MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells
Please cite this paper as: Clark, Jensen, Kluger, Morelock, Hanidu, Qi, Tatake, Pober (2011). MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells. Microcirculation18(2), 102–117. Objective: ECs lining arteries...
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| Veröffentlicht in: | Microcirculation (New York, N.Y. 1994) N.Y. 1994), 2011-02, Vol.18 (2), p.102-117 |
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| creator | CLARK, PAUL R. JENSEN, TODD J. KLUGER, MARTIN S. MORELOCK, MAURICE HANIDU, ADEDAYO QI, ZHENHAO TATAKE, REVATI J. POBER, JORDAN S. |
| description | Please cite this paper as: Clark, Jensen, Kluger, Morelock, Hanidu, Qi, Tatake, Pober (2011). MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells. Microcirculation18(2), 102–117.
Objective: ECs lining arteries respond to LSS by suppressing pro‐inflammatory changes, in part through the activation of MEK5, ERK5 and induction of KLF4. We examined if this anti‐inflammatory pathway operates in human ECs lining microvessels, the principal site of inflammatory responses.
Methods: We used immunofluorescence microscopy of human skin to assess ERK5 activation and KLF4 expression in HDMECs in situ. We applied LSS to or overexpressed MEK5/CA in cultured HDMECs and assessed gene expression by microarrays and qRT‐PCR and protein expression by Western blotting. We assessed effects of MEK5/CA on TNF responses using qRT‐PCR, FACS and measurements of HDMEC monolayer electrical resistance. We used siRNA knockdown to assess the role of ERK5 and KLF4 in these responses.
Results: ERK5 phosphorylation and KLF4 expression is observed in HDMECs in situ. LSS activates ERK5 and induces KLF4 in cultured HDMECs. MEK5/CA‐transduced HDMECs show activated ERK5 and increased KLF4, thrombomodulin, eNOS, and ICAM‐1 expression. MEK5 induction of KLF4 is mediated by ERK5. MEK5/CA‐transduced HDMECs are less responsive to TNF, an effect partly mediated by KLF4.
Conclusions: MEK5 activation by LSS inhibits inflammatory responses in microvascular ECs, in part through ERK5‐dependent induction of KLF4. |
| doi_str_mv | 10.1111/j.1549-8719.2010.00071.x |
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Objective: ECs lining arteries respond to LSS by suppressing pro‐inflammatory changes, in part through the activation of MEK5, ERK5 and induction of KLF4. We examined if this anti‐inflammatory pathway operates in human ECs lining microvessels, the principal site of inflammatory responses.
Methods: We used immunofluorescence microscopy of human skin to assess ERK5 activation and KLF4 expression in HDMECs in situ. We applied LSS to or overexpressed MEK5/CA in cultured HDMECs and assessed gene expression by microarrays and qRT‐PCR and protein expression by Western blotting. We assessed effects of MEK5/CA on TNF responses using qRT‐PCR, FACS and measurements of HDMEC monolayer electrical resistance. We used siRNA knockdown to assess the role of ERK5 and KLF4 in these responses.
Results: ERK5 phosphorylation and KLF4 expression is observed in HDMECs in situ. LSS activates ERK5 and induces KLF4 in cultured HDMECs. MEK5/CA‐transduced HDMECs show activated ERK5 and increased KLF4, thrombomodulin, eNOS, and ICAM‐1 expression. MEK5 induction of KLF4 is mediated by ERK5. MEK5/CA‐transduced HDMECs are less responsive to TNF, an effect partly mediated by KLF4.
Conclusions: MEK5 activation by LSS inhibits inflammatory responses in microvascular ECs, in part through ERK5‐dependent induction of KLF4.</description><identifier>ISSN: 1073-9688</identifier><identifier>EISSN: 1549-8719</identifier><identifier>DOI: 10.1111/j.1549-8719.2010.00071.x</identifier><identifier>PMID: 21166929</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>adhesion molecules ; Base Sequence ; Cells, Cultured ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Enzyme Activation ; Gene Expression Profiling ; Gene Knockdown Techniques ; Humans ; inflammation ; Kruppel-Like Transcription Factors - antagonists & inhibitors ; Kruppel-Like Transcription Factors - biosynthesis ; Kruppel-Like Transcription Factors - genetics ; MAP Kinase Kinase 5 - antagonists & inhibitors ; MAP Kinase Kinase 5 - genetics ; MAP Kinase Kinase 5 - metabolism ; MAP kinases ; Mitogen-Activated Protein Kinase 7 - metabolism ; Oligonucleotide Array Sequence Analysis ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Small Interfering - genetics ; Shear Strength ; skin microvascualture ; Stress, Mechanical ; Tumor Necrosis Factor-alpha - pharmacology ; vascular leak</subject><ispartof>Microcirculation (New York, N.Y. 1994), 2011-02, Vol.18 (2), p.102-117</ispartof><rights>2011 John Wiley & Sons Ltd</rights><rights>2011 John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5271-917929747283c863fc074a744c7ea05e88af3232af45c49f1c9baae1394188623</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1549-8719.2010.00071.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1549-8719.2010.00071.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21166929$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CLARK, PAUL R.</creatorcontrib><creatorcontrib>JENSEN, TODD J.</creatorcontrib><creatorcontrib>KLUGER, MARTIN S.</creatorcontrib><creatorcontrib>MORELOCK, MAURICE</creatorcontrib><creatorcontrib>HANIDU, ADEDAYO</creatorcontrib><creatorcontrib>QI, ZHENHAO</creatorcontrib><creatorcontrib>TATAKE, REVATI J.</creatorcontrib><creatorcontrib>POBER, JORDAN S.</creatorcontrib><title>MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells</title><title>Microcirculation (New York, N.Y. 1994)</title><addtitle>Microcirculation</addtitle><description>Please cite this paper as: Clark, Jensen, Kluger, Morelock, Hanidu, Qi, Tatake, Pober (2011). MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells. Microcirculation18(2), 102–117.
