Inhibition of granuloma‐associated angiogenesis by controlling mast cell mediator release: role of mast cell protease‐5
1 We investigated the role of mast cells in granuloma‐associated angiogenesis in rat by using: (i) a mast cell membrane stabilizer, ketotifen; (ii) a mast cell depleting agent, compound 48/80. Moreover, we focused on the role of chymases, which exhibit proinflammatory and proangiogenic properties by...
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| Veröffentlicht in: | British journal of pharmacology 2005-05, Vol.145 (1), p.24-33 |
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| description | 1
We investigated the role of mast cells in granuloma‐associated angiogenesis in rat by using: (i) a mast cell membrane stabilizer, ketotifen; (ii) a mast cell depleting agent, compound 48/80. Moreover, we focused on the role of chymases, which exhibit proinflammatory and proangiogenic properties by using: (i) chymostatin, an inhibitor of chymase activity; (ii) a specific antisense oligonucleotide (AS‐ODN) designed against rat mast cell protease‐5 (rMCP‐5), the most abundantly expressed chymase in the skin.
2
The formation of granuloma was evaluated, as wet weight, 96 h after the subcutaneous implant of two λ‐carrageenin (1%)‐soaked sponges on the back of male Wistar rats. Angiogenesis was evaluated as haemoglobin content in the granulomatous tissue and as level of tumour necrosis factor‐α (TNF‐α) in the exudates.
3
A single injection of ketotifen (1–5–25 mg kg−1 i.p.) significantly reduced granuloma formation by 31.6, 44.6 and 71.9%, and haemoglobin content by 17.0, 35.0 and 66.2%, suggesting that the release of mediator(s) from mast cells modulates the process. Chymostatin (5–10 nmol−1 site−1 day−1) reduced granuloma‐associated angiogenesis by 57.3 and 70.0%.
4
RT–PCR analysis showed that rMCP‐5 mRNA amounts were significantly reduced by rMCP‐5 AS‐ODN (1.25–2.5–5.0 nmol site−1) by 69.5, 72.5 and 81.8%. In parallel experiments, rMCP‐5 AS‐ODN (1.25, 2.5, 5.0 nmol site−1) strongly reduced granuloma weight (26.1, 45.0 and 56.3%) and haemoglobin content (22.2, 50.4, 62.03%), suggesting that the observed effect is mediated through an antisense mechanism.
5
In conclusion, these data suggest that: (i) inhibition of mast cell mediators release may represent a novel strategy to modulate angiogenesis; (ii) among the chymase family, rMCP‐5 is a key promoter of angiogenesis in the rat.
British Journal of Pharmacology (2005) 145, 24–33. doi:10.1038/sj.bjp.0706112 |
| doi_str_mv | 10.1038/sj.bjp.0706112 |
| format | Article |
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We investigated the role of mast cells in granuloma‐associated angiogenesis in rat by using: (i) a mast cell membrane stabilizer, ketotifen; (ii) a mast cell depleting agent, compound 48/80. Moreover, we focused on the role of chymases, which exhibit proinflammatory and proangiogenic properties by using: (i) chymostatin, an inhibitor of chymase activity; (ii) a specific antisense oligonucleotide (AS‐ODN) designed against rat mast cell protease‐5 (rMCP‐5), the most abundantly expressed chymase in the skin.
2
The formation of granuloma was evaluated, as wet weight, 96 h after the subcutaneous implant of two λ‐carrageenin (1%)‐soaked sponges on the back of male Wistar rats. Angiogenesis was evaluated as haemoglobin content in the granulomatous tissue and as level of tumour necrosis factor‐α (TNF‐α) in the exudates.
3
A single injection of ketotifen (1–5–25 mg kg−1 i.p.) significantly reduced granuloma formation by 31.6, 44.6 and 71.9%, and haemoglobin content by 17.0, 35.0 and 66.2%, suggesting that the release of mediator(s) from mast cells modulates the process. Chymostatin (5–10 nmol−1 site−1 day−1) reduced granuloma‐associated angiogenesis by 57.3 and 70.0%.
