Tails of the unexpected: palatal medial edge epithelium is no more specialized than other embryonic epithelium

Brown, N.J.; Sandy, Jonathan R

doi:10.1111/j.1601-6343.2007.00379.x

Cited by 4 publications

(1 citation statement)

References 71 publications

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“…CLP is the most common congenital facial malformation in humans and occurs in approximately 1/700 live births (Brown and Sandy, 2007 ). However, CPO is the rarest form of oral clefting, with an incidence ranging from 1.3 to 25.3/10,000 live births (Burg et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Chemokine Signaling during Midline Epithelial Seam Disintegration Facilitates Palatal Fusion

Suttorp

Cremers

Rheden

et al. 2017

Front. Cell Dev. Biol.

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Disintegration of the midline epithelial seam (MES) is crucial for palatal fusion, and failure results in cleft palate. Palatal fusion and wound repair share many common signaling pathways related to epithelial-mesenchymal cross-talk. We postulate that chemokine CXCL11, its receptor CXCR3, and the cytoprotective enzyme heme oxygenase (HO), which are crucial during wound repair, also play a decisive role in MES disintegration. Fetal growth restriction and craniofacial abnormalities were present in HO-2 knockout (KO) mice without effects on palatal fusion. CXCL11 and CXCR3 were highly expressed in the disintegrating MES in both wild-type and HO-2 KO animals. Multiple apoptotic DNA fragments were present within the disintegrating MES and phagocytized by recruited CXCR3-positive wt and HO-2 KO macrophages. Macrophages located near the MES were HO-1-positive, and more HO-1-positive cells were present in HO-2 KO mice compared to wild-type. This study of embryonic and palatal development provided evidence that supports the hypothesis that the MES itself plays a prominent role in palatal fusion by orchestrating epithelial apoptosis and macrophage recruitment via CXCL11-CXCR3 signaling.

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Section: Introductionmentioning

confidence: 99%