Publication: Endothelin-1 and endothelinconverting
enzyme-1 in human granulomatous
pathology of eyelid: an immunohistochemical
and in situ hybridization study in chalazia
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Date
2007
Authors
Massai, L. ; Volpi, N. ; Carbotti, P. ; Fruschelli, M. ; Mencarelli, M. ; Pecorelli, A. ; Muscettola, M. ; Aglianò, M. ; Alessandrini, C. ; Grasso, G.
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Publisher
Murcia: F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Endothelin-1 (ET-1), a potent vasoconstrictor
peptide, is involved in several functions of eye
pathophysiology, such as regulation of intraocular
tension and retinal reactive vasoconstriction. As ET-1
pro-inflammatory and fibrosing activity is emerging in
different fields of pathology, we investigated the
expression of ET-1 and endothelin-converting enzyme-1
(ECE-1) in chalazia, granulomatous lesions of the
eyelid.
ET-1 and ECE-1 were analyzed by immunohistochemistry
(IHC) in twenty surgically removed
chalazia, with regard to expression in eyelid structures
and inflammatory infiltrate. Phenotype of ET-1
expressing inflammatory cells was established by double
immunofluorescence. The cellular localization of prepro-
ET-1 (pp-ET-1) mRNA and ECE-1 mRNA was studied
by nonisotopic in situ hybridization (ISH).
Neutrophils (PMNs), macrophages and Tlymphocytes
were scattered in stroma, around alveoli
and grouped in lipogranulomas. PMNs, macrophages,
basal epithelium of meibomian adenomers and central
ducts immunostained for ET-1. ECE-1 protein was found
in meibomian adenomers, conjunctival epithelium, tarsal
mucous glands and in inflammatory cells. Hybridization
signals for pp-ET-1 mRNA and ECE-1 mRNA were
recognized in healthy and degenerating meibomian
ducts, adenomers, inflammatory cells, as well as in
vessel walls. ECE-1 mRNA was also present in
conjunctival epithelium and Henle’s crypts. Our findings suggest that the multifunctional peptide
ET-1 may have a role in molecular genesis of tissue
damage in chalazia. ET-1 cytokine activity is likely to support the migration of inflammatory cells and the
setting of lipogranulomas; ET-1 stimulation might
contribute to proliferation of fibroblasts and collagen
synthesis. ET-1 upregulation on meibomian adenomers
and ducts may further enhance granulomas formation by
stimulating lipid release.
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