4
RT–PCR analysis showed that rMCP‐5 mRNA amounts were significantly reduced by rMCP‐5 AS‐ODN (1.25–2.5–5.0 nmol site−1) by 69.5, 72.5 and 81.8%. In parallel experiments, rMCP‐5 AS‐ODN (1.25, 2.5, 5.0 nmol site−1) strongly reduced granuloma weight (26.1, 45.0 and 56.3%) and haemoglobin content (22.2, 50.4, 62.03%), suggesting that the observed effect is mediated through an antisense mechanism.
5
In conclusion, these data suggest that: (i) inhibition of mast cell mediators release may represent a novel strategy to modulate angiogenesis; (ii) among the chymase family, rMCP‐5 is a key promoter of angiogenesis in the rat.
British Journal of Pharmacology (2005) 145, 24–33. doi:10.1038/sj.bjp.0706112</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0706112</identifier><identifier>PMID: 15723097</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Angiogenesis ; Animals ; Biological and medical sciences ; Cell Degranulation - drug effects ; Cell Degranulation - physiology ; chronic inflammation ; chymases ; Gene Expression - drug effects ; Granuloma - physiopathology ; granuloma formation ; ketotifen ; Ketotifen - pharmacology ; Male ; mast cells ; Mast Cells - drug effects ; Mast Cells - metabolism ; Medical sciences ; Neovascularization, Pathologic - physiopathology ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; rMCP‐5 ; Serine Endopeptidases - metabolism</subject><ispartof>British journal of pharmacology, 2005-05, Vol.145 (1), p.24-33</ispartof><rights>2005 British Pharmacological Society</rights><rights>2005 INIST-CNRS</rights><rights>Copyright Nature Publishing Group May 2005</rights><rights>Copyright 2005, Nature Publishing Group 2005 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4898-78c4d376e36972b468a449098a2291db28517d17c19dd0ed6c91679da79e6bd63</citedby><cites>FETCH-LOGICAL-c4898-78c4d376e36972b468a449098a2291db28517d17c19dd0ed6c91679da79e6bd63</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/PMC1576110/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576110/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1416,1432,27923,27924,45573,45574,46408,46832,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16746353$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15723097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Russo, Annapina</creatorcontrib><creatorcontrib>Russo, Giulia</creatorcontrib><creatorcontrib>Peticca, Manuela</creatorcontrib><creatorcontrib>Pietropaolo, Concetta</creatorcontrib><creatorcontrib>Di Rosa, Massimo</creatorcontrib><creatorcontrib>Iuvone, Teresa</creatorcontrib><title>Inhibition of granuloma‐associated angiogenesis by controlling mast cell mediator release: role of mast cell protease‐5</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1
We investigated the role of mast cells in granuloma‐associated angiogenesis in rat by using: (i) a mast cell membrane stabilizer, ketotifen; (ii) a mast cell depleting agent, compound 48/80. Moreover, we focused on the role of chymases, which exhibit proinflammatory and proangiogenic properties by using: (i) chymostatin, an inhibitor of chymase activity; (ii) a specific antisense oligonucleotide (AS‐ODN) designed against rat mast cell protease‐5 (rMCP‐5), the most abundantly expressed chymase in the skin.
2
The formation of granuloma was evaluated, as wet weight, 96 h after the subcutaneous implant of two λ‐carrageenin (1%)‐soaked sponges on the back of male Wistar rats. Angiogenesis was evaluated as haemoglobin content in the granulomatous tissue and as level of tumour necrosis factor‐α (TNF‐α) in the exudates.
3
A single injection of ketotifen (1–5–25 mg kg−1 i.p.) significantly reduced granuloma formation by 31.6, 44.6 and 71.9%, and haemoglobin content by 17.0, 35.0 and 66.2%, suggesting that the release of mediator(s) from mast cells modulates the process. Chymostatin (5–10 nmol−1 site−1 day−1) reduced granuloma‐associated angiogenesis by 57.3 and 70.0%.
