Platelet activation during tumor development, the potential role of BDNF–TrkB autocrine loop
Platelets are an important place for the storage of angiogenic factors, such as vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The present study aims to investigate the interaction between BDNF–TrkB pathway and platelet activation during tumor development. In...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2006-08, Vol.346 (3), p.981-985 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Yang, Zhen Fan Ho, David W. Lau, Chi Keung Tam, Ka Ho Lam, Chi Tat Poon, Ronnie T.P. Fan, Sheung Tat |
| description | Platelets are an important place for the storage of angiogenic factors, such as vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The present study aims to investigate the interaction between BDNF–TrkB pathway and platelet activation during tumor development. In an orthotopic hepatocellular carcinoma (HCC) model, increased levels of serum and plasma BDNF were detected with tumor progression. Higher numbers of CD62P
+ and TrkB
+ platelets were found in the tumor-bearing rats. In the
in vitro setting, tumor-conditioned-medium (TCM) and BDNF recombinant protein stimulated CD62P upregulation and subsequent BDNF release in the freshly isolated platelets, whereas this effect could be inhibited by TrkB blockade. TCM and BDNF culture augmented the expression of heat shock protein 90 (Hsp90) in the platelets, which could be reversed by TrkB blockade. In conclusion, this study suggested the presence of BDNF–TrkB autocrine loop in platelets and its importance in regulating platelet activation during tumor development. |
| doi_str_mv | 10.1016/j.bbrc.2006.06.007 |
| format | Article |
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+ and TrkB
+ platelets were found in the tumor-bearing rats. In the
in vitro setting, tumor-conditioned-medium (TCM) and BDNF recombinant protein stimulated CD62P upregulation and subsequent BDNF release in the freshly isolated platelets, whereas this effect could be inhibited by TrkB blockade. TCM and BDNF culture augmented the expression of heat shock protein 90 (Hsp90) in the platelets, which could be reversed by TrkB blockade. In conclusion, this study suggested the presence of BDNF–TrkB autocrine loop in platelets and its importance in regulating platelet activation during tumor development.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2006.06.007</identifier><identifier>PMID: 16781670</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Autocrine Communication ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - metabolism ; Cell Line, Tumor ; Cell Separation ; Hepatocellular carcinoma ; Male ; Neoplasms - metabolism ; Neoplasms - pathology ; Platelet ; Platelet Activation ; Protein Binding ; Rats ; Rats, Inbred BUF ; Receptor, trkB - metabolism ; Tyrosine kinase receptor B</subject><ispartof>Biochemical and biophysical research communications, 2006-08, Vol.346 (3), p.981-985</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-49de7d6d2895a9272e8feb594a75610e84e4e6a188d6e2f00e3a9d09d0720a6e3</citedby><cites>FETCH-LOGICAL-c420t-49de7d6d2895a9272e8feb594a75610e84e4e6a188d6e2f00e3a9d09d0720a6e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X06012927$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16781670$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Zhen Fan</creatorcontrib><creatorcontrib>Ho, David W.</creatorcontrib><creatorcontrib>Lau, Chi Keung</creatorcontrib><creatorcontrib>Tam, Ka Ho</creatorcontrib><creatorcontrib>Lam, Chi Tat</creatorcontrib><creatorcontrib>Poon, Ronnie T.P.</creatorcontrib><creatorcontrib>Fan, Sheung Tat</creatorcontrib><title>Platelet activation during tumor development, the potential role of BDNF–TrkB autocrine loop</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Platelets are an important place for the storage of angiogenic factors, such as vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The present study aims to investigate the interaction between BDNF–TrkB pathway and platelet activation during tumor development. In an orthotopic hepatocellular carcinoma (HCC) model, increased levels of serum and plasma BDNF were detected with tumor progression. Higher numbers of CD62P
+ and TrkB
+ platelets were found in the tumor-bearing rats. In the
