Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration
Young Joon Jo, Koh Hei Sonoda, Yuji Oshima, Atsunobu Takeda, Ri Ichiro Kohno, Jun Yamada, Junji Hamuro, Yang Yang, Shoji Notomi, Toshio Hisatomi, Tatsuro Ishibashi
PURPOSE. Subretinal fibrosis causes damage to visual acuity, especially if the lesion is in the macula, as is frequently observed in advanced age-related macular degeneration. Exudate leukocytes form abnormal vessels that initiate regional inflammation accompanied with local glial proliferation and matrix production. The purpose of this study was to establish an animal model of focal subretinal fibrosis. METHODS. Macrophage-rich peritoneal exudate cells (PECs) were injected into the subretinal space of C57BL/6 or MCP-1 knockout (KO) mice. Seven days later, the size of the subretinal fibrotic tissue was evaluated by the adherent area of glial fibrillary acidic protein (GFAP)-positive retinal glial cells on choroidal flat mounts. Myofibroblastic changes and collagen synthesis were detected by α-smooth muscle actin (α-SMA) and Masson trichrome staining of the histologic section, respectively. α-SMA expression was also examined on retinal pigment epithelium (RPE) cells during co-culture with activated macrophages. RESULTS. Subretinal fibrous tissue was observed by funduscopy in PEC-injected mice after 7 days. The tissue consisted of a monotonous, low-cell-density area that expressed α-SMA with collagen synthesis. Both steroid and antioxidant treatment can reduce residual glia. Because PEC-injected MCP-1 KO mice showed less residual glia, not only exogenous macrophages, but also intrinsic macrophages were activated. The macrophages directly induced myofibrotic changes in RPE cells in vitro. CONCLUSIONS. Activated macrophages form subretinal fibrosis when they are placed in the subretinal space and induce myofibrotic changes in RPE cells.
Investigative Ophthalmology and Visual Science
https://doi.org/10.1167/iovs.10-5189
10.1167/iovs.10-5189
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Macular Degeneration Medicine & Life Sciences 100%
Exudates and Transudates Medicine & Life Sciences 69%
Macrophages Medicine & Life Sciences 55%
Retinal Pigment Epithelium Medicine & Life Sciences 54%
Knockout Mice Medicine & Life Sciences 29%
Jo, Y. J., Sonoda, K. H., Oshima, Y., Takeda, A., Kohno, R. I., Yamada, J., Hamuro, J., Yang, Y., Notomi, S., Hisatomi, T., & Ishibashi, T. (2011). Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration. Investigative Ophthalmology and Visual Science, 52(9), 6089-6095. https://doi.org/10.1167/iovs.10-5189
Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration. / Jo, Young Joon; Sonoda, Koh Hei; Oshima, Yuji; Takeda, Atsunobu; Kohno, Ri Ichiro; Yamada, Jun; Hamuro, Junji; Yang, Yang; Notomi, Shoji; Hisatomi, Toshio; Ishibashi, Tatsuro.
In: Investigative Ophthalmology and Visual Science, Vol. 52, No. 9, 08.2011, p. 6089-6095.
Jo, YJ, Sonoda, KH, Oshima, Y, Takeda, A, Kohno, RI, Yamada, J, Hamuro, J, Yang, Y, Notomi, S, Hisatomi, T & Ishibashi, T 2011, 'Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration', Investigative Ophthalmology and Visual Science, vol. 52, no. 9, pp. 6089-6095. https://doi.org/10.1167/iovs.10-5189
Jo YJ, Sonoda KH, Oshima Y, Takeda A, Kohno RI, Yamada J et al. Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration. Investigative Ophthalmology and Visual Science. 2011 Aug;52(9):6089-6095. https://doi.org/10.1167/iovs.10-5189
Jo, Young Joon ; Sonoda, Koh Hei ; Oshima, Yuji ; Takeda, Atsunobu ; Kohno, Ri Ichiro ; Yamada, Jun ; Hamuro, Junji ; Yang, Yang ; Notomi, Shoji ; Hisatomi, Toshio ; Ishibashi, Tatsuro. / Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration. In: Investigative Ophthalmology and Visual Science. 2011 ; Vol. 52, No. 9. pp. 6089-6095.
