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Activation of AMP-activated protein kinase stimulates proopiomelanocortin gene transcription in AtT20 corticotroph cells
1 Department of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Nankoku; and Departments of 2 Medicine and 3 Clinical Pathophysiology, Nagoya University Graduate School of Medicine and Hospital, Nagoya, Japan Submitted 12 March 2006 ; accepted in final form 21 Febr...
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| Published in: | American journal of physiology: endocrinology and metabolism 2007-06, Vol.292 (6), p.E1899-E1905 |
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| container_end_page | E1905 |
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| container_title | American journal of physiology: endocrinology and metabolism |
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| creator | Iwasaki, Yasumasa Nishiyama, Mitsuru Taguchi, Takafumi Kambayashi, Machiko Asai, Masato Yoshida, Masanori Nigawara, Takeshi Hashimoto, Kozo |
| description | 1 Department of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Nankoku; and Departments of 2 Medicine and 3 Clinical Pathophysiology, Nagoya University Graduate School of Medicine and Hospital, Nagoya, Japan
Submitted 12 March 2006
; accepted in final form 21 February 2007
Starvation is known to activate the hypothalamo-pituitary-adrenal (HPA) axis, a representative antistress system in the living organism. In this study, we investigated in vitro whether activation of the AMP-activated protein kinase (AMPK), which is known to occur in intracellular energy depletion, influences the expression of POMC gene that encodes adrenocorticotropin. We first confirmed that each subunit of AMPK was expressed in the AtT20 corticotroph cell line. We then found that AICAR, a cell-permeable AMP analog and an activator of AMPK, potently stimulated the 5'-promoter activity of POMC gene in a dose-dependent manner. The effects were promoter specific because AICAR enhanced the AP1-mediated POMC promoter activities but did not influence other transcription factor-induced transcription. The effect of AICAR on POMC gene transcription was completely eliminated by specific AMPK inhibitor compound C or by dominant negative AMPK, whereas overexpression of constitutively active AMPK mimicked the effect of AICAR. Finally, experiments using specific kinase inhibitors suggested that the PI 3-kinase-mediated signaling pathway is at least partly involved in the effect. Our results suggest that intracellular energy depletion with the resultant activation of AMPK directly stimulates the HPA axis at the pituitary level by increasing the expression of POMC gene.
adenosine 5'-monophosphate; adrenocorticotropin; energy homeostasis; pituitary; starvation
Address for reprint requests and other correspondence: Y. Iwasaki, Dept. of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku 783-8505, Japan (e-mail: iwasaki{at}kochi-u.ac.jp ) |
| doi_str_mv | 10.1152/ajpendo.00116.2006 |
| format | article |
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Submitted 12 March 2006
; accepted in final form 21 February 2007
Starvation is known to activate the hypothalamo-pituitary-adrenal (HPA) axis, a representative antistress system in the living organism. In this study, we investigated in vitro whether activation of the AMP-activated protein kinase (AMPK), which is known to occur in intracellular energy depletion, influences the expression of POMC gene that encodes adrenocorticotropin. We first confirmed that each subunit of AMPK was expressed in the AtT20 corticotroph cell line. We then found that AICAR, a cell-permeable AMP analog and an activator of AMPK, potently stimulated the 5'-promoter activity of POMC gene in a dose-dependent manner. The effects were promoter specific because AICAR enhanced the AP1-mediated POMC promoter activities but did not influence other transcription factor-induced transcription. The effect of AICAR on POMC gene transcription was completely eliminated by specific AMPK inhibitor compound C or by dominant negative AMPK, whereas overexpression of constitutively active AMPK mimicked the effect of AICAR. Finally, experiments using specific kinase inhibitors suggested that the PI 3-kinase-mediated signaling pathway is at least partly involved in the effect. Our results suggest that intracellular energy depletion with the resultant activation of AMPK directly stimulates the HPA axis at the pituitary level by increasing the expression of POMC gene.
