HMGB1-downregulated angulin-1/LSR induces epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells
A non-histone chromatin-associated protein, high mobility group box 1 (HMGB1), which impairs the airway epithelial barrier, is involved in the induction of airway inflammation in patients with allergy, asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Tri...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2020-06, Vol.527 (2), p.553-560 |
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| creator | Kodera, Yuki Chiba, Hirofumi Konno, Takumi Kohno, Takayuki Takahashi, Hiroki Kojima, Takashi |
| description | A non-histone chromatin-associated protein, high mobility group box 1 (HMGB1), which impairs the airway epithelial barrier, is involved in the induction of airway inflammation in patients with allergy, asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Tricellular tight junctions (tTJs) form at the convergence of bicellular tight junctions (bTJs). Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecule present at tricellular contacts and contributes to the epithelial barrier and cellular metabolism. Adenosine monophosphate-activated protein kinase (AMPK) is a central metabolic regulator and has a reciprocal association with TJs. In the present study, to examine how HMGB1 contributes to airway epithelial barrier disruption and the cellular metabolism indicated as mitochondrial respiration, bronchial epithelial Calu-3 cells were transfected with siRNAs of angulin-1/LSR or treated with HMGB1 and the relationship between HMGB1 and angulin-1/LSR was investigated. Knockdown of angulin-1/LSR upregulated the expression of the tight junction molecule claudin-2, AMPK activity, and mitochondrial respiration, and downregulated the epithelial barrier. Treatment with HMGB1 downregulated angulin-1/LSR expression and the epithelial barrier, and upregulated claudin-2 expression, AMPK activity and mitochondrial respiration. Treatment with EW-7197, a transforming growth factor-β (TGF-β) type I receptor kinase inhibitor, prevented all the effects of HMGB1 in Calu-3 cells. HMGB1-downregulated angulin-1/LSR induced epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells. The effects of HMGB1 contribute to TGF-β signaling and EW-7197 shows potential for use in therapy for HMGB1-induced airway inflammation.
•HMGB1-impaired airway epithelial barrier is involved in airway inflammation.•Angulin-1/LSR contributes to the airway epithelial barrier and cellular metabolism.•AMPK has a reciprocal association with cellular metabolism and tight junctions.•Downregulation of angulin-1/LSR induces claudin-2 and AMPK activity.•HMGB1-downregulated LSR induces barrier disruption and cellular metabolism. |
| doi_str_mv | 10.1016/j.bbrc.2020.04.113 |
| format | Article |
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•HMGB1-impaired airway epithelial barrier is involved in airway inflammation.•Angulin-1/LSR contributes to the airway epithelial barrier and cellular metabolism.•AMPK has a reciprocal association with cellular metabolism and tight junctions.•Downregulation of angulin-1/LSR induces claudin-2 and AMPK activity.•HMGB1-downregulated LSR induces barrier disruption and cellular metabolism.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2020.04.113</identifier><identifier>PMID: 32423802</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>AMP-Activated Protein Kinases - metabolism ; AMPK ; Angulin-1/LSR ; Cell Line ; Cellular metabolism ; Claudin-2 ; Claudin-2 - metabolism ; Down-Regulation ; Epithelial barrier ; Epithelial Cells - metabolism ; HMGB1 ; HMGB1 Protein - metabolism ; Humans ; Inflammation - metabolism ; Receptors, Lipoprotein - metabolism ; Respiratory Mucosa - cytology ; Respiratory Mucosa - metabolism ; Tight Junctions - metabolism</subject><ispartof>Biochemical and biophysical research communications, 2020-06, Vol.527 (2), p.553-560</ispartof><rights>2020 The Authors</rights><rights>Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-db0206804d5b70d94e082d35a33d430dee10af921f3513b8d585139c2d611ab93</citedby><cites>FETCH-LOGICAL-c466t-db0206804d5b70d94e082d35a33d430dee10af921f3513b8d585139c2d611ab93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X20308536$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32423802$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kodera, Yuki</creatorcontrib><creatorcontrib>Chiba, Hirofumi</creatorcontrib><creatorcontrib>Konno, Takumi</creatorcontrib><creatorcontrib>Kohno, Takayuki</creatorcontrib><creatorcontrib>Takahashi, Hiroki</creatorcontrib><creatorcontrib>Kojima, Takashi</creatorcontrib><title>HMGB1-downregulated