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Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration
The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four diffe...
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| Published in: | Hepatology (Baltimore, Md.) Md.), 1993-06, Vol.17 (6), p.1109-1116 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | Coni, Pierpaolo Simbula, Gabriella de Prati, Alessandra Carcereri Menegazzi, Marta Suzuki, Hisanori Sarma, Dittakavi S. R. Ledda‐Columbano, Giovanna M. Columbano, Amedeo |
| description | The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four different hepatomitogens: lead nitrate, ethylene dibromide, cyproterone acetate and nafenopin. We show here that whereas c‐fos and c‐jun expression increased soon after partial hepatectomy or carbon tetrachloride administration, an increased expression of c‐jun in the absence of c‐fos expression occurred during direct hyperplasia induced by lead nitrate and ethylene dibromide. When hyperplasia was induced by cyproterone acetate and nafenopin, the mitogenic response of the liver was not associated with an increased expression of c‐jun or c‐fos, despite the fact that the timing of the cell cycle was similar to that observed after partial hepatectomy. Finally, when c‐myc expression was analyzed, it was found that proliferative conditions associated with an increased expression of this gene were characterized by an increased expression of c‐jun. On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c‐fos and c‐jun, was also not associated with an increased c‐myc expression. Similar results were obtained in these experiments with the mitogen nafenopin, a peroxisome proliferator. In fact, liver hyperplasia induced by this compound was not preceded or accompanied by an increased expression of c‐fos and c‐myc. This study suggests that depending on the nature of the proliferative stimulus, an increased expression of c‐fos, c‐jun and c‐myc may not be necessary for in vivo induction of liver cell proliferation. (HEPATOLOGY 1993;17:1109–1116.) |
| doi_str_mv | 10.1002/hep.1840170626 |
| format | article |
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R. ; Ledda‐Columbano, Giovanna M. ; Columbano, Amedeo</creator><creatorcontrib>Coni, Pierpaolo ; Simbula, Gabriella ; de Prati, Alessandra Carcereri ; Menegazzi, Marta ; Suzuki, Hisanori ; Sarma, Dittakavi S. R. ; Ledda‐Columbano, Giovanna M. ; Columbano, Amedeo</creatorcontrib><description>The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four different hepatomitogens: lead nitrate, ethylene dibromide, cyproterone acetate and nafenopin. We show here that whereas c‐fos and c‐jun expression increased soon after partial hepatectomy or carbon tetrachloride administration, an increased expression of c‐jun in the absence of c‐fos expression occurred during direct hyperplasia induced by lead nitrate and ethylene dibromide. When hyperplasia was induced by cyproterone acetate and nafenopin, the mitogenic response of the liver was not associated with an increased expression of c‐jun or c‐fos, despite the fact that the timing of the cell cycle was similar to that observed after partial hepatectomy. Finally, when c‐myc expression was analyzed, it was found that proliferative conditions associated with an increased expression of this gene were characterized by an increased expression of c‐jun. On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c‐fos and c‐jun, was also not associated with an increased c‐myc expression. Similar results were obtained in these experiments with the mitogen nafenopin, a peroxisome proliferator. In fact, liver hyperplasia induced by this compound was not preceded or accompanied by an increased expression of c‐fos and c‐myc. This study suggests that depending on the nature of the proliferative stimulus, an increased expression of c‐fos, c‐jun and c‐myc may not be necessary for in vivo induction of liver cell proliferation. (HEPATOLOGY 1993;17:1109–1116.