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Neurosteroids as regulators of neuroinflammation

Yilmaz, Canelif, Karali, Kanelina, Fodelianaki, Georgia, Gravanis, Achille, Chavakis, Triantafyllos, Charalampopoulos, Ioannis, Alexaki, Vasileia Ismini·2019·Frontiers in Neuroendocrinology
DOI 10.1016/j.yfrne.2019.100788
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Fig. 1 Functions and signaling of 17 β -estradiol in CNS cells. 17 β -estradiol derives in the CNS from neurons, astrocytes and the circulation (Zwain and Yen, 1999; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia it can activate ER α and ER β mediating anti-in fl ammatory e ff ects by suppressing TNF, IL-6 or iNOS expression (Saijo et al., 2011; Smith et al., 2011; Brown et al., 2010; Soucy et al., 2005; Vegeto et al., 2001; Wu et al., 2016; Cerciat et al., 2010; Ishihara et al., 2015; Sarkaki et al., 2013; Barreto et al., 2007; Khaksari et al., 2011; Khaksari et al., 2015; Liu et al., 2005; Bruce-Keller et al., 2000; Sierra et al., 2008). Additionally, through the membrane receptor GPR30 it can activate rapid signaling events, such as Ca 2+ , cAMP or ERK signaling potentially mediating antiin fl ammatory e ff ects (Blasko et al., 2009; Guan et al., 2017; Alexaki et al., 2006; Schaufelberger et al., 2016; Zhang et al., 2018; Prossnitz and Barton, 2014; Prossnitz and Barton, 2011; Liu et al., 2013; Revankar et al., 2005; Filardo et al., 2000; Alexaki et al., 2004). 17 β -estradiol was also reported to negatively regulate infl ammasome activation by a yet unknown mechanism (Thakkar et al., 2016). In astrocytes it can activate ER α signaling diminishing chemokine expression (Spence et al., 2013; Spence et al., 2011; Kuo et al., 2010). The release of 17 β -estradiol is presented by a solid line and its e ff ects by a dashed line. Abbreviations: cAMP: cyclic adenosine monophosphate, CCL2: CC-chemokine ligand 2, CCL7: CC-chemokine ligand 7, ER α : estrogen receptor α , ER β : estrogen receptor β , Ε RK1/2: extracellular signal -regulated kinases 1/2, GPR30: G protein-coupled receptor 30, IL1 β : Interleukin 1 β , IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, NLRP3: NLR family pyrin domain containing 3, TNF: Tumor Necrosis Factor.
Fig. 1 Functions and signaling of 17 β -estradiol in CNS cells. 17 β -estradiol derives in the CNS from neurons, astrocytes and the circulation (Zwain and Yen, 1999; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia it can activate ER α and ER β mediating anti-in fl ammatory e ff ects by suppressing TNF, IL-6 or iNOS expression (Saijo et al., 2011; Smith et al., 2011; Brown et al., 2010; Soucy et al., 2005; Vegeto et al., 2001; Wu et al., 2016; Cerciat et al., 2010; Ishihara et al., 2015; Sarkaki et al., 2013; Barreto et al., 2007; Khaksari et al., 2011; Khaksari et al., 2015; Liu et al., 2005; Bruce-Keller et al., 2000; Sierra et al., 2008). Additionally, through the membrane receptor GPR30 it can activate rapid signaling events, such as Ca 2+ , cAMP or ERK signaling potentially mediating antiin fl ammatory e ff ects (Blasko et al., 2009; Guan et al., 2017; Alexaki et al., 2006; Schaufelberger et al., 2016; Zhang et al., 2018; Prossnitz and Barton, 2014; Prossnitz and Barton, 2011; Liu et al., 2013; Revankar et al., 2005; Filardo et al., 2000; Alexaki et al., 2004). 17 β -estradiol was also reported to negatively regulate infl ammasome activation by a yet unknown mechanism (Thakkar et al., 2016). In astrocytes it can activate ER α signaling diminishing chemokine expression (Spence et al., 2013; Spence et al., 2011; Kuo et al., 2010). The release of 17 β -estradiol is presented by a solid line and its e ff ects by a dashed line. Abbreviations: cAMP: cyclic adenosine monophosphate, CCL2: CC-chemokine ligand 2, CCL7: CC-chemokine ligand 7, ER α : estrogen receptor α , ER β : estrogen receptor β , Ε RK1/2: extracellular signal -regulated kinases 1/2, GPR30: G protein-coupled receptor 30, IL1 β : Interleukin 1 β , IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, NLRP3: NLR family pyrin domain containing 3, TNF: Tumor Necrosis Factor.CC-BY-NC-ND · From the PDF