Objective: ECs lining arteries respond to LSS by suppressing pro‐inflammatory changes, in part through the activation of MEK5, ERK5 and induction of KLF4. We examined if this anti‐inflammatory pathway operates in human ECs lining microvessels, the principal site of inflammatory responses.
Methods: We used immunofluorescence microscopy of human skin to assess ERK5 activation and KLF4 expression in HDMECs in situ. We applied LSS to or overexpressed MEK5/CA in cultured HDMECs and assessed gene expression by microarrays and qRT‐PCR and protein expression by Western blotting. We assessed effects of MEK5/CA on TNF responses using qRT‐PCR, FACS and measurements of HDMEC monolayer electrical resistance. We used siRNA knockdown to assess the role of ERK5 and KLF4 in these responses.
Results: ERK5 phosphorylation and KLF4 expression is observed in HDMECs in situ. LSS activates ERK5 and induces KLF4 in cultured HDMECs. MEK5/CA‐transduced HDMECs show activated ERK5 and increased KLF4, thrombomodulin, eNOS, and ICAM‐1 expression. MEK5 induction of KLF4 is mediated by ERK5. MEK5/CA‐transduced HDMECs are less responsive to TNF, an effect partly mediated by KLF4.
Conclusions: MEK5 activation by LSS inhibits inflammatory responses in microvascular ECs, in part through ERK5‐dependent induction of KLF4.</description><subject>adhesion molecules</subject><subject>Base Sequence</subject><subject>Cells, Cultured</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Enzyme Activation</subject><subject>Gene Expression Profiling</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>inflammation</subject><subject>Kruppel-Like Transcription Factors - antagonists & inhibitors</subject><subject>Kruppel-Like Transcription Factors - biosynthesis</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>MAP Kinase Kinase 5 - antagonists & inhibitors</subject><subject>MAP Kinase Kinase 5 - genetics</subject><subject>MAP Kinase Kinase 5 - metabolism</subject><subject>MAP kinases</subject><subject>Mitogen-Activated Protein Kinase 7 - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>Shear Strength</subject><subject>skin microvascualture</subject><subject>Stress, Mechanical</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>vascular leak</subject><issn>1073-9688</issn><issn>1549-8719</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkV1v0zAUhiMEYmPwF5DvuCHFn7EtIaQttFtZM6RtwKXlOg51yUdnJ6X9D_xoXDoi8I2t8z7nPcd6kwQgOEHxvFtPEKMyFRzJCYaxCiHkaLJ7kpyOwtP4hpykMhPiJHkRwjpCQmD5PDnBCGWZxPI0-VVMrxlwAZyb3m11b0uw3IO7ldUe3PXehvB2lAKY3kZYtyWYt-VgYuF6MaOg70DRlUMdEXB_MwO3Nmy6NkTZteBqaHQLPlrf6BoUzvhuq4OJsAfTtuz6la1dVHJb1-Fl8qzSdbCvHu-z5Mtsep9fpYvPl_P8fJEahjlKJeJxd045FsSIjFQGcqo5pYZbDZkVQlcEE6wrygyVFTJyqbVFRFIkRIbJWfLh6LsZlo0tjW17r2u18a7Rfq867dT_SutW6nu3VQRyJiiNBm8eDXz3MNjQq8YFE7-gW9sNQQkGWYYRyyL5-t9R44y_CUTg_RH46Wq7H3UE1SFptVaHQNUhUHVIWv1JWu1UMc9zjmJ7emx3obe7sV37HyrjhDP17eZSfb3ILsinvFCC_AYZW6rA</recordid><startdate>201102</startdate><enddate>201102</enddate><creator>CLARK, PAUL R.</creator><creator>JENSEN, TODD J.</creator><creator>KLUGER, MARTIN S.</creator><creator>MORELOCK, MAURICE</creator><creator>HANIDU, ADEDAYO</creator><creator>QI, ZHENHAO</creator><creator>TATAKE, REVATI J.</creator><creator>POBER, JORDAN S.</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201102</creationdate><title>MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells</title><author>CLARK, PAUL R. ; JENSEN, TODD J. ; KLUGER, MARTIN S. ; MORELOCK, MAURICE ; HANIDU, ADEDAYO ; QI, ZHENHAO ; TATAKE, REVATI J. ; POBER, JORDAN S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5271-917929747283c863fc074a744c7ea05e88af3232af45c49f1c9baae1394188623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>adhesion molecules</topic><topic>Base Sequence</topic><topic>Cells, Cultured</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Enzyme Activation</topic><topic>Gene Expression Profiling</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>inflammation</topic><topic>Kruppel-Like Transcription Factors - antagonists & inhibitors</topic><topic>Kruppel-Like Transcription Factors - biosynthesis</topic><topic>Kruppel-Like Transcription Factors - genetics</topic><topic>MAP Kinase Kinase 5 - antagonists & inhibitors</topic><topic>MAP Kinase Kinase 5 - genetics</topic><topic>MAP Kinase Kinase 5 - metabolism</topic><topic>MAP kinases</topic><topic>Mitogen-Activated Protein Kinase 7 - metabolism</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>Shear Strength</topic><topic>skin microvascualture</topic><topic>Stress, Mechanical</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>vascular leak</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CLARK, PAUL R.