Loading of mechanical pressure activates mitogen-activated protein kinase and early immediate gene in intestinal epithelial cells
Intestinal mucosa is continuously exposed to mechanical forces. We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pres...
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| Veröffentlicht in: | Digestive diseases and sciences 2001-09, Vol.46 (9), p.1993-2003 |
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| container_end_page | 2003 |
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| container_issue | 9 |
| container_start_page | 1993 |
| container_title | Digestive diseases and sciences |
| container_volume | 46 |
| creator | HIROKAWA, Masahiko MIURA, Soichiro KISHIKAWA, Hiroshi YOSHIDA, Hideo NAKAMIZO, Hiromasa HIGUCHI, Hajime NAKATSUMI, Ruri C SUZUKI, Hidekazu SAITO, Hidetsugu ISHII, Hiromasa |
| description | Intestinal mucosa is continuously exposed to mechanical forces. We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process. |
| doi_str_mv | 10.1023/A:1010607819842 |
| format | Article |
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We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1023/A:1010607819842</identifier><identifier>PMID: 11575455</identifier><identifier>CODEN: DDSCDJ</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; Cell Division ; Cells, Cultured ; Digestive system ; Epithelial Cells - metabolism ; Genes, Immediate-Early - physiology ; Intestinal Mucosa - cytology ; Intestinal Mucosa - physiology ; Investigative techniques, diagnostic techniques (general aspects) ; Medical sciences ; Mitogen-Activated Protein Kinases - metabolism ; Pathology. Cytology. Biochemistry. Spectrometry. 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We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Division</subject><subject>Cells, Cultured</subject><subject>Digestive system</subject><subject>Epithelial Cells - metabolism</subject><subject>Genes, Immediate-Early - physiology</subject><subject>Intestinal Mucosa - cytology</subject><subject>Intestinal Mucosa - physiology</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. 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Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Pressure</topic><topic>Rats</topic><topic>Signal Transduction - physiology</topic><topic>Stress, Mechanical</topic><topic>Transcription Factor AP-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HIROKAWA, Masahiko</creatorcontrib><creatorcontrib>MIURA, Soichiro</creatorcontrib><creatorcontrib>KISHIKAWA, Hiroshi</creatorcontrib><creatorcontrib>YOSHIDA, Hideo</creatorcontrib><creatorcontrib>NAKAMIZO, Hiromasa</creatorcontrib><creatorcontrib>HIGUCHI, Hajime</creatorcontrib><creatorcontrib>NAKATSUMI, Ruri C</creatorcontrib><creatorcontrib>SUZUKI, Hidekazu</creatorcontrib><creatorcontrib>SAITO, Hidetsugu</creatorcontrib><creatorcontrib>ISHII, Hiromasa</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HIROKAWA, Masahiko</au><au>MIURA, Soichiro</au><au>KISHIKAWA, Hiroshi</au><au>YOSHIDA, Hideo</au><au>NAKAMIZO, Hiromasa</au><au>HIGUCHI, Hajime</au><au>NAKATSUMI, Ruri C</au><au>SUZUKI, Hidekazu</au><au>SAITO, Hidetsugu</au><au>ISHII, Hiromasa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loading of mechanical pressure activates mitogen-activated protein kinase and early immediate gene in intestinal epithelial cells</atitle><jtitle>Digestive diseases and sciences</jtitle><addtitle>Dig Dis Sci</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>46</volume><issue>9</issue><spage>1993</spage><epage>2003</epage><pages>1993-2003</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><coden>DDSCDJ</coden><abstract>Intestinal mucosa is continuously exposed to mechanical forces. We examined whether pressure loading activates mitogen-activated protein kinase (MAPK) and expression of early immediate genes in intestinal epithelial cells. Pressure was applied to IEC18 cells by helium gas in a culture flask and pressure-induced cell proliferation was examined. The expression of early immediate genes, MAPK activity, and activation of nuclear factor activator protein-1 (AP-1) were also examined. Pressures significantly promoted cell proliferation with peak effect at 80 mm Hg. Pretreatment with either a protein kinase C inhibitor or tyrosine kinase inhibitors, but not calcium chelating agents significantly inhibited cell proliferation promoted by pressure. Early inductions of c-myc and c-fos proteins, increased activity of MAPK, and activation of AP-1 were observed by pressure loading. Our study showed that intestinal mucosal cell proliferation is promoted by mechanical pressure and various intracellular signaling pathways are involved in the process.</abstract><cop>Heidelberg</cop><pub>Springer</pub><pmid>11575455</pmid><doi>10.1023/A:1010607819842</doi><tpages>11</tpages></addata></record> |
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| ispartof | Digestive diseases and sciences, 2001-09, Vol.46 (9), p.1993-2003 |
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| subjects | Animals Biological and medical sciences Blotting, Western Cell Division Cells, Cultured Digestive system Epithelial Cells - metabolism Genes, Immediate-Early - physiology Intestinal Mucosa - cytology Intestinal Mucosa - physiology Investigative techniques, diagnostic techniques (general aspects) Medical sciences Mitogen-Activated Protein Kinases - metabolism Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Pressure Rats Signal Transduction - physiology Stress, Mechanical Transcription Factor AP-1 - metabolism |
| title | Loading of mechanical pressure activates mitogen-activated protein kinase and early immediate gene in intestinal epithelial cells |
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