Fig. 2 Functions and signaling of progesterone and allopregnanolone in CNS cells. In the CNS progesterone and allopregnanolone derive from the periphery, astrocytes and oligodendrocytes (Zwain and Yen, 1999; Gago et al., 2001; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia progesterone activates membrane PR α and PGMRC1 (Bali et al., 2013; Bali et al., 2013; Roche et al., 2016; Me ff re et al., 2013) and can down-regulate in fl ammasome activation, inhibit the expression of pro-in fl ammatory genes, such as TNF, IL-6, iNOS, MHCII and COX2, and enhance the expression of TREM2, CD206 or TGF β (Aryanpour et al., 2017; Lei et al., 2014; Cutler et al., 2007; Hua et al., 2011). Astrocytes express PR and PGMRC1 (Bali et al., 2013; Bali et al., 2013; Me ff re et al., 2005) and progesterone might induce BDNF release in a Pgrmc1-dependent manner, thereby promoting cell survival (Jodhka et al., 2009; Su et al., 2012; Sun et al., 2016; Kaur et al., 2007; Atif et al., 2013). On the other hand, allopregnanolone binds to GABAA receptors in microglia as well as astrocytes mediating antiin fl ammatory e ff ects through NF κ B inhibition (Singh et al., 2013; Lambert et al., 2003; Lee et al., 2011). The release of progesterone and allopregnanolone is marked by solid lines and their e ff ects by dashed lines. Abbreviations: BDNF: Brain-derived neurotrophic factor, CD206: Cluster of Di ff erentiation 206, COX2: cyclooxygenase 2, GABAAR: γ -aminobutyric acid type A receptor, IL1 β : Interleukin 1 β , IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, MHCII: major histocompatibility complex class II, NLRP3: NLR family pyrin domain containing 3, mPR α : membrane progesterone receptor α , NF κ B: nuclear factor ' kappa-light-chain-enhancer ' of activated B-cells, NLRP3: NLR family pyrin domain containing 3, PGMRC1: progesterone membrane receptor component 1, PR: progesterone receptor, TGF β : Transforming Growth Factor β , TNF: Tumor Necrosis Factor, TREM2: Triggering receptor expressed on myeloid cells 2.
Fig. 2 Functions and signaling of progesterone and allopregnanolone in CNS cells. In the CNS progesterone and allopregnanolone derive from the periphery, astrocytes and oligodendrocytes (Zwain and Yen, 1999; Gago et al., 2001; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia progesterone activates membrane PR α and PGMRC1 (Bali et al., 2013; Bali et al., 2013; Roche et al., 2016; Me ff re et al., 2013) and can down-regulate in fl ammasome activation, inhibit the expression of pro-in fl ammatory genes, such as TNF, IL-6, iNOS, MHCII and COX2, and enhance the expression of TREM2, CD206 or TGF β (Aryanpour et al., 2017; Lei et al., 2014; Cutler et al., 2007; Hua et al., 2011). Astrocytes express PR and PGMRC1 (Bali et al., 2013; Bali et al., 2013; Me ff re et al., 2005) and progesterone might induce BDNF release in a Pgrmc1-dependent manner, thereby promoting cell survival (Jodhka et al., 2009; Su et al., 2012; Sun et al., 2016; Kaur et al., 2007; Atif et al., 2013). On the other hand, allopregnanolone binds to GABAA receptors in microglia as well as astrocytes mediating antiin fl ammatory e ff ects through NF κ B inhibition (Singh et al., 2013; Lambert et al., 2003; Lee et al., 2011). The release of progesterone and allopregnanolone is marked by solid lines and their e ff ects by dashed lines. Abbreviations: BDNF: Brain-derived neurotrophic factor, CD206: Cluster of Di ff erentiation 206, COX2: cyclooxygenase 2, GABAAR: γ -aminobutyric