Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells
Airway remodeling, including increased airway smooth muscle (ASM) mass, is a hallmark feature of asthma and COPD. We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation...
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Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 2017-07, Vol.313 (1), p.L154-L165 |
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creator | Pan, Shi Sharma, Pawan Shah, Sushrut D Deshpande, Deepak A |
description | Airway remodeling, including increased airway smooth muscle (ASM) mass, is a hallmark feature of asthma and COPD. We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation and inhibit mitogen-induced ASM growth. In this study, we explored cellular mechanisms mediating the antimitogenic effect of TAS2R agonists on human ASM cells. Pretreatment of ASM cells with TAS2R agonists chloroquine and quinine resulted in inhibition of cell survival, which was largely reversed by bafilomycin A1, an autophagy inhibitor. Transmission electron microscope studies demonstrated the presence of double-membrane autophagosomes and deformed mitochondria. In ASM cells, TAS2R agonists decreased mitochondrial membrane potential and increased mitochondrial ROS and mitochondrial fragmentation. Inhibiting dynamin-like protein 1 (DLP1) reversed TAS2R agonist-induced mitochondrial membrane potential change and attenuated mitochondrial fragmentation and cell death. Furthermore, the expression of mitochondrial protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) and mitochondrial localization of DLP1 were significantly upregulated by TAS2R agonists. More importantly, inhibiting Bnip3 mitochondrial localization by dominant-negative Bnip3 significantly attenuated cell death induced by TAS2R agonist. Collectively the TAS2R agonists chloroquine and quinine modulate mitochondrial structure and function, resulting in ASM cell death. Furthermore, Bnip3 plays a central role in TAS2R agonist-induced ASM functional changes via a mitochondrial pathway. These findings further establish the cellular mechanisms of antimitogenic effects of TAS2R agonists and identify a novel class of receptors and pathways that can be targeted to mitigate airway remodeling as well as bronchoconstriction in obstructive airway diseases. |
doi_str_mv | 10.1152/ajplung.00106.2017 |
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We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation and inhibit mitogen-induced ASM growth. In this study, we explored cellular mechanisms mediating the antimitogenic effect of TAS2R agonists on human ASM cells. Pretreatment of ASM cells with TAS2R agonists chloroquine and quinine resulted in inhibition of cell survival, which was largely reversed by bafilomycin A1, an autophagy inhibitor. Transmission electron microscope studies demonstrated the presence of double-membrane autophagosomes and deformed mitochondria. In ASM cells, TAS2R agonists decreased mitochondrial membrane potential and increased mitochondrial ROS and mitochondrial fragmentation. Inhibiting dynamin-like protein 1 (DLP1) reversed TAS2R agonist-induced mitochondrial membrane potential change and attenuated mitochondrial fragmentation and cell death. Furthermore, the expression of mitochondrial protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) and mitochondrial localization of DLP1 were significantly upregulated by TAS2R agonists. More importantly, inhibiting Bnip3 mitochondrial localization by dominant-negative Bnip3 significantly attenuated cell death induced by TAS2R agonist. Collectively the TAS2R agonists chloroquine and quinine modulate mitochondrial structure and function, resulting in ASM cell death. Furthermore, Bnip3 plays a central role in TAS2R agonist-induced ASM functional changes via a mitochondrial pathway. These findings further establish the cellular mechanisms of antimitogenic effects of TAS2R agonists and identify a novel class of receptors and pathways that can be targeted to mitigate airway remodeling as well as bronchoconstriction in obstructive airway diseases.</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.00106.2017</identifier><identifier>PMID: 28450286</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adenosine Triphosphate - metabolism ; Asthma ; Autophagy ; Autophagy - drug effects ; Bitter taste ; BNIP3 protein ; Bronchoconstriction ; Bronchodilation ; Cell Death ; Cell survival ; Cells ; Cells, Cultured ; Chloroquine ; Chronic obstructive pulmonary disease ; Dynamin ; Fragmentation ; Genes, Dominant ; GTP Phosphohydrolases - metabolism ; Humans ; Localization ; Lung - cytology ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Membrane Proteins - metabolism ; Membranes ; Microtubule-Associated Proteins - metabolism ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial Dynamics - drug effects ; Mitochondrial Proteins - metabolism ; Models, Biological ; Muscles ; Muscular system ; Myocytes, Smooth Muscle - cytology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Phagocytosis ; Phagosomes ; Pretreatment ; Proteins ; Proto-Oncogene Proteins - metabolism ; Quinazolinones - pharmacology ; Quinine ; Receptors ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - metabolism ; Respiratory tract diseases ; RNA, Small Interfering - metabolism ; Smooth muscle ; Structure-function relationships ; Taste ; Taste - drug effects ; Taste receptors</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2017-07, Vol.313 (1), p.L154-L165</ispartof><rights>Copyright © 2017 the American Physiological Society.