Periostin and tenascin-C interaction promotes angiogenesis in ischemic proliferative retinopathy.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
09 06 2020
Historique:
received: 16 09 2019
accepted: 18 05 2020
entrez: 11 6 2020
pubmed: 11 6 2020
medline: 15 12 2020
Statut: epublish

Résumé

Ischemic proliferative retinopathy (IPR), such as proliferative diabetic retinopathy (PDR), retinal vein occlusion and retinopathy of prematurity is a major cause of vision loss. Our previous studies demonstrated that periostin (PN) and tenascin-C (TNC) are involved in the pathogenesis of IPR. However, the interactive role of PN and TNC in angiogenesis associated with IPR remain unknown. We found significant correlation between concentrations of PN and TNC in PDR vitreous humor. mRNA and protein expression of PN and TNC were found in pre-retinal fibrovascular membranes excised from PDR patients. Interleukin-13 (IL-13) promoted mRNA and protein expression of PN and TNC, and co-immunoprecipitation assay revealed binding between PN and TNC in human microvascular endothelial cells (HRECs). IL-13 promoted angiogenic functions of HRECs. Single inhibition of PN or TNC and their dual inhibition by siRNA suppressed the up-regulated angiogenic functions. Pathological pre-retinal neovessels of oxygen-induced retinopathy (OIR) mice were attenuated in PN knock-out, TNC knock-out and dual knock-out mice compared to wild-type mice. Both in vitro and in vivo, PN inhibition had a stronger inhibitory effect on angiogenesis compared to TNC inhibition, and had a similar effect to dual inhibition of PN and TNC. Furthermore, PN knock-out mice showed scant TNC expression in pre-retinal neovessels of OIR retinas. Our findings suggest that interaction of PN and TNC facilitates pre-retinal angiogenesis, and PN is an effective therapeutic target for IPR such as PDR.

Identifiants

pubmed: 32518264
doi: 10.1038/s41598-020-66278-1
pii: 10.1038/s41598-020-66278-1
pmc: PMC7283227
doi:

Substances chimiques

Cell Adhesion Molecules 0
Interleukin-13 0
POSTN protein, human 0
TNC protein, human 0
Tenascin 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

9299

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Auteurs

Yuki Kubo (Y)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Keijiro Ishikawa (K)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan. keijishi@med.kyushu-u.ac.jp.

Kenichiro Mori (K)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Yoshiyuki Kobayashi (Y)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Takahito Nakama (T)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Mitsuru Arima (M)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Shintaro Nakao (S)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Toshio Hisatomi (T)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Masatoshi Haruta (M)

Department of Ophthalmology, Kurume University School of Medicine, Kurume, Japan.

Koh-Hei Sonoda (KH)

Department of Ophthalmology, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.

Shigeo Yoshida (S)

Department of Ophthalmology, Kurume University School of Medicine, Kurume, Japan.

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