Modulation of bleomycin-induced lung fibrosis by pegylated hyaluronidase and dopamine receptor antagonist in mice
Hyaluronidases are groups of enzymes that degrade hyaluronic acid (HA). To stop enzymatic hydrolysis we modified testicular hyaluronidase (HYAL) by activated polyethylene oxide with the help of electron-beam synthesis. As a result we received pegylated hyaluronidase (pegHYAL). Spiperone is a selecti...
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| Veröffentlicht in: | PloS one 2015-04, Vol.10 (4), p.e0125065 |
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| creator | Skurikhin, Evgenii Germanovich Pershina, Olga Victorovna Reztsova, Alena Mikhaylovna Ermakova, Natalia Nikolaevna Khmelevskaya, Ekaterina Sergeevna Krupin, Vycheslav Andreevich Stepanova, Inna Ernestovna Artamonov, Andrew Vladimirovich Bekarev, Andrew Alexandrovich Madonov, Pavel Gennadjevich Dygai, Alexander Mikhaylovich |
| description | Hyaluronidases are groups of enzymes that degrade hyaluronic acid (HA). To stop enzymatic hydrolysis we modified testicular hyaluronidase (HYAL) by activated polyethylene oxide with the help of electron-beam synthesis. As a result we received pegylated hyaluronidase (pegHYAL). Spiperone is a selective D2 dopamine receptor antagonist. It was demonstrated on the model of a single bleomycin damage of alveolar epithelium that during the inflammatory phase monotherapy by pegHYAL or spiperone reduced the populations of hematopoietic stem /progenitor cells in the lung parenchyma. PegHYAL also reduced the levels of transforming growth factor (TGF)-β, interleukin (IL)-1β, tumor necrosis factor (TNF)-α in the serum and lungs, while spiperone reduced the level of the serum IL-1β. Polytherapy by spiperone and pegHYAL caused the increase of the quantity of hematopoietic stem/ progenitor cells in the lungs. Such an influx of blood cell precursors was observed on the background of considerable fall level of TGF-β and the increase level of TNF-α in the serum and lungs. These results show pegHYAL reduced the bleomycin-induced fibrosis reaction (production and accumulation of collagen) in the lung parenchyma. This effect was observed at a single and repetitive bleomycin damage of alveolar epithelium, the antifibrotic activity of pegHYAL surpassing the activity of testicular HYAL. The antifibrotic effect of pegHYAL is enhanced by an additional instillation of spiperone. Therapy by pegHYAL causes the flow of CD31‒ CD34‒ CD45‒ CD44+ CD73+ CD90+ CD106+-cells into the fibrous lungs. These cells are incapable of differentiating into fibroblast cells. Spiperone instillation separately or together with pegHYAL reduced the MSC-like cells considerably. These data enable us to assume, that pegHYAL is a new and promising instrument both for preventive and therapy of toxic pneumofibrosis. The blockage of D2 dopamine receptors with the following change of hyaluronan matrix can be considered as a new strategy in treatment of pneumofibrosis. |
| doi_str_mv | 10.1371/journal.pone.0125065 |
| format | Article |
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To stop enzymatic hydrolysis we modified testicular hyaluronidase (HYAL) by activated polyethylene oxide with the help of electron-beam synthesis. As a result we received pegylated hyaluronidase (pegHYAL). Spiperone is a selective D2 dopamine receptor antagonist. It was demonstrated on the model of a single bleomycin damage of alveolar epithelium that during the inflammatory phase monotherapy by pegHYAL or spiperone reduced the populations of hematopoietic stem /progenitor cells in the lung parenchyma. PegHYAL also reduced the levels of transforming growth factor (TGF)-β, interleukin (IL)-1β, tumor necrosis factor (TNF)-α in the serum and lungs, while spiperone reduced the level of the serum IL-1β. Polytherapy by spiperone and pegHYAL caused the increase of the quantity of hematopoietic stem/ progenitor cells in the lungs. Such an