</creatorcontrib><creatorcontrib>JENSEN, TODD J.</creatorcontrib><creatorcontrib>KLUGER, MARTIN S.</creatorcontrib><creatorcontrib>MORELOCK, MAURICE</creatorcontrib><creatorcontrib>HANIDU, ADEDAYO</creatorcontrib><creatorcontrib>QI, ZHENHAO</creatorcontrib><creatorcontrib>TATAKE, REVATI J.</creatorcontrib><creatorcontrib>POBER, JORDAN S.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Microcirculation (New York, N.Y. 1994)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CLARK, PAUL R.</au><au>JENSEN, TODD J.</au><au>KLUGER, MARTIN S.</au><au>MORELOCK, MAURICE</au><au>HANIDU, ADEDAYO</au><au>QI, ZHENHAO</au><au>TATAKE, REVATI J.</au><au>POBER, JORDAN S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells</atitle><jtitle>Microcirculation (New York, N.Y. 1994)</jtitle><addtitle>Microcirculation</addtitle><date>2011-02</date><risdate>2011</risdate><volume>18</volume><issue>2</issue><spage>102</spage><epage>117</epage><pages>102-117</pages><issn>1073-9688</issn><eissn>1549-8719</eissn><abstract>Please cite this paper as: Clark, Jensen, Kluger, Morelock, Hanidu, Qi, Tatake, Pober (2011). MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells. Microcirculation18(2), 102–117.
Objective: ECs lining arteries respond to LSS by suppressing pro‐inflammatory changes, in part through the activation of MEK5, ERK5 and induction of KLF4. We examined if this anti‐inflammatory pathway operates in human ECs lining microvessels, the principal site of inflammatory responses.
Methods: We used immunofluorescence microscopy of human skin to assess ERK5 activation and KLF4 expression in HDMECs in situ. We applied LSS to or overexpressed MEK5/CA in cultured HDMECs and assessed gene expression by microarrays and qRT‐PCR and protein expression by Western blotting. We assessed effects of MEK5/CA on TNF responses using qRT‐PCR, FACS and measurements of HDMEC monolayer electrical resistance. We used siRNA knockdown to assess the role of ERK5 and KLF4 in these responses.
Results: ERK5 phosphorylation and KLF4 expression is observed in HDMECs in situ. LSS activates ERK5 and induces KLF4 in cultured HDMECs. MEK5/CA‐transduced HDMECs show activated ERK5 and increased KLF4, thrombomodulin, eNOS, and ICAM‐1 expression. MEK5 induction of KLF4 is mediated by ERK5. MEK5/CA‐transduced HDMECs are less responsive to TNF, an effect partly mediated by KLF4.
Conclusions: MEK5 activation by LSS inhibits inflammatory responses in microvascular ECs, in part through ERK5‐dependent induction of KLF4.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>21166929</pmid><doi>10.1111/j.1549-8719.2010.00071.x</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | adhesion molecules Base Sequence Cells, Cultured Endothelial Cells - drug effects Endothelial Cells - metabolism Enzyme Activation Gene Expression Profiling Gene Knockdown Techniques Humans inflammation Kruppel-Like Transcription Factors - antagonists & inhibitors Kruppel-Like Transcription Factors - biosynthesis Kruppel-Like Transcription Factors - genetics MAP Kinase Kinase 5 - antagonists & inhibitors MAP Kinase Kinase 5 - genetics MAP Kinase Kinase 5 - metabolism MAP kinases Mitogen-Activated Protein Kinase 7 - metabolism Oligonucleotide Array Sequence Analysis RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - genetics Shear Strength skin microvascualture Stress, Mechanical Tumor Necrosis Factor-alpha - pharmacology vascular leak |
| title | MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses in Human Dermal Microvascular Endothelial Cells |
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