Protective effect of P188 in the Model of Acute Trauma to Human Ankle Cartilage: The Mechanism of Action
OBJECTIVE:Because P188 poloxamer is effective in promoting cell survival in models of acute trauma, the objectives were to understand the mechanism of its action focusing on glycogen synthase kinase-3 (GSK3) activation, interleukin-6 (IL-6), and p38 signaling. DESIGN:Sixteen normal human tali were i...
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| Veröffentlicht in: | Journal of orthopaedic trauma 2010-09, Vol.24 (9), p.571-576 |
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| creator | Bajaj, Sarvottam Shoemaker, Thomas Hakimiyan, Arnavaz A Rappoport, Lev Pascual-Garrido, Cecilia Oegema, Theodore R Wimmer, Markus A Chubinskaya, Susan |
| description | OBJECTIVE:Because P188 poloxamer is effective in promoting cell survival in models of acute trauma, the objectives were to understand the mechanism of its action focusing on glycogen synthase kinase-3 (GSK3) activation, interleukin-6 (IL-6), and p38 signaling.
DESIGN:Sixteen normal human tali were impacted using a 4-mm diameter indenter with an impulse of 1 Ns. Eight-millimeter cartilage plugs containing the 4-mm impacted core and 4-mm adjacent nonimpacted ring were removed and cultured with or without P188. Cell lysates were analyzed using Western blots with antibodies against total and phosphorylated extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), p38, ATF-2, GSK3, Stat1, and Stat3. Additional tests were performed with the p38 inhibitor (p38i) SB203580.
RESULTS:Studied pathways were activated after impaction with the peak of activity at 1 hour. P188 completely attenuated phosphorylation of Stat1 and ATF-2 and inhibited p38, Stat3, JNK, ERK, and GSK3. The p38i partially offset phosphorylation of Stat3, GSK3, and ERK suggesting a role of p38 in these three pathways. Additionally, the p38i improved cell survival (P = 0.053) and reduced apoptosis (by approximately 20%, P = 0.046, versus almost 40% by P188), thus confirming that P188 acts (at least in part) through the p38 pathway.
CONCLUSION:Our results report a novel mechanism through which P188 exerts its protective effects on cartilage in the model of acute injury. In addition to its effect on cellular membrane, P188 affects stress-related p38 signaling, apoptosis-related GSK3, and inflammation-related IL-6 signaling. Taken together, these findings suggest that P188 alone or in combination with proanabolic agents may have a therapeutic potential in preventing progressive cartilage degeneration and the development of posttraumatic osteoarthritis. |
| doi_str_mv | 10.1097/BOT.0b013e3181ec4712 |
| format | Article |
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DESIGN:Sixteen normal human tali were impacted using a 4-mm diameter indenter with an impulse of 1 Ns. Eight-millimeter cartilage plugs containing the 4-mm impacted core and 4-mm adjacent nonimpacted ring were removed and cultured with or without P188. Cell lysates were analyzed using Western blots with antibodies against total and phosphorylated extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), p38, ATF-2, GSK3, Stat1, and Stat3. Additional tests were performed with the p38 inhibitor (p38i) SB203580.
RESULTS:Studied pathways were activated after impaction with the peak of activity at 1 hour. P188 completely attenuated phosphorylation of Stat1 and ATF-2 and inhibited p38, Stat3, JNK, ERK, and GSK3. The p38i partially offset phosphorylation of Stat3, GSK3, and ERK suggesting a role of p38 in these three pathways. Additionally, the p38i improved cell survival (P = 0.053) and reduced apoptosis (by approximately 20%, P = 0.046, versus almost 40% by P188), thus confirming that P188 acts (at least in part) through the p38 pathway.
