Platelet-derived growth factor isoforms prevent cell death during starvation of AKR-2B fibroblasts
Confluent AKR‐2B fibroblasts rapidly desintegrate upon removal of serum until a final density of ∼50% of the initial value was reached after 12 h. This density remained unchanged for at least 48 h. Platelet‐derived growth factor (PDGF)‐BB stimulated more than 95% of these cells to divide. PDGF‐AB or...
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| Veröffentlicht in: | Journal of cellular physiology 1994-08, Vol.160 (2), p.295-302 |
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| container_title | Journal of cellular physiology |
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| creator | Simm, Andreas Hoppe, Viviane Hoppe, Jürgen Gazit, Aviv |
| description | Confluent AKR‐2B fibroblasts rapidly desintegrate upon removal of serum until a final density of ∼50% of the initial value was reached after 12 h. This density remained unchanged for at least 48 h. Platelet‐derived growth factor (PDGF)‐BB stimulated more than 95% of these cells to divide. PDGF‐AB or ‐BB added immediately after serum removal caused complete survival of the cells, but did not stimulate cell division as demonstrated by two‐dimensional DNA flow cytometry. PDGF‐AA was less effective leading to ∼75% of the initial cell density. This effect could be augmented by the addition of ocadaic acid, a potent phosphatase inhibitor, suggesting that protein phosphorylation plays a role in this process. By using tyrphostin AG807 it was demonstrated that the signaling mechanism for survival requires receptor tyrosine autophosphorylation. © 1994 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/jcp.1041600211 |
| format | Article |
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This density remained unchanged for at least 48 h. Platelet‐derived growth factor (PDGF)‐BB stimulated more than 95% of these cells to divide. PDGF‐AB or ‐BB added immediately after serum removal caused complete survival of the cells, but did not stimulate cell division as demonstrated by two‐dimensional DNA flow cytometry. PDGF‐AA was less effective leading to ∼75% of the initial cell density. This effect could be augmented by the addition of ocadaic acid, a potent phosphatase inhibitor, suggesting that protein phosphorylation plays a role in this process. By using tyrphostin AG807 it was demonstrated that the signaling mechanism for survival requires receptor tyrosine autophosphorylation. © 1994 Wiley‐Liss, Inc.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.1041600211</identifier><identifier>PMID: 8040188</identifier><identifier>CODEN: JCLLAX</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological and medical sciences ; Catechols - pharmacology ; Cell Death ; Cell Division ; Cell Line ; Cell physiology ; Cell Survival ; Ethers, Cyclic - pharmacology ; Fibroblasts - cytology ; Fibroblasts - metabolism ; Flow Cytometry ; Fundamental and applied biological sciences. Psychology ; Molecular and cellular biology ; Nitriles - pharmacology ; Okadaic Acid ; Phosphorylation ; Platelet-Derived Growth Factor - chemistry ; Platelet-Derived Growth Factor - physiology ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Protein-Tyrosine Kinases - metabolism ; Responses to growth factors, tumor promotors, other factors ; Tyrosine - metabolism ; Tyrphostins</subject><ispartof>Journal of cellular physiology, 1994-08, Vol.160 (2), p.295-302</ispartof><rights>Copyright © 1994 Wiley‐Liss, Inc.</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4731-398521b215c7cf1ddd3fe67063a560cdfc3ed446730e1a27cf01bfeaabf2c3e53</citedby><cites>FETCH-LOGICAL-c4731-398521b215c7cf1ddd3fe67063a560cdfc3ed446730e1a27cf01bfeaabf2c3e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.1041600211$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.1041600211$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4183171$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8040188$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Simm, Andreas</creatorcontrib><creatorcontrib>Hoppe, Viviane</creatorcontrib><creatorcontrib>Hoppe, Jürgen</creatorcontrib><creatorcontrib>Gazit, Aviv</creatorcontrib><title>Platelet-derived growth factor isoforms prevent cell death during starvation of AKR-2B fibroblasts</title><title>Journal of cellular physiology</title><addtitle>J. Cell. Physiol</addtitle><description>Confluent AKR‐2B fibroblasts rapidly desintegrate upon removal of serum until a final density of ∼50% of the initial value was reached after 12 h. This density remained unchanged for at least 48 h. Platelet‐derived growth factor (PDGF)‐BB stimulated more than 95% of these cells to divide. PDGF‐AB or ‐BB added immediately after serum removal caused complete survival of the cells, but did not stimulate cell division as demonstrated by two‐dimensional DNA flow cytometry. PDGF‐AA was less effective leading to ∼75% of the initial cell density. This effect could be augmented by the addition of ocadaic acid, a potent phosphatase inhibitor, suggesting that protein phosphorylation plays a role in this process. By using tyrphostin AG807 it was demonstrated that the signaling mechanism for survival requires receptor tyrosine autophosphorylation. © 1994 Wiley‐Liss, Inc.