2014
DOI: 10.1016/j.amjoto.2013.08.008
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Connexin 32 and 43 mutations: Do they play a role in chronic rhinosinusitis?

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Cited by 2 publications
(2 citation statements)
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“…Cx26 was identified in human fetal tissue, and Cx43 in whole nasal tissue . Mutations of some connexin channels have been investigated as a potential cause for dysfunction of sinonasal epithelium, but were found to be rare . Other research examining the potential role of connexin gap junctions in the rhinologic literature include a group that reported suppressed Cx26 levels in primary human nasal epithelial cells of patients with allergic rhinitis, and concluded that aeroallergens may have a direct effect on the suppression .…”
Section: Discussionmentioning
confidence: 99%
“…Cx26 was identified in human fetal tissue, and Cx43 in whole nasal tissue . Mutations of some connexin channels have been investigated as a potential cause for dysfunction of sinonasal epithelium, but were found to be rare . Other research examining the potential role of connexin gap junctions in the rhinologic literature include a group that reported suppressed Cx26 levels in primary human nasal epithelial cells of patients with allergic rhinitis, and concluded that aeroallergens may have a direct effect on the suppression .…”
Section: Discussionmentioning
confidence: 99%
“…A recent report revealed that 16 connexin genes are expressed in the human sinus mucosa [ 3 ]. One report found that connexin-43 is significantly upregulated in CRS patients compared to healthy controls at both the mRNA and protein levels, whereas other reports searching for a potential cause of dysfunction in the sinonasal epithelium failed to find a significant difference in the expressions of connexin-26, -30, -32, or -43 [ 3 5 ]. Although the relationship between CRS and connexin expression is still controversial, those reports have consistently shown that connexin-43 is expressed in human nasal epithelial cells.…”
mentioning
confidence: 99%