Premium
Enteroendocrine Cell is a Source of VEGF‐A in the Neonatal Intestine
Author(s) -
Yan Xiaocai,
Liu Xueli,
Managlia Elizabeth,
De Plaen Isabelle
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.957.13
Subject(s) - enteroendocrine cell , chromogranin a , biology , paracrine signalling , myenteric plexus , pathology , cd31 , cell type , angiogenesis , small intestine , cell , immunohistochemistry , medicine , endocrinology , cancer research , endocrine system , hormone , biochemistry , genetics , receptor
Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease affecting premature newborns, characterized with a high mortality and chronic morbidity. We have previously found that VEGF‐A is decreased in human and experimental NEC and may play a role in NEC. However, which cell type(s) produce(s) VEGF‐A in the neonatal intestine remains unknown. Here, to determine the cellular origin of VEGF expression in normal mouse and human intestines, fixed small intestinal tissues of newborn mice and a human neonate with intestinal atresia were examined by immunofluorescence staining for VEGF‐A together with CD31, chromogranin A. To determine whether VEGF‐A was expressed in monocytes, intestines from CX3CR1‐GFP mice were used. In both intestinal tissues of mouse and human neonates, we found that VEGF‐A is strongly present in epithelial cells expressing chromogranin A, in myenteric neural plexus cells and in CD31 + cells. However, VEGF‐A was not detected in CX3CR1 + cells in the mouse intestine or in CD45 + cells in the intestine of humans. In conclusion, VEGF‐A is strongly expressed in enteroendocrine cells, myenteric neural plexus cells and endothelial cells, but not in myeloid‐derived cells. Therefore, we speculate that enteroendocrine cells may be critical for supporting the development of the intestinal villi microvasculature. Support or Funding Information Memorial Foundation (Friends of Prentice) and NIH grant R01HD060876 (IDP).