18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile
An aberrant pro-inflammatory microglia response has been associated with most neurodegenerative disorders. Identifying microglia druggable checkpoints to restore their physiological functions is an emerging challenge. Recent data have shown that microglia produce de novo neurosteroids, endogenous mo...
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2025-01, Vol.82 (1), p.34, Article 34 |
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| creator | Germelli, Lorenzo Angeloni, Elisa Da Pozzo, Eleonora Tremolanti, Chiara De Felice, Martina Giacomelli, Chiara Marchetti, Laura Muscatello, Beatrice Barresi, Elisabetta Taliani, Sabrina Da Settimo Passetti, Federico Trincavelli, Maria Letizia Martini, Claudia Costa, Barbara |
| description | An aberrant pro-inflammatory microglia response has been associated with most neurodegenerative disorders. Identifying microglia druggable checkpoints to restore their physiological functions is an emerging challenge. Recent data have shown that microglia produce de novo neurosteroids, endogenous molecules exerting potent anti-inflammatory activity. Here, the role of neurosteroidogenesis in the modulation of microgliosis was explored in human microglia cells. In particular, CYP11A1 inhibition or TSPO pharmacological stimulation, crucial proteins involved in the rate limiting step of the neurosteroidogenic cascade, were employed. CYP11A1 inhibition led microglia to acquire a dysfunctional and hyperreactive phenotype, while selective TSPO ligands promoted the establishment of an anti-inflammatory one. Analysis of specific neurosteroid levels (neurosteroidome) identified allopregnanolone/pregnanolone as crucial metabolites allowing controlled activation of microglia. Importantly, the neurosteroid shift towards a greater androgenic/estrogenic profile supported the transition from pro-inflammatory to neuroprotective microglia, suggesting the therapeutic potential of de novo microglial neurosteroidogenesis stimulation for neuroinflammatory-related disorders. |
| doi_str_mv | 10.1007/s00018-024-05544-1 |
| format | Article |
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Identifying microglia druggable checkpoints to restore their physiological functions is an emerging challenge. Recent data have shown that microglia produce de novo neurosteroids, endogenous molecules exerting potent anti-inflammatory activity. Here, the role of neurosteroidogenesis in the modulation of microgliosis was explored in human microglia cells. In particular, CYP11A1 inhibition or TSPO pharmacological stimulation, crucial proteins involved in the rate limiting step of the neurosteroidogenic cascade, were employed. CYP11A1 inhibition led microglia to acquire a dysfunctional and hyperreactive phenotype, while selective TSPO ligands promoted the establishment of an anti-inflammatory one. Analysis of specific neurosteroid levels (neurosteroidome) identified allopregnanolone/pregnanolone as crucial metabolites allowing controlled activation of microglia. Importantly, the neurosteroid shift towards a greater androgenic/estrogenic profile supported the transition from pro-inflammatory to neuroprotective microglia, suggesting the therapeutic potential of de novo microglial neurosteroidogenesis stimulation for neuroinflammatory-related disorders.</description><identifier>ISSN: 1420-9071</identifier><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-024-05544-1</identifier><identifier>PMID: 39757281</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Anti-inflammatory agents ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Enzymes ; Genotype & phenotype ; Life Sciences ; Ligands ; Metabolites ; Microglia ; Morphology ; Neurodegeneration ; Neurodegenerative diseases ; Neuromodulation ; Neuroprotection ; Neurosciences ; Neurosteroidogenesis ; Neurosteroids ; Original ; Original Article ; Phenotypes ; Physiology ; Pregnanolone ; Stimulation ; Xenoestrogens</subject><ispartof>Cellular and molecular life sciences : CMLS, 2025-01, Vol.82 (1), p.34, Article 34</ispartof><rights>The Author(s) 2025</rights><rights>2025. 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Dec 2025</rights><rights>The Author(s) 2025 2025</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2631-198450ff5e23a698b96173c8fdbee3fe0de24cc5090c0a7788424879ebf694273</cites><orcidid>0000-0002-6244-602X ; 0000-0002-6122-7327 ; 0000-0001-7704-8705 ; 0000-0002-7897-7917 ; 0000-0002-7318-7545 ; 0000-0001-9379-3027 ; 0000-0002-3113-7099 ; 0000-0002-9814-7195 ; 0000-0001-8675-939X ; 0000-0002-2110-9481 ; 0000-0001-8124-977X ; 0000-0002-7598-1275 ; 0000-0003-4762-8949</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700965/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700965/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,41099,41467,42168,42536,51297,51554,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39757281$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Germelli, Lorenzo</creatorcontrib><creatorcontrib>Angeloni, Elisa</creatorcontrib><creatorcontrib>Da Pozzo, Eleonora</creatorcontrib><creatorcontrib>Tremolanti, Chiara</creatorcontrib><creatorcontrib>De Felice, Martina</creatorcontrib><creatorcontrib>Giacomelli, Chiara</creatorcontrib><creatorcontrib>Marchetti, Laura</creatorcontrib><creatorcontrib>Muscatello, Beatrice</creatorcontrib><creatorcontrib>Barresi, Elisabetta</creatorcontrib><creatorcontrib>Taliani, Sabrina</creatorcontrib><creatorcontrib>Da Settimo Passetti, Federico</creatorcontrib><creatorcontrib>Trincavelli, Maria Letizia</creatorcontrib><creatorcontrib>Martini, Claudia</creatorcontrib><creatorcontrib>Costa, Barbara</creatorcontrib><title>18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell. Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>An aberrant pro-inflammatory microglia response has been associated with most neurodegenerative disorders. Identifying microglia druggable checkpoints to restore their physiological functions is an emerging challenge. Recent data have shown that microglia produce de novo neurosteroids, endogenous molecules exerting potent anti-inflammatory activity. Here, the role of neurosteroidogenesis in the modulation of microgliosis was explored in human microglia cells. In particular, CYP11A1 inhibition or TSPO pharmacological stimulation, crucial proteins involved in the rate limiting step of the neurosteroidogenic cascade, were employed. CYP11A1 inhibition led microglia to acquire a dysfunctional and hyperreactive phenotype, while selective TSPO ligands promoted the establishment of an anti-inflammatory one. Analysis of specific neurosteroid levels (neurosteroidome) identified allopregnanolone/pregnanolone as crucial metabolites allowing controlled activation of microglia. Importantly, the neurosteroid shift towards a greater androgenic/estrogenic profile supported the transition from pro-inflammatory to neuroprotective microglia, suggesting the therapeutic potential of de novo microglial neurosteroidogenesis stimulation for neuroinflammatory-related disorders.</description><subject>Anti-inflammatory agents</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Enzymes</subject><subject>Genotype & phenotype</subject><subject>Life Sciences</subject><subject>Ligands</subject><subject>Metabolites</subject><subject>Microglia</subject><subject>Morphology</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neuromodulation</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Neurosteroidogenesis</subject><subject>Neurosteroids</subject><subject>Original</subject><subject>Original Article</subject><subject>Phenotypes</subject><subject>Physiology</subject><subject>Pregnanolone</subject><subject>Stimulation</subject><subject>Xenoestrogens</subject><issn>1420-9071</issn><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kc1u1TAQhSNERUvhBVggS2zYhI4dO7ZXCLX8SZWKRFlbvs4kdUnsi50UwdPwLDwZvvf2DxasbGu-OTPHp6qeUXhFAeRRBgCqamC8BiE4r-mD6oByBrUGSR_eu-9Xj3O-LLRQrH1U7TdaCskUPahmqn7_-npiyfnnT2dktmnA2YeBdMlfYSbrONrkf2JHLpbJBjJ5l-Iwekvm-N2mLhNL1inO6ObCExs6kjDPMdntO-CSYp4xRd_FCTdo70d8Uu31dsz49Po8rL68e3t-_KE-PXv_8fjNae1Y29CaasUF9L1A1thWq5VuqWyc6rsVYtMjdMi4cwI0OLBSKsUZV1Ljqm81Z7I5rF7vdNfLasLOYZiTHc06-cmmHyZab_6uBH9hhnhlKJUAuhVF4eW1QorfluLMTD47HEcbMC7ZNFRQJduyaUFf_INexiWF4m9LSSU0bCi2o8o_5pywv92GgtmkanapmpKq2aZqaGl6ft_HbctNjAVodkAupTBgupv9H9k_6D2v2A</recordid><startdate>20250106</startdate><enddate>20250106</enddate><creator>Germelli, Lorenzo</creator><creator>Angeloni, Elisa</creator><creator>Da Pozzo, Eleonora</creator><creator>Tremolanti, Chiara</creator><creator>De Felice, Martina</creator><creator>Giacomelli, Chiara</creator><creator>Marchetti, Laura</creator><creator>Muscatello, Beatrice</creator><creator>Barresi, Elisabetta</creator><creator>Taliani, Sabrina</creator><creator>Da Settimo Passetti, Federico</creator><creator>Trincavelli, Maria Letizia</creator><creator>Martini, Claudia</creator><creator>Costa, Barbara</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6244-602X</orcidid><orcidid>https://orcid.org/0000-0002-6122-7327</orcidid><orcidid>https://orcid.org/0000-0001-7704-8705</orcidid><orcidid>https://orcid.org/0000-0002-7897-7917</orcidid><orcidid>https://orcid.org/0000-0002-7318-7545</orcidid><orcidid>https://orcid.org/0000-0001-9379-3027</orcidid><orcidid>https://orcid.org/0000-0002-3113-7099</orcidid><orcidid>https://orcid.org/0000-0002-9814-7195</orcidid><orcidid>https://orcid.org/0000-0001-8675-939X</orcidid><orcidid>https://orcid.org/0000-0002-2110-9481</orcidid><orcidid>https://orcid.org/0000-0001-8124-977X</orcidid><orcidid>https://orcid.org/0000-0002-7598-1275</orcidid><orcidid>https://orcid.org/0000-0003-4762-8949</orcidid></search><sort><creationdate>20250106</creationdate><title>18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile</title><author>Germelli, Lorenzo ; 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Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2025-01-06</date><risdate>2025</risdate><volume>82</volume><issue>1</issue><spage>34</spage><pages>34-</pages><artnum>34</artnum><issn>1420-9071</issn><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>An aberrant pro-inflammatory microglia response has been associated with most neurodegenerative disorders. Identifying microglia druggable checkpoints to restore their physiological functions is an emerging challenge. Recent data have shown that microglia produce de novo neurosteroids, endogenous molecules exerting potent anti-inflammatory activity. Here, the role of neurosteroidogenesis in the modulation of microgliosis was explored in human microglia cells. In particular, CYP11A1 inhibition or TSPO pharmacological stimulation, crucial proteins involved in the rate limiting step of the neurosteroidogenic cascade, were employed. 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| subjects | Anti-inflammatory agents Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Enzymes Genotype & phenotype Life Sciences Ligands Metabolites Microglia Morphology Neurodegeneration Neurodegenerative diseases Neuromodulation Neuroprotection Neurosciences Neurosteroidogenesis Neurosteroids Original Original Article Phenotypes Physiology Pregnanolone Stimulation Xenoestrogens |
| title | 18 kDa TSPO targeting drives polarized human microglia towards a protective and restorative neurosteroidome profile |
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