influx of blood cell precursors was observed on the background of considerable fall level of TGF-β and the increase level of TNF-α in the serum and lungs. These results show pegHYAL reduced the bleomycin-induced fibrosis reaction (production and accumulation of collagen) in the lung parenchyma. This effect was observed at a single and repetitive bleomycin damage of alveolar epithelium, the antifibrotic activity of pegHYAL surpassing the activity of testicular HYAL. The antifibrotic effect of pegHYAL is enhanced by an additional instillation of spiperone. Therapy by pegHYAL causes the flow of CD31‒ CD34‒ CD45‒ CD44+ CD73+ CD90+ CD106+-cells into the fibrous lungs. These cells are incapable of differentiating into fibroblast cells. Spiperone instillation separately or together with pegHYAL reduced the MSC-like cells considerably. These data enable us to assume, that pegHYAL is a new and promising instrument both for preventive and therapy of toxic pneumofibrosis. The blockage of D2 dopamine receptors with the following change of hyaluronan matrix can be considered as a new strategy in treatment of pneumofibrosis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0125065</identifier><identifier>PMID: 25927611</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alveoli ; Analysis ; Animals ; Bleomycin ; Bleomycin - toxicity ; Blockage ; Blood cells ; Bone morphogenetic proteins ; CD34 antigen ; CD44 antigen ; CD45 antigen ; CD73 antigen ; CD90 antigen ; Cells (biology) ; Collagen ; Dopamine ; Dopamine Antagonists - therapeutic use ; Dopamine D2 receptors ; Dopamine receptors ; Electron beams ; Enzyme-Linked Immunosorbent Assay ; Enzymes ; Epithelium ; Fibrosis ; Flow Cytometry ; Hematopoietic stem cells ; Hyaluronic acid ; Hyaluronoglucosaminidase - chemistry ; Hyaluronoglucosaminidase - therapeutic use ; IL-1β ; Inflammation ; Interleukins ; Lungs ; Male ; Mice ; Mice, Inbred C57BL ; Parenchyma ; Phenols (Class of compounds) ; Polyethylene ; Polyethylene oxide ; Polyethylenes ; Pulmonary Fibrosis - chemically induced ; Pulmonary Fibrosis - drug therapy ; Receptors ; Spiperone ; Spiperone - therapeutic use ; Testes ; Therapy ; Transforming growth factor ; Transforming growth factors ; Tumor necrosis factor ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2015-04, Vol.10 (4), p.e0125065</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Skurikhin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Skurikhin et al 2015 Skurikhin et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-b7f0751c394c4547daf76a9598983d80f1381201e4299dc362d226287270651e3</citedby><cites>FETCH-LOGICAL-c692t-b7f0751c394c4547daf76a9598983d80f1381201e4299dc362d226287270651e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415936/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415936/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25927611$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Shi, Wei</contributor><creatorcontrib>Skurikhin, Evgenii Germanovich</creatorcontrib><creatorcontrib>Pershina, Olga Victorovna</creatorcontrib><creatorcontrib>Reztsova, Alena Mikhaylovna</creatorcontrib><creatorcontrib>Ermakova, Natalia Nikolaevna</creatorcontrib><creatorcontrib>Khmelevskaya, Ekaterina Sergeevna</creatorcontrib><creatorcontrib>Krupin, Vycheslav Andreevich</creatorcontrib><creatorcontrib>Stepanova, Inna Ernestovna</creatorcontrib><creatorcontrib>Artamonov, Andrew Vladimirovich</creatorcontrib><creatorcontrib>Bekarev, Andrew Alexandrovich</creatorcontrib><creatorcontrib>Madonov, Pavel Gennadjevich</creatorcontrib><creatorcontrib>Dygai, Alexander Mikhaylovich</creatorcontrib><title>Modulation of bleomycin-induced lung fibrosis by pegylated hyaluronidase and dopamine receptor antagonist in mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hyaluronidases are groups of enzymes that degrade hyaluronic acid (HA). To stop enzymatic hydrolysis we modified testicular hyaluronidase (HYAL) by