in vitro setting, tumor-conditioned-medium (TCM) and BDNF recombinant protein stimulated CD62P upregulation and subsequent BDNF release in the freshly isolated platelets, whereas this effect could be inhibited by TrkB blockade. TCM and BDNF culture augmented the expression of heat shock protein 90 (Hsp90) in the platelets, which could be reversed by TrkB blockade. In conclusion, this study suggested the presence of BDNF–TrkB autocrine loop in platelets and its importance in regulating platelet activation during tumor development.</description><subject>Animals</subject><subject>Autocrine Communication</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Separation</subject><subject>Hepatocellular carcinoma</subject><subject>Male</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Platelet</subject><subject>Platelet Activation</subject><subject>Protein Binding</subject><subject>Rats</subject><subject>Rats, Inbred BUF</subject><subject>Receptor, trkB - metabolism</subject><subject>Tyrosine kinase receptor B</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UMtqHDEQFCEhXj9-IAejU06edUue1cxALvHbYGwfbMjJQiv1xNpoRmNJs-Cb_yF_mC-Jhl3ILVBNN3RVQRUhXxjMGTBxvJovl0HPOYCYT4DqA5kxaKDgDMqPZAb5U_CG_dghuzGuABgrRfOZ7DBR1XlgRp4fnEroMFGlk12rZH1PzRhs_5OmsfOBGlyj80OHfTqi6QXp4FO-rXI0eIfUt_T0_O7yz_vvx_DrlKoxeZ3lSJ33wz751CoX8WC798jT5cXj2XVxe391c_b9ttAlh1SUjcHKCMPrZqEaXnGsW1wumlJVC8EA6xJLFIrVtRHIWwA8UY2BjIqDEniyR75ufIfgX0eMSXY2anRO9ejHKEW9EHWOn4l8Q9TBxxiwlUOwnQpvkoGcWpUrObUqp1blBKiy6HDrPi47NP8k2xoz4duGgDnj2mKQUVvsNRobUCdpvP2f_180tIoZ</recordid><startdate>20060804</startdate><enddate>20060804</enddate><creator>Yang, Zhen Fan</creator><creator>Ho, David W.</creator><creator>Lau, Chi Keung</creator><creator>Tam, Ka Ho</creator><creator>Lam, Chi Tat</creator><creator>Poon, Ronnie T.P.</creator><creator>Fan, Sheung Tat</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20060804</creationdate><title>Platelet activation during tumor development, the potential role of BDNF–TrkB autocrine loop</title><author>Yang, Zhen Fan ; Ho, David W. ; Lau, Chi Keung ; Tam, Ka Ho ; Lam, Chi Tat ; Poon, Ronnie T.P. ; Fan, Sheung Tat</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-49de7d6d2895a9272e8feb594a75610e84e4e6a188d6e2f00e3a9d09d0720a6e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Autocrine Communication</topic><topic>Brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Separation</topic><topic>Hepatocellular carcinoma</topic><topic>Male</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Platelet</topic><topic>Platelet Activation</topic><topic>Protein Binding</topic><topic>Rats</topic><topic>Rats, Inbred BUF</topic><topic>Receptor, trkB - metabolism</topic><topic>Tyrosine kinase receptor B</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Zhen Fan</creatorcontrib><creatorcontrib>Ho, David W.</creatorcontrib><creatorcontrib>Lau, Chi Keung</creatorcontrib><creatorcontrib>Tam, Ka Ho</creatorcontrib><creatorcontrib>Lam, Chi Tat</creatorcontrib><creatorcontrib>Poon, Ronnie T.P.</creatorcontrib><creatorcontrib>Fan, Sheung Tat</creatorcontrib><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>Yang, Zhen Fan</au><au>Ho, David W.</au><au>Lau, Chi Keung</au><au>Tam, Ka Ho</au><au>Lam, Chi Tat</au><au>Poon, Ronnie T.P.</au><au>Fan, Sheung Tat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet activation during tumor development, the potential role of BDNF–TrkB autocrine loop</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-08-04</date><risdate>2006</risdate><volume>346</volume><issue>3</issue><spage>981</spage><epage>985</epage><pages>981-985</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Platelets are an important place for the storage of angiogenic factors, such as vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The present study aims to investigate the interaction between BDNF–TrkB pathway and platelet activation during tumor development. In an orthotopic hepatocellular carcinoma (HCC) model, increased levels of serum and plasma BDNF were detected with tumor progression. Higher numbers of CD62P
+ and TrkB
+ platelets were found in the tumor-bearing rats. In the
in vitro setting, tumor-conditioned-medium (TCM) and BDNF recombinant protein stimulated CD62P upregulation and subsequent BDNF release in the freshly isolated platelets, whereas this effect could be inhibited by TrkB blockade. TCM and BDNF culture augmented the expression of heat shock protein 90 (Hsp90) in the platelets, which could be reversed by TrkB blockade. In conclusion, this study suggested the presence of BDNF–TrkB autocrine loop in platelets and its importance in regulating platelet activation during tumor development.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16781670</pmid><doi>10.1016/j.bbrc.2006.06.007</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Autocrine Communication Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Cell Line, Tumor Cell Separation Hepatocellular carcinoma Male Neoplasms - metabolism Neoplasms - pathology Platelet Platelet Activation Protein Binding Rats Rats, Inbred BUF Receptor, trkB - metabolism Tyrosine kinase receptor B |
| title | Platelet activation during tumor development, the potential role of BDNF–TrkB autocrine loop |
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