Flexor tendon wound healing in vitro: Lactate up-regulation of TGF-β expression and functional activity
Flexor tendon wound healing in zone II is complicated by adhesions to the surrounding fibro-osseous sheath. These adhesions can significantly alter tendon gliding and ultimately hand function. Lactate and transforming growth factor-beta (TGF-beta) are two important mediators of wound healing that ha...
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| Veröffentlicht in: | Plastic and reconstructive surgery (1963) 2004-02, Vol.113 (2), p.625-632 |
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| creator | YALAMANCHI, Naveen KLEIN, Matthew B PHAM, Hung M LONGAKER, Michael T CHANG, James |
| description | Flexor tendon wound healing in zone II is complicated by adhesions to the surrounding fibro-osseous sheath. These adhesions can significantly alter tendon gliding and ultimately hand function. Lactate and transforming growth factor-beta (TGF-beta) are two important mediators of wound healing that have been demonstrated to independently increase collagen production by cells of the tendon sheath, epitenon, and endotenon. This study examined the effects of lactate on TGF-beta peptide and receptor production by flexor tendon cells. Tendon sheath fibroblasts, epitenon tenocytes, and endotenon tenocytes were isolated from rabbit flexor tendons and cultured separately. Cell cultures were supplemented with 50 mM lactate, and the expression of three TGF-beta peptide isoforms (beta1, beta2, and beta3) and three receptor isoforms (R1, R2, and R3) was quantified with enzyme-linked immunosorbent assays. TGF-beta functional activity was also assessed with the addition of tendon cell conditioned media to mink lung epithelial cells transfected with a luciferase reporter gene expression construct responsive to TGF-beta. Supplementation of the cell culture medium with lactate significantly (p < 0.05) increased the expression of all TGF-beta peptide and receptor isoforms in all three cell lines. Tendon sheath fibroblasts exhibited the greatest increases in beta1 and beta2 peptide isoform expression (30 and 23 percent, respectively), whereas endotenon tenocytes demonstrated the greatest increase in beta3 peptide expression (32 percent). Epitenon tenocytes exhibited the greatest increases in receptor isoform R1 and R2 expression (17 and 19 percent, respectively). All three tendon cell types demonstrated significant (p < 0.05) increases in TGF-beta functional activity when exposed to lactate. Epitenon tenocytes demonstrated the greatest increase in activity (>4 times control values), whereas tendon sheath fibroblasts demonstrated the highest overall levels of total TGF-beta functional activity. Lactate significantly increased TGF-beta peptide (beta1, beta2, and beta3) expression, receptor (R1, R2, and R3) expression, and functional activity, suggesting a common pathway regulating tendon cell collagen production. Modulation of lactate and TGF-beta levels may provide a means of modulating the effects of TGF-beta on adhesion formation in flexor tendon wound healing. |
| doi_str_mv | 10.1097/01.PRS.0000101529.47062.34 |
| format | Article |
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These adhesions can significantly alter tendon gliding and ultimately hand function. Lactate and transforming growth factor-beta (TGF-beta) are two important mediators of wound healing that have been demonstrated to independently increase collagen production by cells of the tendon sheath, epitenon, and endotenon. This study examined the effects of lactate on TGF-beta peptide and receptor production by flexor tendon cells. Tendon sheath fibroblasts, epitenon tenocytes, and endotenon tenocytes were isolated from rabbit flexor tendons and cultured separately. Cell cultures were supplemented with 50 mM lactate, and the expression of three TGF-beta peptide isoforms (beta1, beta2, and beta3) and three receptor isoforms (R1, R2, and R3) was quantified with enzyme-linked immunosorbent assays. TGF-beta functional activity was also assessed with the addition of tendon cell conditioned media to mink lung epithelial cells transfected with a luciferase reporter gene expression construct responsive to TGF-beta. Supplementation of the cell culture medium with lactate significantly (p < 0.05) increased the expression of all TGF-beta peptide and receptor isoforms in all three cell lines. Tendon sheath fibroblasts exhibited the greatest increases in beta1 and beta2 peptide isoform expression (30 and 23 percent, respectively), whereas endotenon tenocytes demonstrated the greatest increase in beta3 peptide expression (32 percent). Epitenon tenocytes exhibited the greatest increases in receptor isoform R1 and R2 expression (17 and 19 percent, respectively). All three tendon cell types demonstrated significant (p < 0.05) increases in TGF-beta functional activity when exposed to lactate. Epitenon tenocytes demonstrated the greatest increase in activity (>4 times control values), whereas tendon sheath fibroblasts demonstrated the highest overall levels of total TGF-beta functional activity. Lactate significantly increased TGF-beta peptide (beta1, beta2, and beta3) expression, receptor (R1, R2, and R3) expression, and functional activity, suggesting a common pathway regulating tendon cell collagen production. Modulation of lactate and TGF-beta levels may provide a means of modulating the effects of TGF-beta on adhesion formation in flexor tendon wound healing.