activated polyethylene oxide with the help of electron-beam synthesis. As a result we received pegylated hyaluronidase (pegHYAL). Spiperone is a selective D2 dopamine receptor antagonist. It was demonstrated on the model of a single bleomycin damage of alveolar epithelium that during the inflammatory phase monotherapy by pegHYAL or spiperone reduced the populations of hematopoietic stem /progenitor cells in the lung parenchyma. PegHYAL also reduced the levels of transforming growth factor (TGF)-β, interleukin (IL)-1β, tumor necrosis factor (TNF)-α in the serum and lungs, while spiperone reduced the level of the serum IL-1β. Polytherapy by spiperone and pegHYAL caused the increase of the quantity of hematopoietic stem/ progenitor cells in the lungs. Such an influx of blood cell precursors was observed on the background of considerable fall level of TGF-β and the increase level of TNF-α in the serum and lungs. These results show pegHYAL reduced the bleomycin-induced fibrosis reaction (production and accumulation of collagen) in the lung parenchyma. This effect was observed at a single and repetitive bleomycin damage of alveolar epithelium, the antifibrotic activity of pegHYAL surpassing the activity of testicular HYAL. The antifibrotic effect of pegHYAL is enhanced by an additional instillation of spiperone. Therapy by pegHYAL causes the flow of CD31‒ CD34‒ CD45‒ CD44+ CD73+ CD90+ CD106+-cells into the fibrous lungs. These cells are incapable of differentiating into fibroblast cells. Spiperone instillation separately or together with pegHYAL reduced the MSC-like cells considerably. These data enable us to assume, that pegHYAL is a new and promising instrument both for preventive and therapy of toxic pneumofibrosis. The blockage of D2 dopamine receptors with the following change of hyaluronan matrix can be considered as a new strategy in treatment of pneumofibrosis.</description><subject>Alveoli</subject><subject>Analysis</subject><subject>Animals</subject><subject>Bleomycin</subject><subject>Bleomycin - toxicity</subject><subject>Blockage</subject><subject>Blood cells</subject><subject>Bone morphogenetic proteins</subject><subject>CD34 antigen</subject><subject>CD44 antigen</subject><subject>CD45 antigen</subject><subject>CD73 antigen</subject><subject>CD90 antigen</subject><subject>Cells (biology)</subject><subject>Collagen</subject><subject>Dopamine</subject><subject>Dopamine Antagonists - therapeutic use</subject><subject>Dopamine D2 receptors</subject><subject>Dopamine receptors</subject><subject>Electron beams</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Enzymes</subject><subject>Epithelium</subject><subject>Fibrosis</subject><subject>Flow Cytometry</subject><subject>Hematopoietic stem cells</subject><subject>Hyaluronic acid</subject><subject>Hyaluronoglucosaminidase - chemistry</subject><subject>Hyaluronoglucosaminidase - therapeutic use</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Interleukins</subject><subject>Lungs</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Parenchyma</subject><subject>Phenols (Class of compounds)</subject><subject>Polyethylene</subject><subject>Polyethylene oxide</subject><subject>Polyethylenes</subject><subject>Pulmonary Fibrosis - chemically induced</subject><subject>Pulmonary Fibrosis - drug therapy</subject><subject>Receptors</subject><subject>Spiperone</subject><subject>Spiperone - therapeutic use</subject><subject>Testes</subject><subject>Therapy</subject><subject>Transforming growth factor</subject><subject>Transforming growth factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis 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Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Skurikhin, Evgenii Germanovich</au><au>Pershina, Olga Victorovna</au><au>Reztsova, Alena Mikhaylovna</au><au>Ermakova, Natalia Nikolaevna</au><au>Khmelevskaya, Ekaterina Sergeevna</au><au>Krupin, Vycheslav Andreevich</au><au>Stepanova, Inna