4
RT–PCR analysis showed that rMCP‐5 mRNA amounts were significantly reduced by rMCP‐5 AS‐ODN (1.25–2.5–5.0 nmol site−1) by 69.5, 72.5 and 81.8%. In parallel experiments, rMCP‐5 AS‐ODN (1.25, 2.5, 5.0 nmol site−1) strongly reduced granuloma weight (26.1, 45.0 and 56.3%) and haemoglobin content (22.2, 50.4, 62.03%), suggesting that the observed effect is mediated through an antisense mechanism.
5
In conclusion, these data suggest that: (i) inhibition of mast cell mediators release may represent a novel strategy to modulate angiogenesis; (ii) among the chymase family, rMCP‐5 is a key promoter of angiogenesis in the rat.
British Journal of Pharmacology (2005) 145, 24–33. doi:10.1038/sj.bjp.0706112</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Degranulation - drug effects</subject><subject>Cell Degranulation - physiology</subject><subject>chronic inflammation</subject><subject>chymases</subject><subject>Gene Expression - drug effects</subject><subject>Granuloma - physiopathology</subject><subject>granuloma formation</subject><subject>ketotifen</subject><subject>Ketotifen - pharmacology</subject><subject>Male</subject><subject>mast cells</subject><subject>Mast Cells - drug effects</subject><subject>Mast Cells - metabolism</subject><subject>Medical sciences</subject><subject>Neovascularization, Pathologic - physiopathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>rMCP‐5</subject><subject>Serine Endopeptidases - metabolism</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkb1uFDEUhS1ERJZAS4ksJMrZ-GfGPxRIIQISKRIUUFse2zvxyGsv9ixolSaPwDPyJHi1I5ZUqW5xvnvu0T0AvMJoiREV52Vc9uNmiThiGJMnYIFbzpqOCvwULBBCvMFYiFPwvJQRoSry7hk4xR0nFEm-AHfX8db3fvIpwrSCQ9ZxG9Ja_7n_rUtJxuvJWajj4NPgoiu-wH4HTYpTTiH4OMC1LhM0LgS4drbiKcPsgtPFvYOVcXvbI7PJadpr1b97AU5WOhT3cp5n4Punj98ur5qbL5-vLy9uGtMKKRouTGspZ44yyUnfMqHbViIpNCES256IDnOLucHSWuQsMxIzLq3m0rHeMnoG3h98N9u-ZjSuhtdBbbJf67xTSXv1UIn-Vg3pp6pvql9F1eDNbJDTj60rkxrTNseaWRHMsaSd2EPLA2RyKiW71b8DGKl9V6qMqnal5q7qwuv_Yx3xuZwKvJ0BXYwOq9qN8eXIMd4y2tHK0QP3ywe3e-Ss-vD1iggi6F83GrHv</recordid><startdate>200505</startdate><enddate>200505</enddate><creator>Russo, Annapina</creator><creator>Russo, Giulia</creator><creator>Peticca, Manuela</creator><creator>Pietropaolo, Concetta</creator><creator>Di Rosa, Massimo</creator><creator>Iuvone, Teresa</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200505</creationdate><title>Inhibition of granuloma‐associated angiogenesis by controlling mast cell mediator release: role of mast cell protease‐5</title><author>Russo, Annapina ; Russo, Giulia ; Peticca, Manuela ; Pietropaolo, Concetta ; Di Rosa, Massimo ; Iuvone, Teresa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4898-78c4d376e36972b468a449098a2291db28517d17c19dd0ed6c91679da79e6bd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Degranulation - drug effects</topic><topic>Cell Degranulation - physiology</topic><topic>chronic inflammation</topic><topic>chymases</topic><topic>Gene Expression - drug effects</topic><topic>Granuloma - physiopathology</topic><topic>granuloma formation</topic><topic>ketotifen</topic><topic>Ketotifen - pharmacology</topic><topic>Male</topic><topic>mast cells</topic><topic>Mast Cells - drug effects</topic><topic>Mast Cells - metabolism</topic><topic>Medical sciences</topic><topic>Neovascularization, Pathologic - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>rMCP‐5</topic><topic>Serine Endopeptidases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Russo, Annapina</creatorcontrib><creatorcontrib>Russo, Giulia</creatorcontrib><creatorcontrib>Peticca, Manuela</creatorcontrib><creatorcontrib>Pietropaolo, Concetta</creatorcontrib><creatorcontrib>Di