adenosine 5'-monophosphate; adrenocorticotropin; energy homeostasis; pituitary; starvation
Address for reprint requests and other correspondence: Y. Iwasaki, Dept. of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku 783-8505, Japan (e-mail: iwasaki{at}kochi-u.ac.jp )</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00116.2006</identifier><identifier>PMID: 17341551</identifier><identifier>CODEN: AJPMD9</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adrenocorticotropic Hormone - secretion ; Aminoimidazole Carboxamide - administration & dosage ; Aminoimidazole Carboxamide - analogs & derivatives ; Aminoimidazole Carboxamide - pharmacology ; AMP-Activated Protein Kinases ; Animals ; Cell Line ; Cellular biology ; Corticotrophs - metabolism ; Corticotropin-Releasing Hormone - genetics ; Dose-Response Relationship, Drug ; Enzyme Activation - physiology ; Gene expression ; Gene Expression - drug effects ; Gene Expression Regulation ; Kinases ; Metabolism ; Multienzyme Complexes - metabolism ; Phosphorylation - drug effects ; Pro-Opiomelanocortin - genetics ; Promoter Regions, Genetic - drug effects ; Protein-Serine-Threonine Kinases - metabolism ; Ribonucleotides - administration & dosage ; Ribonucleotides - pharmacology ; RNA, Messenger - metabolism ; Signal Transduction - physiology ; Transcription Factor AP-1 - physiology ; Transcription, Genetic - drug effects ; Transcription, Genetic - physiology</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2007-06, Vol.292 (6), p.E1899-E1905</ispartof><rights>Copyright American Physiological Society Jun 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-3089d62976145d2cce9fe02b7b9774b74c73f4fce9ba4c449187746a3be1a4173</citedby><cites>FETCH-LOGICAL-c449t-3089d62976145d2cce9fe02b7b9774b74c73f4fce9ba4c449187746a3be1a4173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17341551$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Iwasaki, Yasumasa</creatorcontrib><creatorcontrib>Nishiyama, Mitsuru</creatorcontrib><creatorcontrib>Taguchi, Takafumi</creatorcontrib><creatorcontrib>Kambayashi, Machiko</creatorcontrib><creatorcontrib>Asai, Masato</creatorcontrib><creatorcontrib>Yoshida, Masanori</creatorcontrib><creatorcontrib>Nigawara, Takeshi</creatorcontrib><creatorcontrib>Hashimoto, Kozo</creatorcontrib><title>Activation of AMP-activated protein kinase stimulates proopiomelanocortin gene transcription in AtT20 corticotroph cells</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>1 Department of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Nankoku; and Departments of 2 Medicine and 3 Clinical Pathophysiology, Nagoya University Graduate School of Medicine and Hospital, Nagoya, Japan
Submitted 12 March 2006
; accepted in final form 21 February 2007
Starvation is known to activate the hypothalamo-pituitary-adrenal (HPA) axis, a representative antistress system in the living organism. In this study, we investigated in vitro whether activation of the AMP-activated protein kinase (AMPK), which is known to occur in intracellular energy depletion, influences the expression of POMC gene that encodes adrenocorticotropin. We first confirmed that each subunit of AMPK was expressed in the AtT20 corticotroph cell line. We then found that AICAR, a cell-permeable AMP analog and an activator of AMPK, potently stimulated the 5'-promoter activity of POMC gene in a dose-dependent manner. The effects were promoter specific because AICAR enhanced the AP1-mediated POMC promoter activities but did not influence other transcription factor-induced transcription. The effect of AICAR on POMC gene transcription was completely eliminated by specific AMPK inhibitor compound C or by dominant negative AMPK, whereas overexpression of constitutively active AMPK mimicked the effect of AICAR. Finally, experiments using specific kinase inhibitors suggested that the PI 3-kinase-mediated signaling pathway is at least partly involved in the effect. Our results suggest that intracellular energy depletion with the resultant activation of AMPK directly stimulates the HPA axis at the pituitary level by increasing the expression of POMC gene.
adenosine 5'-monophosphate; adrenocorticotropin; energy homeostasis; pituitary; starvation
Address for reprint requests and other correspondence: Y. Iwasaki, Dept. of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku 783-8505, Japan (e-mail: iwasaki{at}kochi-u.ac.jp )</description><subject>Adrenocorticotropic Hormone - secretion</subject><subject>Aminoimidazole Carboxamide - administration & dosage</subject><subject>Aminoimidazole Carboxamide - analogs & derivatives</subject><subject>Aminoimidazole Carboxamide - pharmacology</subject><subject>AMP-Activated Protein Kinases</subject><subject>Animals</subject><subject>Cell Line</subject><subject>Cellular biology</subject><subject>Corticotrophs - metabolism</subject><subject>Corticotropin-Releasing Hormone - genetics</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Activation - physiology</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Gene Expression Regulation</subject><subject>Kinases</subject><subject>Metabolism</subject><subject>Multienzyme Complexes - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Pro-Opiomelanocortin - genetics</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Ribonucleotides - administration & dosage</subject><subject>Ribonucleotides - pharmacology</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Transcription Factor AP-1 - physiology</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transcription, Genetic - physiology</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1DAUhS1ERaelL8ACRSzYZbAd_8TsRlVbkIrKYlhbjuPMeEjsYDvQeXucmSkgJMTCsnTud47u1QHgFYJLhCh-p3ajca1fQogQW2II2TOwyANcIkrpc7CASFQlqok4Bxcx7iCEnBL8ApwjXpHMoAV4XOlkv6tkvSt8V6w-fS7VUTFtMQafjHXFV-tUNEVMdpj6PInzxI_WD6ZXzmsfUqY2xpkiBeWiDnY8JGZ1ldYYFgdE-xT8uC206fv4Epx1qo_m6vRfgi-3N-vrD-X9w93H69V9qQkRqaxgLVqGBWeI0BZrbURnIG54IzgnDSeaVx3pstwoMltQnXWmqsYgRfKdl-DtMTev_G0yMcnBxnkD5YyfouSQMs4Z_i-IRE0pFiyDb_4Cd34KLh8hcYUrSPPLED5COvgYg-nkGOygwl4iKOf25Kk9eWhPzu1l0-tT8tQMpv1tOdWVgeUR2NrN9ocNRo7bfbS-95v9r0AssGTyBtVCZMP7fxtup75fm8f05PzDKMe2q34Cdqu-Tw</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Iwasaki, Yasumasa</creator><creator>Nishiyama, Mitsuru</creator><creator>Taguchi, Takafumi</creator><creator>Kambayashi, Machiko</creator><creator>Asai, Masato</creator><creator>Yoshida, Masanori</creator><creator>Nigawara, Takeshi</creator><creator>Hashimoto, Kozo</creator><general>American Physiological Society</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>7QP</scope><scope>7TS</scope><scope>7U7</scope><scope>C1K</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20070601</creationdate><title>Activation of AMP-activated protein kinase stimulates proopiomelanocortin gene transcription in AtT20 corticotroph cells</title><author>Iwasaki, Yasumasa ; 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and Departments of 2 Medicine and 3 Clinical Pathophysiology, Nagoya University Graduate School of Medicine and Hospital, Nagoya, Japan
Submitted 12 March 2006
; accepted in final form 21 February 2007
Starvation is known to activate the hypothalamo-pituitary-adrenal (HPA) axis, a representative antistress system in the living organism. In this study, we investigated in vitro whether activation of the AMP-activated protein kinase (AMPK), which is known to occur in intracellular energy depletion, influences the expression of POMC gene that encodes adrenocorticotropin. We first confirmed that each subunit of AMPK was expressed in the AtT20 corticotroph cell line. We then found that AICAR, a cell-permeable AMP analog and an activator of AMPK, potently stimulated the 5'-promoter activity of POMC gene in a dose-dependent manner. The effects were promoter specific because AICAR enhanced the AP1-mediated POMC promoter activities but did not influence other transcription factor-induced transcription. The effect of AICAR on POMC gene transcription was completely eliminated by specific AMPK inhibitor compound C or by dominant negative AMPK, whereas overexpression of constitutively active AMPK mimicked the effect of AICAR. Finally, experiments using specific kinase inhibitors suggested that the PI 3-kinase-mediated signaling pathway is at least partly involved in the effect. Our results suggest that intracellular energy depletion with the resultant activation of AMPK directly stimulates the HPA axis at the pituitary level by increasing the expression of POMC gene.
adenosine 5'-monophosphate; adrenocorticotropin; energy homeostasis; pituitary; starvation
Address for reprint requests and other correspondence: Y. Iwasaki, Dept. of Endocrinology, Metabolism, and Nephrology, Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku 783-8505, Japan (e-mail: iwasaki{at}kochi-u.ac.jp )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>17341551</pmid><doi>10.1152/ajpendo.00116.2006</doi></addata></record> |
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| ispartof | American journal of physiology: endocrinology and metabolism, 2007-06, Vol.292 (6), p.E1899-E1905 |
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| source | American Physiological Society Free |
| subjects | Adrenocorticotropic Hormone - secretion Aminoimidazole Carboxamide - administration & dosage Aminoimidazole Carboxamide - analogs & derivatives Aminoimidazole Carboxamide - pharmacology AMP-Activated Protein Kinases Animals Cell Line Cellular biology Corticotrophs - metabolism Corticotropin-Releasing Hormone - genetics Dose-Response Relationship, Drug Enzyme Activation - physiology Gene expression Gene Expression - drug effects Gene Expression Regulation Kinases Metabolism Multienzyme Complexes - metabolism Phosphorylation - drug effects Pro-Opiomelanocortin - genetics Promoter Regions, Genetic - drug effects Protein-Serine-Threonine Kinases - metabolism Ribonucleotides - administration & dosage Ribonucleotides - pharmacology RNA, Messenger - metabolism Signal Transduction - physiology Transcription Factor AP-1 - physiology Transcription, Genetic - drug effects Transcription, Genetic - physiology |
| title | Activation of AMP-activated protein kinase stimulates proopiomelanocortin gene transcription in AtT20 corticotroph cells |
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