</rights><rights>Copyright American Physiological Society Jul 2017</rights><rights>Copyright © 2017 the American Physiological Society 2017 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-60de1906c6288ac1de5b7d604156784691e65c2028e97758799f15afc80ae46d3</citedby><cites>FETCH-LOGICAL-c430t-60de1906c6288ac1de5b7d604156784691e65c2028e97758799f15afc80ae46d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28450286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Shi</creatorcontrib><creatorcontrib>Sharma, Pawan</creatorcontrib><creatorcontrib>Shah, Sushrut D</creatorcontrib><creatorcontrib>Deshpande, Deepak A</creatorcontrib><title>Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Airway remodeling, including increased airway smooth muscle (ASM) mass, is a hallmark feature of asthma and COPD. We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation and inhibit mitogen-induced ASM growth. In this study, we explored cellular mechanisms mediating the antimitogenic effect of TAS2R agonists on human ASM cells. Pretreatment of ASM cells with TAS2R agonists chloroquine and quinine resulted in inhibition of cell survival, which was largely reversed by bafilomycin A1, an autophagy inhibitor. Transmission electron microscope studies demonstrated the presence of double-membrane autophagosomes and deformed mitochondria. In ASM cells, TAS2R agonists decreased mitochondrial membrane potential and increased mitochondrial ROS and mitochondrial fragmentation. Inhibiting dynamin-like protein 1 (DLP1) reversed TAS2R agonist-induced mitochondrial membrane potential change and attenuated mitochondrial fragmentation and cell death. Furthermore, the expression of mitochondrial protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) and mitochondrial localization of DLP1 were significantly upregulated by TAS2R agonists. More importantly, inhibiting Bnip3 mitochondrial localization by dominant-negative Bnip3 significantly attenuated cell death induced by TAS2R agonist. Collectively the TAS2R agonists chloroquine and quinine modulate mitochondrial structure and function, resulting in ASM cell death. Furthermore, Bnip3 plays a central role in TAS2R agonist-induced ASM functional changes via a mitochondrial pathway. These findings further establish the cellular mechanisms of antimitogenic effects of TAS2R agonists and identify a novel class of receptors and pathways that can be targeted to mitigate airway remodeling as well as bronchoconstriction in obstructive airway diseases.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Asthma</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Bitter taste</subject><subject>BNIP3 protein</subject><subject>Bronchoconstriction</subject><subject>Bronchodilation</subject><subject>Cell Death</subject><subject>Cell survival</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Chloroquine</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Dynamin</subject><subject>Fragmentation</subject><subject>Genes, Dominant</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>Humans</subject><subject>Localization</subject><subject>Lung - cytology</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Membrane Proteins - metabolism</subject><subject>Membranes</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Dynamics - drug effects</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Models, Biological</subject><subject>Muscles</subject><subject>Muscular system</subject><subject>Myocytes, Smooth Muscle - cytology</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Phagocytosis</subject><subject>Phagosomes</subject><subject>Pretreatment</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Quinazolinones - pharmacology</subject><subject>Quinine</subject><subject>Receptors</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Respiratory tract diseases</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Smooth muscle</subject><subject>Structure-function relationships</subject><subject>Taste</subject><subject>Taste - drug effects</subject><subject>Taste receptors</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU-LFDEQxYMo7jr6BTxIwIuXHivdSTp9EXRxVVjwoudQm07PZOhO2vxxmW9vxh0X9VSh3qtHHj9CXjLYMibat3hY5-J3WwAGctsC6x-Ryyq0DRPAH9c3cGhAgrggz1I6AIAAkE_JRau4gFbJS-I_uJxtpBlTtjRaY9ccIsVd8C7lRHE-qYvLweyDH6PDmU7Fm-yCp-hH6vxYjKVYclj3uDvWBUUX7_BI0xJC3tOlJDNbauw8p-fkyYRzsi_Oc0O-X3_8dvW5ufn66cvV-5vG8A5yI2G0bABpZKsUGjZacduPEjgTsldcDsxKYdpawQ59L1Q_DBMTOBkFaLkcuw15d5-7ltvFjsb6HHHWa3QLxqMO6PS_ind7vQs_tRCdUnKoAW_OATH8KDZlvbh0qoDehpI0U0MnuJTVvyGv_7MeQom-1tNsEBK6jouuutp7l4khpWinh88w0Cec-oxT_8apTzjr0au_azyc_OHX_QKhNZ9P</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Pan, Shi</creator><creator>Sharma, Pawan</creator><creator>Shah, Sushrut D</creator><creator>Deshpande, Deepak A</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170701</creationdate><title>Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells</title><author>Pan, Shi ; Sharma, Pawan ; Shah, Sushrut D ; Deshpande, Deepak A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-60de1906c6288ac1de5b7d604156784691e65c2028e97758799f15afc80ae46d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Asthma</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Bitter