angulin-1/LSR induces epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>A non-histone chromatin-associated protein, high mobility group box 1 (HMGB1), which impairs the airway epithelial barrier, is involved in the induction of airway inflammation in patients with allergy, asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Tricellular tight junctions (tTJs) form at the convergence of bicellular tight junctions (bTJs). Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecule present at tricellular contacts and contributes to the epithelial barrier and cellular metabolism. Adenosine monophosphate-activated protein kinase (AMPK) is a central metabolic regulator and has a reciprocal association with TJs. In the present study, to examine how HMGB1 contributes to airway epithelial barrier disruption and the cellular metabolism indicated as mitochondrial respiration, bronchial epithelial Calu-3 cells were transfected with siRNAs of angulin-1/LSR or treated with HMGB1 and the relationship between HMGB1 and angulin-1/LSR was investigated. Knockdown of angulin-1/LSR upregulated the expression of the tight junction molecule claudin-2, AMPK activity, and mitochondrial respiration, and downregulated the epithelial barrier. Treatment with HMGB1 downregulated angulin-1/LSR expression and the epithelial barrier, and upregulated claudin-2 expression, AMPK activity and mitochondrial respiration. Treatment with EW-7197, a transforming growth factor-β (TGF-β) type I receptor kinase inhibitor, prevented all the effects of HMGB1 in Calu-3 cells. HMGB1-downregulated angulin-1/LSR induced epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells. The effects of HMGB1 contribute to TGF-β signaling and EW-7197 shows potential for use in therapy for HMGB1-induced airway inflammation.
•HMGB1-impaired airway epithelial barrier is involved in airway inflammation.•Angulin-1/LSR contributes to the airway epithelial barrier and cellular metabolism.•AMPK has a reciprocal association with cellular metabolism and tight junctions.•Downregulation of angulin-1/LSR induces claudin-2 and AMPK activity.•HMGB1-downregulated LSR induces barrier disruption and cellular metabolism.</description><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>AMPK</subject><subject>Angulin-1/LSR</subject><subject>Cell Line</subject><subject>Cellular metabolism</subject><subject>Claudin-2</subject><subject>Claudin-2 - metabolism</subject><subject>Down-Regulation</subject><subject>Epithelial barrier</subject><subject>Epithelial Cells - metabolism</subject><subject>HMGB1</subject><subject>HMGB1 Protein - metabolism</subject><subject>Humans</subject><subject>Inflammation - metabolism</subject><subject>Receptors, Lipoprotein - metabolism</subject><subject>Respiratory Mucosa - cytology</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Tight Junctions - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFu1DAQhi0EokvLC3BAPnJJOmN700TiUlbQom4FoiBxsxx7Frxykq2dtOqjcONZeDKcbkGcOI0P___JMx9jLxBKBKyOt2XbRlsKEFCCKhHlI7ZAaKAQCOoxWwBAVYgGvx6wZyltARBV1TxlB1IoIWsQC_bj_PLsDRZuuO0jfZuCGclx0-eX7ws8Xl994r53k6XEaefH7xS8Cbw1MXqK3PkUp93oh57feMNtMJPLPZEJjlsKIQMj72g07RB86u5Tp5cfLzKUGx9vzd2_2JUJUyF__Zyb6Yg92ZiQ6PnDPGRf3r39vDov1h_O3q9O14VVVTUWrs3rVzUot2xPwDWKoBZOLo2UTklwRAhm0wjcyCXKtnbLOs_GClchmraRh-zVnruLw_VEadSdT_MPTE_DlLRQoCpZ48kcFfuojUNKkTZ6F31n4p1G0LMSvdWzEj0r0aB0VpJLLx_4U9uR-1v54yAHXu8DlLe8yWfVyXrqLTkfyY7aDf5__N-Vq54l</recordid><startdate>20200625</startdate><enddate>20200625</enddate><creator>Kodera, Yuki</creator><creator>Chiba, Hirofumi</creator><creator>Konno, Takumi</creator><creator>Kohno, Takayuki</creator><creator>Takahashi, Hiroki</creator><creator>Kojima, Takashi</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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><scope>7X8</scope></search><sort><creationdate>20200625</creationdate><title>HMGB1-downregulated angulin-1/LSR induces epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells</title><author>Kodera, Yuki ; Chiba, Hirofumi ; Konno, Takumi ; Kohno, Takayuki ; Takahashi, Hiroki ; Kojima, Takashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-db0206804d5b70d94e082d35a33d430dee10af921f3513b8d585139c2d611ab93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>AMPK</topic><topic>Angulin-1/LSR</topic><topic>Cell Line</topic><topic>Cellular metabolism</topic><topic>Claudin-2</topic><topic>Claudin-2 - metabolism</topic><topic>Down-Regulation</topic><topic>Epithelial barrier</topic><topic>Epithelial Cells - metabolism</topic><topic>HMGB1</topic><topic>HMGB1 Protein - metabolism</topic><topic>Humans</topic><topic>Inflammation - metabolism</topic><topic>Receptors, Lipoprotein - metabolism</topic><topic>Respiratory Mucosa - cytology</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Tight Junctions - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kodera, Yuki</creatorcontrib><creatorcontrib>Chiba, Hirofumi</creatorcontrib><creatorcontrib>Konno, Takumi</creatorcontrib><creatorcontrib>Kohno, Takayuki</creatorcontrib><creatorcontrib>Takahashi, Hiroki</creatorcontrib><creatorcontrib>Kojima, Takashi</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kodera, Yuki</au><au>Chiba, Hirofumi</au><au>Konno, Takumi</au><au>Kohno, Takayuki</au><au>Takahashi, Hiroki</au><au>Kojima, Takashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HMGB1-downregulated angulin-1/LSR induces epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2020-06-25</date><risdate>2020</risdate><volume>527</volume><issue>2</issue><spage>553</spage><epage>560</epage><pages>553-560</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>A non-histone chromatin-associated protein, high mobility group box 1 (HMGB1), which impairs the airway epithelial barrier, is involved in the induction of airway inflammation in patients with allergy, asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Tricellular tight junctions (tTJs) form at the convergence of bicellular tight junctions (bTJs). Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecule present at tricellular contacts and contributes to the epithelial barrier and cellular metabolism. Adenosine monophosphate-activated protein kinase (AMPK) is a central metabolic regulator and has a reciprocal association with TJs. In the present study, to examine how HMGB1 contributes to airway epithelial barrier disruption and the cellular metabolism indicated as mitochondrial respiration, bronchial epithelial Calu-3 cells were transfected with siRNAs of angulin-1/LSR or treated with HMGB1 and the relationship between HMGB1 and angulin-1/LSR was investigated. Knockdown of angulin-1/LSR upregulated the expression of the tight junction molecule claudin-2, AMPK activity, and mitochondrial respiration, and downregulated the epithelial barrier. Treatment with HMGB1 downregulated angulin-1/LSR expression and the epithelial barrier, and upregulated claudin-2 expression, AMPK activity and mitochondrial respiration. Treatment with EW-7197, a transforming growth factor-β (TGF-β) type I receptor kinase inhibitor, prevented all the effects of HMGB1 in Calu-3 cells. HMGB1-downregulated angulin-1/LSR induced epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells. The effects of HMGB1 contribute to TGF-β signaling and EW-7197 shows potential for use in therapy for HMGB1-induced airway inflammation.
•HMGB1-impaired airway epithelial barrier is involved in airway inflammation.•Angulin-1/LSR contributes to the airway epithelial barrier and cellular metabolism.•AMPK has a reciprocal association with cellular metabolism and tight junctions.•Downregulation of angulin-1/LSR induces claudin-2 and AMPK activity.•HMGB1-downregulated LSR induces barrier disruption and cellular metabolism.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>32423802</pmid><doi>10.1016/j.bbrc.2020.04.113</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AMP-Activated Protein Kinases - metabolism AMPK Angulin-1/LSR Cell Line Cellular metabolism Claudin-2 Claudin-2 - metabolism Down-Regulation Epithelial barrier Epithelial Cells - metabolism HMGB1 HMGB1 Protein - metabolism Humans Inflammation - metabolism Receptors, Lipoprotein - metabolism Respiratory Mucosa - cytology Respiratory Mucosa - metabolism Tight Junctions - metabolism |
| title | HMGB1-downregulated angulin-1/LSR induces epithelial barrier disruption via claudin-2 and cellular metabolism via AMPK in airway epithelial Calu-3 cells |
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