acid type A receptor, IL1 β : Interleukin 1 β , IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, MHCII: major histocompatibility complex class II, NLRP3: NLR family pyrin domain containing 3, mPR α : membrane progesterone receptor α , NF κ B: nuclear factor ' kappa-light-chain-enhancer ' of activated B-cells, NLRP3: NLR family pyrin domain containing 3, PGMRC1: progesterone membrane receptor component 1, PR: progesterone receptor, TGF β : Transforming Growth Factor β , TNF: Tumor Necrosis Factor, TREM2: Triggering receptor expressed on myeloid cells 2.CC-BY-NC-ND · From the PDF
Fig. 3 Functions and signaling of DHEA in CNS cells. DHEA is synthesized in astrocytes and neurons, while it also derives from the circulation (Zwain and Yen, 1999; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia it exerts anti-in fl ammatory e ff ects through activation of the NGF receptor TrkA, which triggers the AKT/CREB signaling cascade leading to enhanced Jmjd3 expression (Lazaridis et al., 2011; Alexaki et al., 2018). Moreover, it can be metabolized to ADIOL, which binds to ER β thereby negatively regulating pro-in fl ammatory gene expression (Saijo et al., 2011). Through regulation of cytokine and NO secretion it a ff ects astrocyte activation and neuronal survival (Glass et al., 2010). The release of DHEA is shown by a solid line, its e ff ects by a dashed line. Abbreviations: ADIOL: 5-androstene-3 beta, 17 beta-diol, CREB: cAMP response element-binding protein, CtBP: C-terminal-binding protein 1, DHEA: Dehydroepiandrosterone, ER β : estrogen receptor β , HSD17 β 14: 17 β 14-Hydroxysteroid dehydrogenase, IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, Jmjd3: Jumonji Domain Containing 3, TNF: Tumor Necrosis Factor, TrkA: tropomyosin related kinase.
Fig. 3 Functions and signaling of DHEA in CNS cells. DHEA is synthesized in astrocytes and neurons, while it also derives from the circulation (Zwain and Yen, 1999; Mellon and Gri ffi n, 2002; Schumacher et al., 2003; Starka et al., 2015). In microglia it exerts anti-in fl ammatory e ff ects through activation of the NGF receptor TrkA, which triggers the AKT/CREB signaling cascade leading to enhanced Jmjd3 expression (Lazaridis et al., 2011; Alexaki et al., 2018). Moreover, it can be metabolized to ADIOL, which binds to ER β thereby negatively regulating pro-in fl ammatory gene expression (Saijo et al., 2011). Through regulation of cytokine and NO secretion it a ff ects astrocyte activation and neuronal survival (Glass et al., 2010). The release of DHEA is shown by a solid line, its e ff ects by a dashed line. Abbreviations: ADIOL: 5-androstene-3 beta, 17 beta-diol, CREB: cAMP response element-binding protein, CtBP: C-terminal-binding protein 1, DHEA: Dehydroepiandrosterone, ER β : estrogen receptor β , HSD17 β 14: 17 β 14-Hydroxysteroid dehydrogenase, IL6: Interleukin 6, iNOS: inducible nitric oxide synthase, Jmjd3: Jumonji Domain Containing 3, TNF: Tumor Necrosis Factor, TrkA: tropomyosin related kinase.CC-BY-NC-ND · From the PDF

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Metadata

Authors
Yilmaz, C., Karali, K., Fodelianaki, G., Gravanis, A., Chavakis, T., Charalampopoulos, I., & Alexaki, V. I.
Venue
Frontiers in Neuroendocrinology
Publisher
Elsevier BV
Published
2019-10
Volume
55
Pages
100788
ISSN
0091-3022
DOI
10.1016/j.yfrne.2019.100788
Cited by
213
References
60
Language
en
Licence
Funders
  • Horizon 2020
  • Deutsche Forschungsgemeinschaft

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Yilmaz, C., Karali, K., Fodelianaki, G., Gravanis, A., Chavakis, T., Charalampopoulos, I., & Alexaki, V. I. (2019). Neurosteroids as regulators of neuroinflammation. Frontiers in Neuroendocrinology. https://doi.org/10.1016/j.yfrne.2019.100788

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