Periostin promotes the generation of fibrous membranes in proliferative vitreoretinopathy

Ishikawa, Keijiro; Yoshida, Shigeo; Nakao, Shintaro; Nakama, Takahito; Kita, Takeshi; Asato, Ryo; Sassa, Yukio; Arita, Ryoichi; Miyazaki, Masao; Enaida, Hiroshi; Oshima, Yuji; Murakami, Noboru; Niiro, Hiroaki; Ono, Junya; Matsuda, Akira; Goto, Yoshinobu; Akashi, Koichi; Izuhara, Kenji; Kudo, Akira; Kono, Toshihiro; Hafezi-Moghadam, Ali; Ishibashi, Tatsuro

doi:10.1096/fj.13-229740

Cited by 56 publications

(54 citation statements)

References 48 publications

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“…We recently reported an increased expression of periostin in the vitreous and ERMs obtained from patients with PDR and proliferative vitreoretinopathy 14 22 23. In the present study, we showed a higher correlation between the vitreous levels of M-CSF, sCD163 and periostin in eyes with PDR.…”

Section: Discussionsupporting

confidence: 68%

Increased expression of M-CSF and IL-13 in vitreous of patients with proliferative diabetic retinopathy: implications for M2 macrophage-involving fibrovascular membrane formation

et al. 2014

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Section: Discussionsupporting

confidence: 68%

Increased expression of M-CSF and IL-13 in vitreous of patients with proliferative diabetic retinopathy: implications for M2 macrophage-involving fibrovascular membrane formation

et al. 2014

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“…Periostin has been shown to induce proliferation by activating phosphatidylinositol 3-kinase (PI3K)-dependent pathways (18,32). LY294002, an inhibitor that competes with the ATP binding site in the catalytic domain of PI3K, significantly decreased HTS fibroblast proliferation both in the presence and absence of matrix-associated periostin (P < 0.05, data not shown).…”

Section: Resultsmentioning

confidence: 98%

Periostin induces fibroblast proliferation and myofibroblast persistence in hypertrophic scarring

Crawford

Nygard

Gan

et al. 2015

Experimental Dermatology

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Hypertrophic scarring is characterized by the excessive development and persistence of myofibroblasts. These cells contract the surrounding extracellular matrix resulting in the increased tissue density characteristic of scar tissue. Periostin is a matricellular protein that is abnormally abundant in fibrotic dermis, however, its roles in hypertrophic scarring are largely unknown. In this report, we assessed the ability of matrix-associated periostin to promote the proliferation and myofibroblast differentiation of dermal fibroblasts isolated from the dermis of hypertrophic scars or healthy skin. Supplementation of a thin type-I collagen cell culture substrate with recombinant periostin induced a significant increase in the proliferation of hypertrophic scar fibroblasts but not normal dermal fibroblasts. Periostin induced significant increases in supermature focal adhesion formation, α smooth muscle actin levels and collagen contraction in fibroblasts cultured from hypertrophic scars under conditions of increased matrix tension in three-dimensional type-I collagen lattices. Inhibition of Rho-associated protein kinase activity significantly attenuated the effects of matrix-associated periostin on hypertrophic scar fibroblasts and myofibroblasts. Depletion of endogenous periostin expression in hypertrophic scar myofibroblasts resulted in a sustained decrease in α smooth muscle actin levels under conditions of reducing matrix tension, while matrix-associated periostin levels caused the cells to retain high levels of a smooth muscle actin under these conditions. These findings indicate that periostin promotes Rho-associated protein kinase-dependent proliferation and myofibroblast persistence of hypertrophic scar fibroblasts and implicate periostin as a potential therapeutic target to enhance the resolution of scars.

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“…27 Briefly, 5 Â 10 4 cells were seeded in each well and transfected with or without siRNAs. After 1 hour of pretreatment with Dulbecco's modified Eagle's medium with 3% fetal bovine serum containing recombinant TGF-b2 with 5 mmol/L aphidicolin (Sigma-Aldrich) to inhibit cell division, the stoppers were removed to allow cells to migrate into the detection zone.…”

Section: Cell Migration Assaymentioning

confidence: 99%

αB-Crystallin Regulates Subretinal Fibrosis by Modulation of Epithelial-Mesenchymal Transition

Ishikawa

Sreekumar

Spee

et al. 2016

The American Journal of Pathology

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Subretinal fibrosis is an end stage of neovascular age-related macular degeneration, characterized by fibrous membrane formation after choroidal neovascularization. An initial step of the pathogenesis is an epithelial-mesenchymal transition (EMT) of retinal pigment epithelium cells. aB-crystallin plays multiple roles in age-related macular degeneration, including cytoprotection and angiogenesis. However, the role of aB-crystallin in subretinal EMT and fibrosis is unknown. Herein, we showed attenuation of subretinal fibrosis after regression of laser-induced choroidal neovascularization and a decrease in mesenchymal retinal pigment epithelium cells in aB-crystallin knockout mice compared with wild-type mice. aB-crystallin was prominently expressed in subretinal fibrotic lesions in mice. In vitro, overexpression of aB-crystallin induced EMT, whereas suppression of aB-crystallin induced a mesenchymal-epithelial transition. Transforming growth factor-b2einduced EMT was further enhanced by overexpression of aB-crystallin but was inhibited by suppression of aB-crystallin. Silencing of aB-crystallin inhibited multiple fibrotic processes, including cell proliferation, migration, and fibronectin production. Bone morphogenetic protein 4 upregulated aB-crystallin, and its EMT induction was inhibited by knockdown of aB-crystallin. Furthermore, inhibition of aB-crystallin enhanced monotetraubiquitination of SMAD4, which can impair its nuclear localization. Overexpression of aB-crystallin enhanced nuclear translocation and accumulation of SMAD4 and SMAD5. Thus, aB-crystallin is an important regulator of EMT, acting as a molecular chaperone for SMAD4 and as its potential therapeutic target for preventing subretinal fibrosis development in neovascular age-related macular degeneration. (Am J Pathol 2016, 186: 859e873; http:// dx

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Periostin promotes the generation of fibrous membranes in proliferative vitreoretinopathy

Cited by 56 publications

References 48 publications

Increased expression of M-CSF and IL-13 in vitreous of patients with proliferative diabetic retinopathy: implications for M2 macrophage-involving fibrovascular membrane formation

Increased expression of M-CSF and IL-13 in vitreous of patients with proliferative diabetic retinopathy: implications for M2 macrophage-involving fibrovascular membrane formation

Periostin induces fibroblast proliferation and myofibroblast persistence in hypertrophic scarring

αB-Crystallin Regulates Subretinal Fibrosis by Modulation of Epithelial-Mesenchymal Transition

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