taste</topic><topic>BNIP3 protein</topic><topic>Bronchoconstriction</topic><topic>Bronchodilation</topic><topic>Cell Death</topic><topic>Cell survival</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Chloroquine</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Dynamin</topic><topic>Fragmentation</topic><topic>Genes, Dominant</topic><topic>GTP Phosphohydrolases - metabolism</topic><topic>Humans</topic><topic>Localization</topic><topic>Lung - cytology</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Membrane Proteins - metabolism</topic><topic>Membranes</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Dynamics - drug effects</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Models, Biological</topic><topic>Muscles</topic><topic>Muscular system</topic><topic>Myocytes, Smooth Muscle - cytology</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Phagocytosis</topic><topic>Phagosomes</topic><topic>Pretreatment</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Quinazolinones - pharmacology</topic><topic>Quinine</topic><topic>Receptors</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Respiratory tract diseases</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Smooth muscle</topic><topic>Structure-function relationships</topic><topic>Taste</topic><topic>Taste - drug effects</topic><topic>Taste receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pan, Shi</creatorcontrib><creatorcontrib>Sharma, Pawan</creatorcontrib><creatorcontrib>Shah, Sushrut D</creatorcontrib><creatorcontrib>Deshpande, Deepak A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pan, Shi</au><au>Sharma, Pawan</au><au>Shah, Sushrut D</au><au>Deshpande, Deepak A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>313</volume><issue>1</issue><spage>L154</spage><epage>L165</epage><pages>L154-L165</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>Airway remodeling, including increased airway smooth muscle (ASM) mass, is a hallmark feature of asthma and COPD. We previously identified the expression of bitter taste receptors (TAS2Rs) on human ASM cells and demonstrated that known TAS2R agonists could promote ASM relaxation and bronchodilation and inhibit mitogen-induced ASM growth. In this study, we explored cellular mechanisms mediating the antimitogenic effect of TAS2R agonists on human ASM cells. Pretreatment of ASM cells with TAS2R agonists chloroquine and quinine resulted in inhibition of cell survival, which was largely reversed by bafilomycin A1, an autophagy inhibitor. Transmission electron microscope studies demonstrated the presence of double-membrane autophagosomes and deformed mitochondria. In ASM cells, TAS2R agonists decreased mitochondrial membrane potential and increased mitochondrial ROS and mitochondrial fragmentation. Inhibiting dynamin-like protein 1 (DLP1) reversed TAS2R agonist-induced mitochondrial membrane potential change and attenuated mitochondrial fragmentation and cell death. Furthermore, the expression of mitochondrial protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) and mitochondrial localization of DLP1 were significantly upregulated by TAS2R agonists. More importantly, inhibiting Bnip3 mitochondrial localization by dominant-negative Bnip3 significantly attenuated cell death induced by TAS2R agonist. Collectively the TAS2R agonists chloroquine and quinine modulate mitochondrial structure and function, resulting in ASM cell death. Furthermore, Bnip3 plays a central role in TAS2R agonist-induced ASM functional changes via a mitochondrial pathway. These findings further establish the cellular mechanisms of antimitogenic effects of TAS2R agonists and identify a novel class of receptors and pathways that can be targeted to mitigate airway remodeling as well as bronchoconstriction in obstructive airway diseases.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>28450286</pmid><doi>10.1152/ajplung.00106.2017</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adenosine Triphosphate - metabolism Asthma Autophagy Autophagy - drug effects Bitter taste BNIP3 protein Bronchoconstriction Bronchodilation Cell Death Cell survival Cells Cells, Cultured Chloroquine Chronic obstructive pulmonary disease Dynamin Fragmentation Genes, Dominant GTP Phosphohydrolases - metabolism Humans Localization Lung - cytology Membrane potential Membrane Potential, Mitochondrial - drug effects Membrane Proteins - metabolism Membranes Microtubule-Associated Proteins - metabolism Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Dynamics - drug effects Mitochondrial Proteins - metabolism Models, Biological Muscles Muscular system Myocytes, Smooth Muscle - cytology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Phagocytosis Phagosomes Pretreatment Proteins Proto-Oncogene Proteins - metabolism Quinazolinones - pharmacology Quinine Receptors Receptors, G-Protein-Coupled - agonists Receptors, G-Protein-Coupled - metabolism Respiratory tract diseases RNA, Small Interfering - metabolism Smooth muscle Structure-function relationships Taste Taste - drug effects Taste receptors |
title | Bitter taste receptor agonists alter mitochondrial function and induce autophagy in airway smooth muscle cells |
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