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.1840170626</identifier><identifier>PMID: 8514261</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Animals ; Biological and medical sciences ; Carbon Tetrachloride - pharmacology ; Cell Division - drug effects ; Cyproterone Acetate - pharmacology ; Degeneration. Regeneration. Wound healing. Graft ; Ethylene Dibromide - pharmacology ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Genes, fos ; Genes, jun ; Genes, myc ; Hepatectomy ; Hyperplasia ; Lead - pharmacology ; Liver - cytology ; Liver - drug effects ; Liver - pathology ; Liver Regeneration - physiology ; Male ; Nafenopin - pharmacology ; Nitrates - pharmacology ; Rats ; Rats, Wistar ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Hepatology (Baltimore, Md.), 1993-06, Vol.17 (6), p.1109-1116</ispartof><rights>Copyright © 1993 American Association for the Study of Liver Diseases</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4756-6ed8c4420be8587d19cfae22d42638269afd9c07809ce5dbbb73038e26711e443</citedby><cites>FETCH-LOGICAL-c4756-6ed8c4420be8587d19cfae22d42638269afd9c07809ce5dbbb73038e26711e443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4864102$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8514261$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Coni, Pierpaolo</creatorcontrib><creatorcontrib>Simbula, Gabriella</creatorcontrib><creatorcontrib>de Prati, Alessandra Carcereri</creatorcontrib><creatorcontrib>Menegazzi, Marta</creatorcontrib><creatorcontrib>Suzuki, Hisanori</creatorcontrib><creatorcontrib>Sarma, Dittakavi S. R.</creatorcontrib><creatorcontrib>Ledda‐Columbano, Giovanna M.</creatorcontrib><creatorcontrib>Columbano, Amedeo</creatorcontrib><title>Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four different hepatomitogens: lead nitrate, ethylene dibromide, cyproterone acetate and nafenopin. We show here that whereas c‐fos and c‐jun expression increased soon after partial hepatectomy or carbon tetrachloride administration, an increased expression of c‐jun in the absence of c‐fos expression occurred during direct hyperplasia induced by lead nitrate and ethylene dibromide. When hyperplasia was induced by cyproterone acetate and nafenopin, the mitogenic response of the liver was not associated with an increased expression of c‐jun or c‐fos, despite the fact that the timing of the cell cycle was similar to that observed after partial hepatectomy. Finally, when c‐myc expression was analyzed, it was found that proliferative conditions associated with an increased expression of this gene were characterized by an increased expression of c‐jun. On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c‐fos and c‐jun, was also not associated with an increased c‐myc expression. Similar results were obtained in these experiments with the mitogen nafenopin, a peroxisome proliferator. In fact, liver hyperplasia induced by this compound was not preceded or accompanied by an increased expression of c‐fos and c‐myc. This study suggests that depending on the nature of the proliferative stimulus, an increased expression of c‐fos, c‐jun and c‐myc may not be necessary for in vivo induction of liver cell proliferation. (HEPATOLOGY 1993;17:1109–1116.)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carbon Tetrachloride - pharmacology</subject><subject>Cell Division - drug effects</subject><subject>Cyproterone Acetate - pharmacology</subject><subject>Degeneration. Regeneration. Wound healing. Graft</subject><subject>Ethylene Dibromide - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Genes, fos</subject><subject>Genes, jun</subject><subject>Genes, myc</subject><subject>Hepatectomy</subject><subject>Hyperplasia</subject><subject>Lead - pharmacology</subject><subject>Liver - cytology</subject><subject>Liver - drug effects</subject><subject>Liver - pathology</subject><subject>Liver Regeneration - physiology</subject><subject>Male</subject><subject>Nafenopin - pharmacology</subject><subject>Nitrates - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNqFkE1P3DAQhq0KRBfKtbdKPvTYLGPHSZwj4rMSAoTKOXLs8a5R4qzsLCi3_gTO_Dx-SV12RXvjNKOZ552Pl5CvDOYMgB8tcTVnUgCroOTlJzJjBa-yPC9gh8yAV5DVLK8_k_0YHwCgFlzukT1ZMMFLNiMvp85aDOg1Ruo8HZdI44jKTK-_n-OoRqQdPmIX6WCpTjU7xB9vycPaU-XNW95PmvYYI_oFBnp3fUzNOji_oL0bhwX6hDhv1hoN7dxjQhZheBqXG_3Qr9BHNQ5hogETjUGNbvBfyK5VXcTDbTwg9-dnv04us6ubi58nx1eZFlVRZiUaqYXg0KIsZGVYra1Czk16MJe8rJU1tYZKQq2xMG3bVjnkEnlZMYZC5AdkvpmrwxBjQNusgutVmBoGzV-Pm-Rx88_jJPi2EazWbY_mHd-amvrft30VtepsUF67-I4JWQoGPGH1BntyHU4fLG0uz27_O-EP6W2cZA</recordid><startdate>199306</startdate><enddate>199306</enddate><creator>Coni, Pierpaolo</creator><creator>Simbula, Gabriella</creator><creator>de Prati, Alessandra Carcereri</creator><creator>Menegazzi, Marta</creator><creator>Suzuki, Hisanori</creator><creator>Sarma, Dittakavi S. R.</creator><creator>Ledda‐Columbano, Giovanna M.