@article{b29c5b662f2844ed817246d85614926e,
title = "Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration",
abstract = "PURPOSE. Subretinal fibrosis causes damage to visual acuity, especially if the lesion is in the macula, as is frequently observed in advanced age-related macular degeneration. Exudate leukocytes form abnormal vessels that initiate regional inflammation accompanied with local glial proliferation and matrix production. The purpose of this study was to establish an animal model of focal subretinal fibrosis. METHODS. Macrophage-rich peritoneal exudate cells (PECs) were injected into the subretinal space of C57BL/6 or MCP-1 knockout (KO) mice. Seven days later, the size of the subretinal fibrotic tissue was evaluated by the adherent area of glial fibrillary acidic protein (GFAP)-positive retinal glial cells on choroidal flat mounts. Myofibroblastic changes and collagen synthesis were detected by α-smooth muscle actin (α-SMA) and Masson trichrome staining of the histologic section, respectively. α-SMA expression was also examined on retinal pigment epithelium (RPE) cells during co-culture with activated macrophages. RESULTS. Subretinal fibrous tissue was observed by funduscopy in PEC-injected mice after 7 days. The tissue consisted of a monotonous, low-cell-density area that expressed α-SMA with collagen synthesis. Both steroid and antioxidant treatment can reduce residual glia. Because PEC-injected MCP-1 KO mice showed less residual glia, not only exogenous macrophages, but also intrinsic macrophages were activated. The macrophages directly induced myofibrotic changes in RPE cells in vitro. CONCLUSIONS. Activated macrophages form subretinal fibrosis when they are placed in the subretinal space and induce myofibrotic changes in RPE cells.",
author = "Jo, {Young Joon} and Sonoda, {Koh Hei} and Yuji Oshima and Atsunobu Takeda and Kohno, {Ri Ichiro} and Jun Yamada and Junji Hamuro and Yang Yang and Shoji Notomi and Toshio Hisatomi and Tatsuro Ishibashi",
doi = "10.1167/iovs.10-5189",
journal = "Investigative Ophthalmology",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
T1 - Establishment of a new animal model of focal subretinal fibrosis that resembles disciform lesion in advanced age-related macular degeneration
AU - Jo, Young Joon
AU - Sonoda, Koh Hei
AU - Oshima, Yuji
AU - Takeda, Atsunobu
AU - Kohno, Ri Ichiro
AU - Hamuro, Junji
AU - Yang, Yang
AU - Notomi, Shoji
AU - Hisatomi, Toshio
AU - Ishibashi, Tatsuro
N2 - PURPOSE. Subretinal fibrosis causes damage to visual acuity, especially if the lesion is in the macula, as is frequently observed in advanced age-related macular degeneration. Exudate leukocytes form abnormal vessels that initiate regional inflammation accompanied with local glial proliferation and matrix production. The purpose of this study was to establish an animal model of focal subretinal fibrosis. METHODS. Macrophage-rich peritoneal exudate cells (PECs) were injected into the subretinal space of C57BL/6 or MCP-1 knockout (KO) mice. Seven days later, the size of the subretinal fibrotic tissue was evaluated by the adherent area of glial fibrillary acidic protein (GFAP)-positive retinal glial cells on choroidal flat mounts. Myofibroblastic changes and collagen synthesis were detected by α-smooth muscle actin (α-SMA) and Masson trichrome staining of the histologic section, respectively. α-SMA expression was also examined on retinal pigment epithelium (RPE) cells during co-culture with activated macrophages. RESULTS. Subretinal fibrous tissue was observed by funduscopy in PEC-injected mice after 7 days. The tissue consisted of a monotonous, low-cell-density area that expressed α-SMA with collagen synthesis. Both steroid and antioxidant treatment can reduce residual glia. Because PEC-injected MCP-1 KO mice showed less residual glia, not only exogenous macrophages, but also intrinsic macrophages were activated. The macrophages directly induced myofibrotic changes in RPE cells in vitro. CONCLUSIONS. Activated macrophages form subretinal fibrosis when they are placed in the subretinal space and induce myofibrotic changes in RPE cells.
AB - PURPOSE. Subretinal fibrosis causes damage to visual acuity, especially if the lesion is in the macula, as is frequently observed in advanced age-related macular degeneration. Exudate leukocytes form abnormal vessels that initiate regional inflammation accompanied with local glial proliferation and matrix production. The purpose of this study was to establish an animal model of focal subretinal fibrosis. METHODS. Macrophage-rich peritoneal exudate cells (PECs) were injected into the subretinal space of C57BL/6 or MCP-1 knockout (KO) mice. Seven days later, the size of the subretinal fibrotic tissue was evaluated by the adherent area of glial fibrillary acidic protein (GFAP)-positive retinal glial cells on choroidal flat mounts. Myofibroblastic changes and collagen synthesis were detected by α-smooth muscle actin (α-SMA) and Masson trichrome staining of the histologic section, respectively. α-SMA expression was also examined on retinal pigment epithelium (RPE) cells during co-culture with activated macrophages. RESULTS. Subretinal fibrous tissue was observed by funduscopy in PEC-injected mice after 7 days. The tissue consisted of a monotonous, low-cell-density area that expressed α-SMA with collagen synthesis. Both steroid and antioxidant treatment can reduce residual glia. Because PEC-injected MCP-1 KO mice showed less residual glia, not only exogenous macrophages, but also intrinsic macrophages were activated. The macrophages directly induced myofibrotic changes in RPE cells in vitro. CONCLUSIONS. Activated macrophages form subretinal fibrosis when they are placed in the subretinal space and induce myofibrotic changes in RPE cells.
U2 - 10.1167/iovs.10-5189
DO - 10.1167/iovs.10-5189
JO - Investigative Ophthalmology
JF - Investigative Ophthalmology