Rosa, Massimo</creatorcontrib><creatorcontrib>Iuvone, Teresa</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>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Russo, Annapina</au><au>Russo, Giulia</au><au>Peticca, Manuela</au><au>Pietropaolo, Concetta</au><au>Di Rosa, Massimo</au><au>Iuvone, Teresa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of granuloma‐associated angiogenesis by controlling mast cell mediator release: role of mast cell protease‐5</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2005-05</date><risdate>2005</risdate><volume>145</volume><issue>1</issue><spage>24</spage><epage>33</epage><pages>24-33</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>1
We investigated the role of mast cells in granuloma‐associated angiogenesis in rat by using: (i) a mast cell membrane stabilizer, ketotifen; (ii) a mast cell depleting agent, compound 48/80. Moreover, we focused on the role of chymases, which exhibit proinflammatory and proangiogenic properties by using: (i) chymostatin, an inhibitor of chymase activity; (ii) a specific antisense oligonucleotide (AS‐ODN) designed against rat mast cell protease‐5 (rMCP‐5), the most abundantly expressed chymase in the skin.
2
The formation of granuloma was evaluated, as wet weight, 96 h after the subcutaneous implant of two λ‐carrageenin (1%)‐soaked sponges on the back of male Wistar rats. Angiogenesis was evaluated as haemoglobin content in the granulomatous tissue and as level of tumour necrosis factor‐α (TNF‐α) in the exudates.
3
A single injection of ketotifen (1–5–25 mg kg−1 i.p.) significantly reduced granuloma formation by 31.6, 44.6 and 71.9%, and haemoglobin content by 17.0, 35.0 and 66.2%, suggesting that the release of mediator(s) from mast cells modulates the process. Chymostatin (5–10 nmol−1 site−1 day−1) reduced granuloma‐associated angiogenesis by 57.3 and 70.0%.
4
RT–PCR analysis showed that rMCP‐5 mRNA amounts were significantly reduced by rMCP‐5 AS‐ODN (1.25–2.5–5.0 nmol site−1) by 69.5, 72.5 and 81.8%. In parallel experiments, rMCP‐5 AS‐ODN (1.25, 2.5, 5.0 nmol site−1) strongly reduced granuloma weight (26.1, 45.0 and 56.3%) and haemoglobin content (22.2, 50.4, 62.03%), suggesting that the observed effect is mediated through an antisense mechanism.
5
In conclusion, these data suggest that: (i) inhibition of mast cell mediators release may represent a novel strategy to modulate angiogenesis; (ii) among the chymase family, rMCP‐5 is a key promoter of angiogenesis in the rat.
British Journal of Pharmacology (2005) 145, 24–33. doi:10.1038/sj.bjp.0706112</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15723097</pmid><doi>10.1038/sj.bjp.0706112</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Animals Biological and medical sciences Cell Degranulation - drug effects Cell Degranulation - physiology chronic inflammation chymases Gene Expression - drug effects Granuloma - physiopathology granuloma formation ketotifen Ketotifen - pharmacology Male mast cells Mast Cells - drug effects Mast Cells - metabolism Medical sciences Neovascularization, Pathologic - physiopathology Pharmacology. Drug treatments Rats Rats, Wistar rMCP‐5 Serine Endopeptidases - metabolism |
| title | Inhibition of granuloma‐associated angiogenesis by controlling mast cell mediator release: role of mast cell protease‐5 |
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