Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression
Abstract Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosph...
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| Veröffentlicht in: | Medical hypotheses 2015-09, Vol.85 (3), p.291-294 |
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| creator | Jovicic, Milica J Lukic, Iva Radojcic, Marija Adzic, Miroslav Maric, Nadja P |
| description | Abstract Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression. |
| doi_str_mv | 10.1016/j.mehy.2015.05.015 |
| format | Article |
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Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression.</description><identifier>ISSN: 0306-9877</identifier><identifier>EISSN: 1532-2777</identifier><identifier>DOI: 10.1016/j.mehy.2015.05.015</identifier><identifier>PMID: 26052031</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Depressive Disorder, Major - metabolism ; Depressive Disorder, Major - therapy ; Humans ; Internal Medicine ; JNK Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation ; Receptors, Glucocorticoid - metabolism ; Signal Transduction</subject><ispartof>Medical hypotheses, 2015-09, Vol.85 (3), p.291-294</ispartof><rights>Elsevier Ltd</rights><rights>2015 Elsevier Ltd</rights><rights>Copyright © 2015 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-256b6b75bd593cce77854b256c465310e4c6a89fe6ecdc8348b2a0ec0da5ea833</citedby><cites>FETCH-LOGICAL-c580t-256b6b75bd593cce77854b256c465310e4c6a89fe6ecdc8348b2a0ec0da5ea833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.mehy.2015.05.015$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,315,781,785,886,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26052031$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jovicic, Milica J</creatorcontrib><creatorcontrib>Lukic, Iva</creatorcontrib><creatorcontrib>Radojcic, Marija</creatorcontrib><creatorcontrib>Adzic, Miroslav</creatorcontrib><creatorcontrib>Maric, Nadja P</creatorcontrib><title>Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression</title><title>Medical hypotheses</title><addtitle>Med Hypotheses</addtitle><description>Abstract Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression.</description><subject>Depressive Disorder, Major - metabolism</subject><subject>Depressive Disorder, Major - therapy</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>Signal Transduction</subject><issn>0306-9877</issn><issn>1532-2777</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kl2P1CAUhonRuOPoH_DCcOlNRz5KPxKzidmsX1n1Qr0m9PR0hm5bKtBN5if4r6WZcaNemBwgwMvLgecQ8pyzHWe8eNXvRjwcd4JxtWMpuHpANlxJkYmyLB-SDZOsyOqqLC_IkxB6xlidy-oxuRAFU4JJviE_P7l2GUy0bqKuo5B9XCb6OYvoRzuZgd6mPiANdp9mdtpTM7U0zAi2s0D3wwIOnI8WnG2pR8A5Ok_ngwup-ePZ2U40HpBGjyaOOMX1qtH0Sdni7DGEJHpKHnVmCPjsPG7J97fX367eZzdf3n24enOTgapYzIQqmqIpVdOqWgJgWVYqb9Iq5IWSnGEOhanqDguEFiqZV40wDIG1RqGppNySy5PvvDQjtpDS8WbQs7ej8UftjNV_70z2oPfuTucqr3klksHLs4F3PxYMUY82AA6DmdAtQfOSFaosOM-TVJyk4F0IHrv7azjTK0Pd65WhXhlqliLh25IXfyZ4f-Q3tCR4fRJg-qY7i14HsDgBtjYRiLp19v_-l_8ch0TWghlu8Yihd4tPrNM7dBCa6a9rFa1FxBVjgkspfwHklcdV</recordid><startdate>20150901</startdate><enddate>20150901</enddate><creator>Jovicic, Milica J</creator><creator>Lukic, Iva</creator><creator>Radojcic, Marija</creator><creator>Adzic, Miroslav</creator><creator>Maric, Nadja P</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150901</creationdate><title>Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression</title><author>Jovicic, Milica J ; Lukic, Iva ; Radojcic, Marija ; Adzic, Miroslav ; Maric, Nadja P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-256b6b75bd593cce77854b256c465310e4c6a89fe6ecdc8348b2a0ec0da5ea833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Depressive Disorder, Major - metabolism</topic><topic>Depressive Disorder, Major - therapy</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jovicic, Milica J</creatorcontrib><creatorcontrib>Lukic, Iva</creatorcontrib><creatorcontrib>Radojcic, Marija</creatorcontrib><creatorcontrib>Adzic, Miroslav</creatorcontrib><creatorcontrib>Maric, Nadja P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Medical hypotheses</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jovicic, Milica J</au><au>Lukic, Iva</au><au>Radojcic, Marija</au><au>Adzic, Miroslav</au><au>Maric, Nadja P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression</atitle><jtitle>Medical hypotheses</jtitle><addtitle>Med Hypotheses</addtitle><date>2015-09-01</date><risdate>2015</risdate><volume>85</volume><issue>3</issue><spage>291</spage><epage>294</epage><pages>291-294</pages><issn>0306-9877</issn><eissn>1532-2777</eissn><abstract>Abstract Glucocorticoid resistance is a common finding in major depressive disorder. Increased glucocorticoid receptor (GR) phosphorylation at serine 226 is associated with increased glucocorticoid resistance. Previously we have demonstrated that depressed patients exhibit higher levels of GR phosphorylated at serine 226 compared to healthy controls. The enzyme that is involved in this specific GR phosphorylation is c-Jun N-terminal kinase (JNK). We propose that modulation of glucocorticoid phosphorylation at serine 226, by targeting JNK signaling pathway, could be a potential strategy for antidepressant treatment. We base this assumption on the results of previous research that examined GR phosphorylation and JNK signaling in animal models and human studies. We also discuss the potential challenges in targeting JNK signaling pathway in depression.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>26052031</pmid><doi>10.1016/j.mehy.2015.05.015</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Medical hypotheses, 2015-09, Vol.85 (3), p.291-294 |
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| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Depressive Disorder, Major - metabolism Depressive Disorder, Major - therapy Humans Internal Medicine JNK Mitogen-Activated Protein Kinases - metabolism Phosphorylation Receptors, Glucocorticoid - metabolism Signal Transduction |
| title | Modulation of c-Jun N-terminal kinase signaling and specific glucocorticoid receptor phosphorylation in the treatment of major depression |
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