</creator><creator>Columbano, Amedeo</creator><general>W.B. Saunders</general><general>Wiley</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>199306</creationdate><title>Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration</title><author>Coni, Pierpaolo ; Simbula, Gabriella ; de Prati, Alessandra Carcereri ; Menegazzi, Marta ; Suzuki, Hisanori ; Sarma, Dittakavi S. R. ; Ledda‐Columbano, Giovanna M. ; Columbano, Amedeo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4756-6ed8c4420be8587d19cfae22d42638269afd9c07809ce5dbbb73038e26711e443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carbon Tetrachloride - pharmacology</topic><topic>Cell Division - drug effects</topic><topic>Cyproterone Acetate - pharmacology</topic><topic>Degeneration. Regeneration. Wound healing. Graft</topic><topic>Ethylene Dibromide - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>Genes, fos</topic><topic>Genes, jun</topic><topic>Genes, myc</topic><topic>Hepatectomy</topic><topic>Hyperplasia</topic><topic>Lead - pharmacology</topic><topic>Liver - cytology</topic><topic>Liver - drug effects</topic><topic>Liver - pathology</topic><topic>Liver Regeneration - physiology</topic><topic>Male</topic><topic>Nafenopin - pharmacology</topic><topic>Nitrates - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Coni, Pierpaolo</creatorcontrib><creatorcontrib>Simbula, Gabriella</creatorcontrib><creatorcontrib>de Prati, Alessandra Carcereri</creatorcontrib><creatorcontrib>Menegazzi, Marta</creatorcontrib><creatorcontrib>Suzuki, Hisanori</creatorcontrib><creatorcontrib>Sarma, Dittakavi S. R.</creatorcontrib><creatorcontrib>Ledda‐Columbano, Giovanna M.</creatorcontrib><creatorcontrib>Columbano, Amedeo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Coni, Pierpaolo</au><au>Simbula, Gabriella</au><au>de Prati, Alessandra Carcereri</au><au>Menegazzi, Marta</au><au>Suzuki, Hisanori</au><au>Sarma, Dittakavi S. R.</au><au>Ledda‐Columbano, Giovanna M.</au><au>Columbano, Amedeo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1993-06</date><risdate>1993</risdate><volume>17</volume><issue>6</issue><spage>1109</spage><epage>1116</epage><pages>1109-1116</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>The steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA were investigated in rat liver tissue after proliferative stimuli of different nature‐namely, compensatory regeneration induced by partial hepatectomy or carbon tetrachloride administration ‐ and direct hyperplasia induced by four different hepatomitogens: lead nitrate, ethylene dibromide, cyproterone acetate and nafenopin. We show here that whereas c‐fos and c‐jun expression increased soon after partial hepatectomy or carbon tetrachloride administration, an increased expression of c‐jun in the absence of c‐fos expression occurred during direct hyperplasia induced by lead nitrate and ethylene dibromide. When hyperplasia was induced by cyproterone acetate and nafenopin, the mitogenic response of the liver was not associated with an increased expression of c‐jun or c‐fos, despite the fact that the timing of the cell cycle was similar to that observed after partial hepatectomy. Finally, when c‐myc expression was analyzed, it was found that proliferative conditions associated with an increased expression of this gene were characterized by an increased expression of c‐jun. On the contrary, the hyperplasia induced by cyproterone acetate and nafenopin, which is characterized by a lack of increase in the expression of c‐fos and c‐jun, was also not associated with an increased c‐myc expression. Similar results were obtained in these experiments with the mitogen nafenopin, a peroxisome proliferator. In fact, liver hyperplasia induced by this compound was not preceded or accompanied by an increased expression of c‐fos and c‐myc. This study suggests that depending on the nature of the proliferative stimulus, an increased expression of c‐fos, c‐jun and c‐myc may not be necessary for in vivo induction of liver cell proliferation. (HEPATOLOGY 1993;17:1109–1116.)</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>8514261</pmid><doi>10.1002/hep.1840170626</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hepatology (Baltimore, Md.), 1993-06, Vol.17 (6), p.1109-1116 |
| issn | 0270-9139 1527-3350 |
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| source | Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Carbon Tetrachloride - pharmacology Cell Division - drug effects Cyproterone Acetate - pharmacology Degeneration. Regeneration. Wound healing. Graft Ethylene Dibromide - pharmacology Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Genes, fos Genes, jun Genes, myc Hepatectomy Hyperplasia Lead - pharmacology Liver - cytology Liver - drug effects Liver - pathology Liver Regeneration - physiology Male Nafenopin - pharmacology Nitrates - pharmacology Rats Rats, Wistar RNA, Messenger - genetics RNA, Messenger - metabolism Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Differences in the steady‐state levels of c‐fos, c‐jun and c‐myc messenger RNA during mitogen‐induced liver growth and compensatory regeneration |
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