 in an Fgf9-dependent fashion. The p-Erk/Fst/Fstl1-expressing cells were most consistent with intestinal mesenchymal stem cells (iMSCs). We found that isolated iMSCs expressed p-Erk, Fst and Fstl1, and could repress the differentiation of intestinal myofibroblasts in co-culture. These data suggest a model in which epithelial-derived Fgf9 stimulates iMSCs that in turn regulate underlying mesenchymal fibroblast proliferation and differentiation at least in part through inhibition of Tgfbeta signaling in the mesenchyme. Taken together, the interaction of FGF and TGFbeta signaling pathways in the intestinal mesenchyme could represent novel targets for future short bowel syndrome therapies.
PMID: 18653563 http://www.ncbi.nlm.nih.gov/pubmed/18653563
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678066/?tool=pubmed
2003
Timetable for intestinal rotation in staged human embryos and fetuses
Birth Defects Res A Clin Mol Teratol. 2003 Nov;67(11):941-5.
Kim WK, Kim H, Ahn DH, Kim MH, Park HW.
Department of Anatomy, College of Medicine, Hanyang University, Seoul, South Korea. hwoopark@yumc.yonsei.ac.kr Abstract BACKGROUND: The existing data on intestinal rotation during human development are contradictory regarding the timing of major events, and as such an exact timetable for rotation of the intestine in humans is not yet available.
METHODS: We studied the initial formation and rotation of the intestine by microdissection and histological observations in 72 human embryos and fetuses at two to 12 weeks postfertilization. The embryos were classified according to the Carnegie staging system.
RESULTS: The primordium of the primitive gut was first observed as a yolk sac at stage 5. With the formation of the embryonic foldings, three divisions of the primitive gut (the foregut, midgut, and hindgut) were observed at stage 10. At stage 12, the primitive gut was located on the midline. At stage 15, a 90 degrees counterclockwise rotation of the intestine began. At stage 16, herniation of the intestine into the umbilical cord was not evident in observations of the external form or a transversely sectioned embryo, but was evident in a sagittally sectioned embryo. There was another 90 degrees counterclockwise rotation at stage 20. Reduction of the intestine was a rapid process, since it was still in the cord in fetuses of <40 mm crown-rump length (CRL), and was reduced above 40 mm in general during nine weeks of development. When the intestine returned to the abdominal cavity, the cecum was located in the right lower quadrant (the adult position).
CONCLUSIONS: We have developed a standard timetable to describe the rotation of the intestine. The current results will be helpful in studies describing the pathogenesis of some developmental abnormalities in the intestine due to abnormal rotation.
Copyright 2003 Wiley-Liss, Inc. PMID: 14745932 http://www.ncbi.nlm.nih.gov/pubmed/14745932
1991
Small intestinal length: a factor essential for gut adaptation
Gut. 1991 Nov;32(11):1321-3.
Weaver LT, Austin S, Cole TJ. Source MRC Dunn Nutrition Unit, Cambridge.
Abstract
Changes in small intestinal structure, cytokinetics, and function are dynamic ways in which the gut adapts to diet, disease, and damage. Adequate length provides a static 'reserve' permitting an immediate response to pathophysiological changes. The length of the small intestine from conception to adulthood using data taken from eight published reports of necropsy measurement of 1010 guts is described. Mean length at 20 weeks' gestation was 125 cm, at 30 weeks' 200 cm, at term 275 cm, at 1 year 380 cm, at 5 years 450 cm, at 10 years 500 cm, and at 20 years 575 cm. Prenatal small intestinal growth exceeded that of body length according to the law: small intestinal length alpha body length to the power 4/3. After birth there was a noticeable deceleration: small intestinal length alpha body length to the power 1/2. The coefficient of variation of small intestinal length postnatally was 24%, sixfold greater than for body length. The rapid prenatal small intestinal growth rate ensures that the mature newborn has adequate small intestine to meet postnatal nutritional demands, but handicaps the preterm infant who undergoes intestinal resection. The wide variation in lengths suggests a 'surplus' surface area that is immediately available to respond, independent of dynamic mucosal changes, to fluctuations in food availability, local intestinal disease, damage, rapid transit, and resection.
PMID: 1752463 http://www.ncbi.nlm.nih.gov/pubmed/1752463
Postulated functional regions
Duodenum - principal site for iron absorption. Ileocecal valve - only site in the gastrointestinal tract for Vitamin B12 and bile acid absorption?
