Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure

Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important...
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Autor*in:	Joana Ferreira-Silva [verfasserIn] Inês D. Aires [verfasserIn] Raquel Boia [verfasserIn] António Francisco Ambrósio [verfasserIn] Ana Raquel Santiago [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	adenosine A elevated hydrostatic pressure glaucoma microglia neuroinflammation

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 21(2020), 19, p 7218
Übergeordnetes Werk:	volume:21 ; year:2020 ; number:19, p 7218

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms21197218

Katalog-ID:	DOAJ03782869X

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allfields	10.3390/ijms21197218 doi (DE-627)DOAJ03782869X (DE-599)DOAJ71e576a0481648a6b7684001a3aa2c4b DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Joana Ferreira-Silva verfasserin aut Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation. adenosine A<sub<3</sub< receptor elevated hydrostatic pressure glaucoma microglia neuroinflammation Biology (General) Chemistry Inês D. Aires verfasserin aut Raquel Boia verfasserin aut António Francisco Ambrósio verfasserin aut Ana Raquel Santiago verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 19, p 7218 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:19, p 7218 https://doi.org/10.3390/ijms21197218 kostenfrei https://doaj.org/article/71e576a0481648a6b7684001a3aa2c4b kostenfrei https://www.mdpi.com/1422-0067/21/19/7218 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 19, p 7218
spelling	10.3390/ijms21197218 doi (DE-627)DOAJ03782869X (DE-599)DOAJ71e576a0481648a6b7684001a3aa2c4b DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Joana Ferreira-Silva verfasserin aut Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation. adenosine A<sub<3</sub< receptor elevated hydrostatic pressure glaucoma microglia neuroinflammation Biology (General) Chemistry Inês D. Aires verfasserin aut Raquel Boia verfasserin aut António Francisco Ambrósio verfasserin aut Ana Raquel Santiago verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 19, p 7218 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:19, p 7218 https://doi.org/10.3390/ijms21197218 kostenfrei https://doaj.org/article/71e576a0481648a6b7684001a3aa2c4b kostenfrei https://www.mdpi.com/1422-0067/21/19/7218 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 19, p 7218
allfields_unstemmed	10.3390/ijms21197218 doi (DE-627)DOAJ03782869X (DE-599)DOAJ71e576a0481648a6b7684001a3aa2c4b DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Joana Ferreira-Silva verfasserin aut Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation. adenosine A<sub<3</sub< receptor elevated hydrostatic pressure glaucoma microglia neuroinflammation Biology (General) Chemistry Inês D. Aires verfasserin aut Raquel Boia verfasserin aut António Francisco Ambrósio verfasserin aut Ana Raquel Santiago verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 19, p 7218 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:19, p 7218 https://doi.org/10.3390/ijms21197218 kostenfrei https://doaj.org/article/71e576a0481648a6b7684001a3aa2c4b kostenfrei https://www.mdpi.com/1422-0067/21/19/7218 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 19, p 7218
allfieldsGer	10.3390/ijms21197218 doi (DE-627)DOAJ03782869X (DE-599)DOAJ71e576a0481648a6b7684001a3aa2c4b DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Joana Ferreira-Silva verfasserin aut Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation. adenosine A<sub<3</sub< receptor elevated hydrostatic pressure glaucoma microglia neuroinflammation Biology (General) Chemistry Inês D. Aires verfasserin aut Raquel Boia verfasserin aut António Francisco Ambrósio verfasserin aut Ana Raquel Santiago verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 19, p 7218 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:19, p 7218 https://doi.org/10.3390/ijms21197218 kostenfrei https://doaj.org/article/71e576a0481648a6b7684001a3aa2c4b kostenfrei https://www.mdpi.com/1422-0067/21/19/7218 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 19, p 7218
allfieldsSound	10.3390/ijms21197218 doi (DE-627)DOAJ03782869X (DE-599)DOAJ71e576a0481648a6b7684001a3aa2c4b DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Joana Ferreira-Silva verfasserin aut Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation. adenosine A<sub<3</sub< receptor elevated hydrostatic pressure glaucoma microglia neuroinflammation Biology (General) Chemistry Inês D. Aires verfasserin aut Raquel Boia verfasserin aut António Francisco Ambrósio verfasserin aut Ana Raquel Santiago verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 19, p 7218 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:19, p 7218 https://doi.org/10.3390/ijms21197218 kostenfrei https://doaj.org/article/71e576a0481648a6b7684001a3aa2c4b kostenfrei https://www.mdpi.com/1422-0067/21/19/7218 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 19, p 7218
language	English
source	In International Journal of Molecular Sciences 21(2020), 19, p 7218 volume:21 year:2020 number:19, p 7218
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author	Joana Ferreira-Silva
spellingShingle	Joana Ferreira-Silva misc QH301-705.5 misc QD1-999 misc adenosine A<sub<3</sub< receptor misc elevated hydrostatic pressure misc glaucoma misc microglia misc neuroinflammation misc Biology (General) misc Chemistry Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure
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title	Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure
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title_sort	activation of adenosine a<sub<3</sub< receptor inhibits microglia reactivity elicited by elevated pressure
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title_auth	Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure
abstract	Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation.
abstractGer	Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation.
abstract_unstemmed	Glaucoma is a progressive chronic retinal degenerative disease and a leading cause of global irreversible blindness, characterized by optic nerve damage and retinal ganglion cell (RGC) death. Elevated intraocular pressure (IOP) is a main risk factor of glaucoma. Neuroinflammation plays an important role in glaucoma. We have been demonstrating that elevated pressure triggers microglia reactivity that contribute to the loss of RGCs. Adenosine, acting on adenosine receptors, is a crucial modulator of microglia phenotype. Microglia express all adenosine receptors. Previously, we demonstrated that the activation of adenosine A<sub<3</sub< receptor (A<sub<3</sub<R) affords protection to the retina, including RGCs, unveiling the possibility for a new strategy for glaucoma treatment. Since microglial cells express A<sub<3</sub<R, we now studied the ability of a selective A<sub<3</sub<R agonist (2-Cl-IB-MECA) in controlling microglia reactivity induced by elevated hydrostatic pressure (EHP), used to mimic elevated IOP. The activation of A<sub<3</sub<R reduced EHP-induced inducible nitric oxide synthase (iNOS) expression, microglia migration and phagocytosis in BV-2 cells. In retinal microglia, proliferation and phagocytosis elicited by EHP were also decreased by A<sub<3</sub<R activation. This work demonstrates that 2-Cl-IB-MECA, the selective agonist of A<sub<3</sub<R, is able to hinder microglia reactivity, suggesting that A<sub<3</sub<R agonists could afford protection against glaucomatous degeneration through the control of neuroinflammation.
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Activation of Adenosine A<sub<3</sub< Receptor Inhibits Microglia Reactivity Elicited by Elevated Pressure

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