title: Involvement of periostin in regression of hyaloidvascular system during ocular development.
abstract: OBJECTIVE
  A timely regression of the hyaloid vascular system (HVS) is required for the normal ocular development. Although macrophages have a critical role in this process, the exact mechanism remains undetermined. Periostin is a matricellular protein involved in tissue and vascular remodeling. The purpose of our study was to determine whether periostin is involved in the HVS regression.
  
  
  METHODS
  We used wild type (WT) and periostin knockout (KO) mice. Indocyanine green angiography and immunohistochemistry with isolectin B4 were used to evaluate the HVS regression. TUNEL-labeling was used to quantify the number of apoptotic hyaloid vascular endothelial cells. F4/80 and Iba-1 staining was performed to determine the number and location of macrophages in the vitreous. The location of periostin also was investigated by immunohistochemistry. To determine the functional role of periostin, the degree of adhesion of human monocytes to fibronectin was measured by an adhesion assay.
  
  
  RESULTS
  The HVS regression and peak in the number of TUNEL-positive apoptotic endothelial cells were delayed in periostin KO mice. The number of F4/80 positive cells in the vitreous was higher in periostin KO mice. Only a small number of Iba-1-positive cells near the hyaloid vessels was co-stained with periostin, and peripheral blood monocytes were not stained with periostin. Adhesion assay showed that periostin increased the degree of attachment of monocytes to fibronectin.
  
  
  CONCLUSIONS
  These results suggest that periostin, which is secreted by the intraocular macrophages, enhances the HVS regression by intensifying the adhesion of macrophages to hyaloid vessels.
authors.affiliation: Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Arima
authors.forename: Shigeo
authors.initials: S
authors.lastname: Yoshida
authors.forename: Takahito
authors.initials: T
authors.lastname: Nakama
authors.forename: Keijiro
authors.initials: K
authors.lastname: Ishikawa
authors.forename: Shintaro
authors.initials: S
authors.lastname: Nakao
authors.forename: Takeru
authors.initials: T
authors.lastname: Yoshimura
authors.forename: Ryo
authors.initials: R
authors.lastname: Asato
authors.forename: Yukio
authors.initials: Y
authors.lastname: Sassa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Enaida
authors.forename: Yuji
authors.initials: Y
authors.lastname: Oshima
authors.forename: Akira
authors.initials: A
authors.lastname: Matsuda
authors.forename: Akira
authors.initials: A
authors.lastname: Kudo
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Ishibashi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002448:Cell Adhesion / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000235:genetics* / Q000378:metabolism; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology*; D005353:Fibronectins / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D006801:Humans; D008264:Macrophages / Q000166:cytology / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009000:Monocytes / Q000166:cytology / Q000502:physiology; D009414:Nerve Growth Factors / Q000235:genetics / Q000378:metabolism; D012171:Retinal Vessels / Q000254:growth & development* / Q000502:physiology; D014822:Vitreous Body / Q000098:blood supply* / Q000254:growth & development* / Q000502:physiology
chemical_list: D015815:Cell Adhesion Molecules; D015816:Cell Adhesion Molecules, Neuronal; D005353:Fibronectins; D009414:Nerve Growth Factors; C484439:Ninj1 protein, mouse; C082838:Postn protein, mouse