CONCLUSION:Our results report a novel mechanism through which P188 exerts its protective effects on cartilage in the model of acute injury. In addition to its effect on cellular membrane, P188 affects stress-related p38 signaling, apoptosis-related GSK3, and inflammation-related IL-6 signaling. Taken together, these findings suggest that P188 alone or in combination with proanabolic agents may have a therapeutic potential in preventing progressive cartilage degeneration and the development of posttraumatic osteoarthritis.</description><identifier>ISSN: 0890-5339</identifier><identifier>EISSN: 1531-2291</identifier><identifier>DOI: 10.1097/BOT.0b013e3181ec4712</identifier><identifier>PMID: 20736797</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Ankle Injuries - drug therapy ; Ankle Injuries - metabolism ; Ankle Injuries - pathology ; Ankle Joint - drug effects ; Apoptosis - drug effects ; Biological and medical sciences ; Cartilage, Articular - drug effects ; Cartilage, Articular - injuries ; Cartilage, Articular - pathology ; Chondrocytes - drug effects ; Chondrocytes - metabolism ; Chondrocytes - pathology ; Diseases of the osteoarticular system ; Enzyme Inhibitors - pharmacology ; Fractures, Cartilage - drug therapy ; Fractures, Cartilage - metabolism ; Fractures, Cartilage - pathology ; Glycogen Synthase Kinase 3 - metabolism ; Humans ; Imidazoles - pharmacology ; Injuries of the limb. Injuries of the spine ; Interleukin-6 - metabolism ; Medical sciences ; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases - metabolism ; Poloxamer - pharmacology ; Pyridines - pharmacology ; Signal Transduction - drug effects ; Surface-Active Agents - pharmacology ; Talus - drug effects ; Talus - injuries ; Traumas. Diseases due to physical agents ; Wound Healing - drug effects</subject><ispartof>Journal of orthopaedic trauma, 2010-09, Vol.24 (9), p.571-576</ispartof><rights>2010 Lippincott Williams & Wilkins, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5483-3e5ab54f46968d52a5a7f387ff14f6f46fb08130f1d4aeb52986673917638ca63</citedby><cites>FETCH-LOGICAL-c5483-3e5ab54f46968d52a5a7f387ff14f6f46fb08130f1d4aeb52986673917638ca63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,309,310,314,780,784,789,790,885,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23204368$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20736797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bajaj, Sarvottam</creatorcontrib><creatorcontrib>Shoemaker, Thomas</creatorcontrib><creatorcontrib>Hakimiyan, Arnavaz A</creatorcontrib><creatorcontrib>Rappoport, Lev</creatorcontrib><creatorcontrib>Pascual-Garrido, Cecilia</creatorcontrib><creatorcontrib>Oegema, Theodore R</creatorcontrib><creatorcontrib>Wimmer, Markus A</creatorcontrib><creatorcontrib>Chubinskaya, Susan</creatorcontrib><title>Protective effect of P188 in the Model of Acute Trauma to Human Ankle Cartilage: The Mechanism of Action</title><title>Journal of orthopaedic trauma</title><addtitle>J Orthop Trauma</addtitle><description>OBJECTIVE:Because P188 poloxamer is effective in promoting cell survival in models of acute trauma, the objectives were to understand the mechanism of its action focusing on glycogen synthase kinase-3 (GSK3) activation, interleukin-6 (IL-6), and p38 signaling.
DESIGN:Sixteen normal human tali were impacted using a 4-mm diameter indenter with an impulse of 1 Ns. Eight-millimeter cartilage plugs containing the 4-mm impacted core and 4-mm adjacent nonimpacted ring were removed and cultured with or without P188. Cell lysates were analyzed using Western blots with antibodies against total and phosphorylated extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), p38, ATF-2, GSK3, Stat1, and Stat3. Additional tests were performed with the p38 inhibitor (p38i) SB203580.
RESULTS:Studied pathways were activated after impaction with the peak of activity at 1 hour. P188 completely attenuated phosphorylation of Stat1 and ATF-2 and inhibited p38, Stat3, JNK, ERK, and GSK3. The p38i partially offset phosphorylation of Stat3, GSK3, and ERK suggesting a role of p38 in these three pathways. Additionally, the p38i improved cell survival (P = 0.053) and reduced apoptosis (by approximately 20%, P = 0.046, versus almost 40% by P188), thus confirming that P188 acts (at least in part) through the p38 pathway.
