Humans, Mice, and Mechanisms of Intestinal Atresias: A Window into Understanding Early Intestinal Development

Nichol, Peter F.; Reeder, Amy L.; Botham, Robert A.

doi:10.1007/s11605-010-1400-y

Cited by 27 publications

(18 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mice were bred on a C57BL6 background. Using the previously described HPRT‐Cre system Fgfr2IIIb −/− (null) embryos were generated by mating Fgfr2IIIb flox/+ ; HprtCre /+ females with Fgfr2IIIb flox/flox males. Fgfr2IIIb flox/flox (control) embryos were generated within the same litters without the HPRT‐Cre allele.…”

Section: Methodsmentioning

confidence: 99%

“…Null embryos in this model have been shown to form a number of congenital defects . Of note for this study, these mutant mice present with distal colonic atresia with 100% penetrance across all homozygous mutant embryos . Given the anatomic precision and fidelity of colonic atresia formation in this model, we focused on this distal colonic region as a discreet location where cellular differences during organogenesis would be of interest.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lack of discreet colocalization of epithelial apoptosis to the atretic precursor in the colon of the Fibroblast growth factor receptor 2IIIb mouse and staining consistent with cellular movement suggest a revised model of atresia formation

Kowalkowski

Zaremba

Rogers

et al. 2020

Developmental Dynamics

Self Cite

View full text Add to dashboard Cite

Background: Colonic atresias in the Fibroblast growth factor receptor 2IIIb (Fgfr2IIIb) mouse model have been attributed to increased epithelial apoptosis and decreased epithelial proliferation at embryonic day (E) 10.5. We therefore hypothesized that these processes would colocalize to the distal colon where atresias occur (atretic precursor) and would be excluded or minimized from the proximal colon and small intestine. Results: We observed a global increase in intestinal epithelial apoptosis in Fgfr2IIIb −/− intestines from E9.5 to E10.5 that did not colocalize to the atretic precursor. Additionally, epithelial proliferations rates in Fgfr2IIIb −/− intestines were statistically indistinguishable to that of controls at E10.5 and E11.5. At E11.5 distal colonic epithelial cells in mutants failed to assume the expected pseudostratified columnar architecture and the continuity of the adjacent basal lamina was disrupted. Individual E-cadherin-positive cells were observed in the colonic mesenchyme. Conclusions: Our observations suggest that alterations in proliferation and apoptosis alone are insufficient to account for intestinal atresias and that these defects may arise from both a failure of distal colonic epithelial cells to develop normally and local disruptions in basal lamina architecture.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lack of discreet colocalization of epithelial apoptosis to the atretic precursor in the colon of the Fibroblast growth factor receptor 2IIIb mouse and staining consistent with cellular movement suggest a revised model of atresia formation

Kowalkowski

Zaremba

Rogers

et al. 2020

Developmental Dynamics

Self Cite

View full text Add to dashboard Cite

show abstract

“…Although jejunal and ileal atresias are usually bundled together as one and the same disease, their clinical presentation and postoperative course often differ, suggesting 1 of 2 possibilities: the aetiologies are different or the 2 segments respond differently to obstruction and altered blood supply owing to regional, anatomical, and functional differences (42,43).…”

Section: Jejunal and Ileal Atresiasmentioning

confidence: 99%

Recent Advances in the Molecular and Genetic Understanding of Congenital Gastrointestinal Malformations

Dauvé

Mclin²

2013

J. pediatr. gastroenterol. nutr.

View full text Add to dashboard Cite

Major developmental paradigms are highly conserved among vertebrates. The contribution of developmental biology to the understanding of human disease and regeneration has soared recently. We review advances in the molecular and genetic understanding of gastrointestinal development using evidence from both mammalian and nonmammalian models. When appropriate, we highlight relevance and applicability to human disease.

show abstract

“…7 Atresias are categorized depending on increased importance of the anomaly in base of 3 facts: 1) amount of absent gut tissue, 2) interruption of the vasculature, and 3) the number of co-existing anomalies in the intestine. 8 Accordingly, atresias are classified into 3 types: type 1: membrane atresia with a membrane occluding the lumen, type 2: cord atresia, produced by blind-ends connected by a tissue string (of muscular and/or fibrous origin) suspended or not by its mesentery, and type 3: blind-end atresia characterized by loss of intestinal tissue with separated blind-ends and a cooccurring cleft in the mesentery. They also described a fourth type, in fact a variant of type 3, exclusive to man, named "apple peel" or "Christmas tree" atresia.…”

Section: Introductionmentioning

confidence: 99%

“…They also described a fourth type, in fact a variant of type 3, exclusive to man, named "apple peel" or "Christmas tree" atresia. 7,8 …”

Section: Introductionmentioning

confidence: 99%

An unusual colon atresia in a calf: at the junction of the distal loop and transverse colon. A brief overview

Lombardero

Yllera

2014

Organogenesis

View full text Add to dashboard Cite

Congenital defects are those abnormalities present at birth. During embryogenesis, many anomalies can occur. The primitive gut tube lengthens quickly and rotates, allowing the gastrointestinal tract acquire its final position and orientation. Because the colon of large animals is complex, most changes occur in this segment. Thus, in ruminants, colon atresia is the most frequent malformation, affecting mainly ascending colon, at the level of the spiral loop. There are no previous references about a very atypical colon atresia at the junction of distal loop and transverse colon, such we have described in a 5-day-old calf, after a history of abdominal distention and absence of feces at birth, even with a patent anal opening. Atresia coli was detected at distal position of the typical colon atresia, at the junction of distal loop and transverse colon. In addition, the distal blind end was bent into a U-shape supported by the mesocolon. Besides the anatomical findings of this worthwhile atresia coli we discuss its possible etiology, in which local factors, such as a compromised blood supply during embryogenesis, are more consistent than genetic factors. Finding out the causes of atresia coli would help to reduce its incidence, lessen animal suffering and economic loss.

show abstract

Humans, Mice, and Mechanisms of Intestinal Atresias: A Window into Understanding Early Intestinal Development

Cited by 27 publications

References 57 publications

Lack of discreet colocalization of epithelial apoptosis to the atretic precursor in the colon of the Fibroblast growth factor receptor 2IIIb mouse and staining consistent with cellular movement suggest a revised model of atresia formation

Lack of discreet colocalization of epithelial apoptosis to the atretic precursor in the colon of the Fibroblast growth factor receptor 2IIIb mouse and staining consistent with cellular movement suggest a revised model of atresia formation

Recent Advances in the Molecular and Genetic Understanding of Congenital Gastrointestinal Malformations

An unusual colon atresia in a calf: at the junction of the distal loop and transverse colon. A brief overview

Contact Info

Product

Resources

About