Ernestovna</au><au>Artamonov, Andrew Vladimirovich</au><au>Bekarev, Andrew Alexandrovich</au><au>Madonov, Pavel Gennadjevich</au><au>Dygai, Alexander Mikhaylovich</au><au>Shi, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of bleomycin-induced lung fibrosis by pegylated hyaluronidase and dopamine receptor antagonist in mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-04-30</date><risdate>2015</risdate><volume>10</volume><issue>4</issue><spage>e0125065</spage><pages>e0125065-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Hyaluronidases are groups of enzymes that degrade hyaluronic acid (HA). To stop enzymatic hydrolysis we modified testicular hyaluronidase (HYAL) by activated polyethylene oxide with the help of electron-beam synthesis. As a result we received pegylated hyaluronidase (pegHYAL). Spiperone is a selective D2 dopamine receptor antagonist. It was demonstrated on the model of a single bleomycin damage of alveolar epithelium that during the inflammatory phase monotherapy by pegHYAL or spiperone reduced the populations of hematopoietic stem /progenitor cells in the lung parenchyma. PegHYAL also reduced the levels of transforming growth factor (TGF)-β, interleukin (IL)-1β, tumor necrosis factor (TNF)-α in the serum and lungs, while spiperone reduced the level of the serum IL-1β. Polytherapy by spiperone and pegHYAL caused the increase of the quantity of hematopoietic stem/ progenitor cells in the lungs. Such an influx of blood cell precursors was observed on the background of considerable fall level of TGF-β and the increase level of TNF-α in the serum and lungs. These results show pegHYAL reduced the bleomycin-induced fibrosis reaction (production and accumulation of collagen) in the lung parenchyma. This effect was observed at a single and repetitive bleomycin damage of alveolar epithelium, the antifibrotic activity of pegHYAL surpassing the activity of testicular HYAL. The antifibrotic effect of pegHYAL is enhanced by an additional instillation of spiperone. Therapy by pegHYAL causes the flow of CD31‒ CD34‒ CD45‒ CD44+ CD73+ CD90+ CD106+-cells into the fibrous lungs. These cells are incapable of differentiating into fibroblast cells. Spiperone instillation separately or together with pegHYAL reduced the MSC-like cells considerably. These data enable us to assume, that pegHYAL is a new and promising instrument both for preventive and therapy of toxic pneumofibrosis. The blockage of D2 dopamine receptors with the following change of hyaluronan matrix can be considered as a new strategy in treatment of pneumofibrosis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25927611</pmid><doi>10.1371/journal.pone.0125065</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-04, Vol.10 (4), p.e0125065 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1677376614 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Alveoli Analysis Animals Bleomycin Bleomycin - toxicity Blockage Blood cells Bone morphogenetic proteins CD34 antigen CD44 antigen CD45 antigen CD73 antigen CD90 antigen Cells (biology) Collagen Dopamine Dopamine Antagonists - therapeutic use Dopamine D2 receptors Dopamine receptors Electron beams Enzyme-Linked Immunosorbent Assay Enzymes Epithelium Fibrosis Flow Cytometry Hematopoietic stem cells Hyaluronic acid Hyaluronoglucosaminidase - chemistry Hyaluronoglucosaminidase - therapeutic use IL-1β Inflammation Interleukins Lungs Male Mice Mice, Inbred C57BL Parenchyma Phenols (Class of compounds) Polyethylene Polyethylene oxide Polyethylenes Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - drug therapy Receptors Spiperone Spiperone - therapeutic use Testes Therapy Transforming growth factor Transforming growth factors Tumor necrosis factor Tumor necrosis factor-α |
| title | Modulation of bleomycin-induced lung fibrosis by pegylated hyaluronidase and dopamine receptor antagonist in mice |
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