CONCLUSION:Our results report a novel mechanism through which P188 exerts its protective effects on cartilage in the model of acute injury. In addition to its effect on cellular membrane, P188 affects stress-related p38 signaling, apoptosis-related GSK3, and inflammation-related IL-6 signaling. Taken together, these findings suggest that P188 alone or in combination with proanabolic agents may have a therapeutic potential in preventing progressive cartilage degeneration and the development of posttraumatic osteoarthritis.</description><subject>Ankle Injuries - drug therapy</subject><subject>Ankle Injuries - metabolism</subject><subject>Ankle Injuries - pathology</subject><subject>Ankle Joint - drug effects</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cartilage, Articular - drug effects</subject><subject>Cartilage, Articular - injuries</subject><subject>Cartilage, Articular - pathology</subject><subject>Chondrocytes - drug effects</subject><subject>Chondrocytes - metabolism</subject><subject>Chondrocytes - pathology</subject><subject>Diseases of the osteoarticular system</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fractures, Cartilage - drug therapy</subject><subject>Fractures, Cartilage - metabolism</subject><subject>Fractures, Cartilage - pathology</subject><subject>Glycogen Synthase Kinase 3 - metabolism</subject><subject>Humans</subject><subject>Imidazoles - pharmacology</subject><subject>Injuries of the limb. Injuries of the spine</subject><subject>Interleukin-6 - metabolism</subject><subject>Medical sciences</subject><subject>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Poloxamer - pharmacology</subject><subject>Pyridines - pharmacology</subject><subject>Signal Transduction - drug effects</subject><subject>Surface-Active Agents - pharmacology</subject><subject>Talus - drug effects</subject><subject>Talus - injuries</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Wound Healing - drug effects</subject><issn>0890-5339</issn><issn>1531-2291</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUktv1DAQjhCIbgv_ACFfEKcUvxLbHJC2K0qRitrDcrYc77gxdeJiO6349yTapQUO1oxnvoelz1X1huBTgpX4cHa1PcUdJgwYkQQsF4Q-q1akYaSmVJHn1QpLheuGMXVUHef8A2MsMaUvqyOKBWuFEquqv06xgC3-HhA4N3coOnRNpER-RKUH9C3uICzDtZ0KoG0y02BQiehiriNaj7cB0Mak4oO5gY9ou3DA9mb0edjzio_jq-qFMyHD60M9qb6ff95uLurLqy9fN-vL2jZcsppBY7qGO96qVu4aahojHJPCOcJdO49dhyVh2JEdN9A1VMm2FUwR0TJpTctOqk973bupG2BnYSzJBH2X_GDSLx2N1_9uRt_rm3ivmcQN5WoWeH8QSPHnBLnowWcLIZgR4pS14FJJodRixfdIm2LOCdyjC8F6yUjPGen_M5ppb_9-4SPpTygz4N0BYLI1wSUzWp-fcIxizlr55P8QQ4GUb8P0AEn3YELp9Zw2bsjyGTDBWM23ej6Esd-rMqm9</recordid><startdate>201009</startdate><enddate>201009</enddate><creator>Bajaj, Sarvottam</creator><creator>Shoemaker, Thomas</creator><creator>Hakimiyan, Arnavaz A</creator><creator>Rappoport, Lev</creator><creator>Pascual-Garrido, Cecilia</creator><creator>Oegema, Theodore R</creator><creator>Wimmer, Markus A</creator><creator>Chubinskaya, Susan</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>201009</creationdate><title>Protective effect of P188 in the Model of Acute Trauma to Human Ankle Cartilage: The Mechanism of Action</title><author>Bajaj, Sarvottam ; Shoemaker, Thomas ; Hakimiyan, Arnavaz A ; Rappoport, Lev ; Pascual-Garrido, Cecilia ; Oegema, Theodore R ; Wimmer, Markus A ; Chubinskaya, Susan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5483-3e5ab54f46968d52a5a7f387ff14f6f46fb08130f1d4aeb52986673917638ca63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Ankle Injuries - drug therapy</topic><topic>Ankle Injuries - metabolism</topic><topic>Ankle Injuries - pathology</topic><topic>Ankle Joint - drug effects</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cartilage, Articular - drug effects</topic><topic>Cartilage, Articular - injuries</topic><topic>Cartilage, Articular - pathology</topic><topic>Chondrocytes - drug effects</topic><topic>Chondrocytes - metabolism</topic><topic>Chondrocytes - pathology</topic><topic>Diseases of the osteoarticular system</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fractures, Cartilage - drug therapy</topic><topic>Fractures, Cartilage - metabolism</topic><topic>Fractures, Cartilage - pathology</topic><topic>Glycogen Synthase Kinase 3 - metabolism</topic><topic>Humans</topic><topic>Imidazoles - pharmacology</topic><topic>Injuries of the limb. Injuries of the spine</topic><topic>Interleukin-6 - metabolism</topic><topic>Medical sciences</topic><topic>p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Poloxamer - pharmacology</topic><topic>Pyridines - pharmacology</topic><topic>Signal Transduction - drug effects</topic><topic>Surface-Active Agents - pharmacology</topic><topic>Talus - drug effects</topic><topic>Talus - injuries</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Wound Healing - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bajaj, Sarvottam</creatorcontrib><creatorcontrib>Shoemaker, Thomas</creatorcontrib><creatorcontrib>Hakimiyan, Arnavaz A</creatorcontrib><creatorcontrib>Rappoport, Lev</creatorcontrib><creatorcontrib>Pascual-Garrido, Cecilia</creatorcontrib><creatorcontrib>Oegema, Theodore R</creatorcontrib><creatorcontrib>Wimmer, Markus A</creatorcontrib><creatorcontrib>Chubinskaya, Susan</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of orthopaedic trauma</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bajaj, Sarvottam</au><au>Shoemaker, Thomas</au><au>Hakimiyan, Arnavaz A</au><au>Rappoport, Lev</au><au>Pascual-Garrido, Cecilia</au><au>Oegema, Theodore R</au><au>Wimmer, Markus A</au><au>Chubinskaya, Susan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effect of P188 in the Model of Acute Trauma to Human Ankle Cartilage: The Mechanism of Action</atitle><jtitle>Journal of orthopaedic trauma</jtitle><addtitle>J Orthop Trauma</addtitle><date>2010-09</date><risdate>2010</risdate><volume>24</volume><issue>9</issue><spage>571</spage><epage>576</epage><pages>571-576</pages><issn>0890-5339</issn><eissn>1531-2291</eissn><abstract>OBJECTIVE:Because P188 poloxamer is effective in promoting cell survival in models of acute trauma, the objectives were to understand the mechanism of its action focusing on glycogen synthase kinase-3 (GSK3) activation, interleukin-6 (IL-6), and p38 signaling.
DESIGN:Sixteen normal human tali were impacted using a 4-mm diameter indenter with an impulse of 1 Ns. Eight-millimeter cartilage plugs containing the 4-mm impacted core and 4-mm adjacent nonimpacted ring were removed and cultured with or without P188. Cell lysates were analyzed using Western blots with antibodies against total and phosphorylated extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), p38, ATF-2, GSK3, Stat1, and Stat3. Additional tests were performed with the p38 inhibitor (p38i) SB203580.
RESULTS:Studied pathways were activated after impaction with the peak of activity at 1 hour. P188 completely attenuated phosphorylation of Stat1 and ATF-2 and inhibited p38, Stat3, JNK, ERK, and GSK3. The p38i partially offset phosphorylation of Stat3, GSK3, and ERK suggesting a role of p38 in these three pathways. Additionally, the p38i improved cell survival (P = 0.053) and reduced apoptosis (by approximately 20%, P = 0.046, versus almost 40% by P188), thus confirming that P188 acts (at least in part) through the p38 pathway.
CONCLUSION:Our results report a novel mechanism through which P188 exerts its protective effects on cartilage in the model of acute injury. In addition to its effect on cellular membrane, P188 affects stress-related p38 signaling, apoptosis-related GSK3, and inflammation-related IL-6 signaling. Taken together, these findings suggest that P188 alone or in combination with proanabolic agents may have a therapeutic potential in preventing progressive cartilage degeneration and the development of posttraumatic osteoarthritis.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>20736797</pmid><doi>10.1097/BOT.0b013e3181ec4712</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of orthopaedic trauma, 2010-09, Vol.24 (9), p.571-576 |
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| subjects | Ankle Injuries - drug therapy Ankle Injuries - metabolism Ankle Injuries - pathology Ankle Joint - drug effects Apoptosis - drug effects Biological and medical sciences Cartilage, Articular - drug effects Cartilage, Articular - injuries Cartilage, Articular - pathology Chondrocytes - drug effects Chondrocytes - metabolism Chondrocytes - pathology Diseases of the osteoarticular system Enzyme Inhibitors - pharmacology Fractures, Cartilage - drug therapy Fractures, Cartilage - metabolism Fractures, Cartilage - pathology Glycogen Synthase Kinase 3 - metabolism Humans Imidazoles - pharmacology Injuries of the limb. Injuries of the spine Interleukin-6 - metabolism Medical sciences p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors p38 Mitogen-Activated Protein Kinases - metabolism Poloxamer - pharmacology Pyridines - pharmacology Signal Transduction - drug effects Surface-Active Agents - pharmacology Talus - drug effects Talus - injuries Traumas. Diseases due to physical agents Wound Healing - drug effects |
| title | Protective effect of P188 in the Model of Acute Trauma to Human Ankle Cartilage: The Mechanism of Action |
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