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Catechols - pharmacology</subject><subject>Cell Death</subject><subject>Cell Division</subject><subject>Cell Line</subject><subject>Cell physiology</subject><subject>Cell Survival</subject><subject>Ethers, Cyclic - pharmacology</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - metabolism</subject><subject>Flow Cytometry</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Molecular and cellular biology</subject><subject>Nitriles - pharmacology</subject><subject>Okadaic Acid</subject><subject>Phosphorylation</subject><subject>Platelet-Derived Growth Factor - chemistry</subject><subject>Platelet-Derived Growth Factor - physiology</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Responses to growth factors, tumor promotors, other factors</subject><subject>Tyrosine - metabolism</subject><subject>Tyrphostins</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1vGyEQxVHVKnXSXnuLxKHXdZiFXXaPjpU4X0qsqlWPiIUhwV17LSBO8t8Xy5arnnIC5v3ezPAI-QZsDIyVZwuzzhcBdX4AfCAjYK0sRF2VH8loWyvaSsBnchzjgjHWtpwfkaOGCQZNMyLdvNcJe0yFxeA3aOljGF7SE3XapCFQHwc3hGWk64AbXCVqsO-pRZ0R-xz86pHGpMNGJz-s6ODo5PZHUZ5T57swdL2OKX4hn5zuI37dnyfk1-XFz-lVcfcwu55O7gojJIeCt01VQldCZaRxYK3lDmvJaq6rmhnrDEcrRC05Q9BlZhh0DrXuXJmlip-Q8a6vCUOMAZ1aB7_U4U0BU9usVM5K_csqG053hvVzt0R7wPfhZP37XtfR6N4FvTI-HjABDQe5bdPusBff49s7Q9XNdP7fCsXO62PC14NXhz8qf1RW6vf9TJ1LeSXu57Wq-V-BipJb</recordid><startdate>199408</startdate><enddate>199408</enddate><creator>Simm, Andreas</creator><creator>Hoppe, Viviane</creator><creator>Hoppe, Jürgen</creator><creator>Gazit, Aviv</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><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></search><sort><creationdate>199408</creationdate><title>Platelet-derived growth factor isoforms prevent cell death during starvation of AKR-2B fibroblasts</title><author>Simm, Andreas ; Hoppe, Viviane ; Hoppe, Jürgen ; Gazit, Aviv</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4731-398521b215c7cf1ddd3fe67063a560cdfc3ed446730e1a27cf01bfeaabf2c3e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Catechols - pharmacology</topic><topic>Cell Death</topic><topic>Cell Division</topic><topic>Cell Line</topic><topic>Cell physiology</topic><topic>Cell Survival</topic><topic>Ethers, Cyclic - pharmacology</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - metabolism</topic><topic>Flow Cytometry</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Molecular and cellular biology</topic><topic>Nitriles - pharmacology</topic><topic>Okadaic Acid</topic><topic>Phosphorylation</topic><topic>Platelet-Derived Growth Factor - chemistry</topic><topic>Platelet-Derived Growth Factor - physiology</topic><topic>Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Responses to growth factors, tumor promotors, other factors</topic><topic>Tyrosine - metabolism</topic><topic>Tyrphostins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Simm, Andreas</creatorcontrib><creatorcontrib>Hoppe, Viviane</creatorcontrib><creatorcontrib>Hoppe, Jürgen</creatorcontrib><creatorcontrib>Gazit, Aviv</creatorcontrib><collection>Istex</collection><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><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Simm, Andreas</au><au>Hoppe, Viviane</au><au>Hoppe, Jürgen</au><au>Gazit, Aviv</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet-derived growth factor isoforms prevent cell death during starvation of AKR-2B fibroblasts</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>1994-08</date><risdate>1994</risdate><volume>160</volume><issue>2</issue><spage>295</spage><epage>302</epage><pages>295-302</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><coden>JCLLAX</coden><abstract>Confluent AKR‐2B fibroblasts rapidly desintegrate upon removal of serum until a final density of ∼50% of the initial value was reached after 12 h. This density remained unchanged for at least 48 h. Platelet‐derived growth factor (PDGF)‐BB stimulated more than 95% of these cells to divide. PDGF‐AB or ‐BB added immediately after serum removal caused complete survival of the cells, but did not stimulate cell division as demonstrated by two‐dimensional DNA flow cytometry. PDGF‐AA was less effective leading to ∼75% of the initial cell density. This effect could be augmented by the addition of ocadaic acid, a potent phosphatase inhibitor, suggesting that protein phosphorylation plays a role in this process. By using tyrphostin AG807 it was demonstrated that the signaling mechanism for survival requires receptor tyrosine autophosphorylation. © 1994 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8040188</pmid><doi>10.1002/jcp.1041600211</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of cellular physiology, 1994-08, Vol.160 (2), p.295-302 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Biological and medical sciences Catechols - pharmacology Cell Death Cell Division Cell Line Cell physiology Cell Survival Ethers, Cyclic - pharmacology Fibroblasts - cytology Fibroblasts - metabolism Flow Cytometry Fundamental and applied biological sciences. Psychology Molecular and cellular biology Nitriles - pharmacology Okadaic Acid Phosphorylation Platelet-Derived Growth Factor - chemistry Platelet-Derived Growth Factor - physiology Protein-Tyrosine Kinases - antagonists & inhibitors Protein-Tyrosine Kinases - metabolism Responses to growth factors, tumor promotors, other factors Tyrosine - metabolism Tyrphostins |
| title | Platelet-derived growth factor isoforms prevent cell death during starvation of AKR-2B fibroblasts |
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