</description><identifier>ISSN: 0032-1052</identifier><identifier>EISSN: 1529-4242</identifier><identifier>DOI: 10.1097/01.PRS.0000101529.47062.34</identifier><identifier>PMID: 14758225</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Biological Assay ; Cell Line ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Forelimb ; Lactic Acid - pharmacology ; Male ; Medical sciences ; Rabbits ; Receptors, Transforming Growth Factor beta - biosynthesis ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Tendon Injuries - metabolism ; Tendons - cytology ; Tendons - metabolism ; Transforming Growth Factor beta - biosynthesis ; Transforming Growth Factor beta - pharmacology ; Up-Regulation ; Wound Healing</subject><ispartof>Plastic and reconstructive surgery (1963), 2004-02, Vol.113 (2), p.625-632</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c294t-e32a94fe9584b3b6d97f17d25923882e702a72f2b0cfefd57d4fa4dc7f9df8203</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15458099$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14758225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YALAMANCHI, Naveen</creatorcontrib><creatorcontrib>KLEIN, Matthew B</creatorcontrib><creatorcontrib>PHAM, Hung M</creatorcontrib><creatorcontrib>LONGAKER, Michael T</creatorcontrib><creatorcontrib>CHANG, James</creatorcontrib><title>Flexor tendon wound healing in vitro: Lactate up-regulation of TGF-β expression and functional activity</title><title>Plastic and reconstructive surgery (1963)</title><addtitle>Plast Reconstr Surg</addtitle><description>Flexor tendon wound healing in zone II is complicated by adhesions to the surrounding fibro-osseous sheath. These adhesions can significantly alter tendon gliding and ultimately hand function. Lactate and transforming growth factor-beta (TGF-beta) are two important mediators of wound healing that have been demonstrated to independently increase collagen production by cells of the tendon sheath, epitenon, and endotenon. This study examined the effects of lactate on TGF-beta peptide and receptor production by flexor tendon cells. Tendon sheath fibroblasts, epitenon tenocytes, and endotenon tenocytes were isolated from rabbit flexor tendons and cultured separately. Cell cultures were supplemented with 50 mM lactate, and the expression of three TGF-beta peptide isoforms (beta1, beta2, and beta3) and three receptor isoforms (R1, R2, and R3) was quantified with enzyme-linked immunosorbent assays. TGF-beta functional activity was also assessed with the addition of tendon cell conditioned media to mink lung epithelial cells transfected with a luciferase reporter gene expression construct responsive to TGF-beta. Supplementation of the cell culture medium with lactate significantly (p < 0.05) increased the expression of all TGF-beta peptide and receptor isoforms in all three cell lines. Tendon sheath fibroblasts exhibited the greatest increases in beta1 and beta2 peptide isoform expression (30 and 23 percent, respectively), whereas endotenon tenocytes demonstrated the greatest increase in beta3 peptide expression (32 percent). Epitenon tenocytes exhibited the greatest increases in receptor isoform R1 and R2 expression (17 and 19 percent, respectively). All three tendon cell types demonstrated significant (p < 0.05) increases in TGF-beta functional activity when exposed to lactate. Epitenon tenocytes demonstrated the greatest increase in activity (>4 times control values), whereas tendon sheath fibroblasts demonstrated the highest overall levels of total TGF-beta functional activity. Lactate significantly increased TGF-beta peptide (beta1, beta2, and beta3) expression, receptor (R1, R2, and R3) expression, and functional activity, suggesting a common pathway regulating tendon cell collagen production. Modulation of lactate and TGF-beta levels may provide a means of modulating the effects of TGF-beta on adhesion formation in flexor tendon wound healing.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Assay</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Forelimb</subject><subject>Lactic Acid - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Rabbits</subject><subject>Receptors, Transforming Growth Factor beta - biosynthesis</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Tendon Injuries - metabolism</subject><subject>Tendons - cytology</subject><subject>Tendons - metabolism</subject><subject>Transforming Growth Factor beta - biosynthesis</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Up-Regulation</subject><subject>Wound Healing</subject><issn>0032-1052</issn><issn>1529-4242</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0FFLwzAQB_AgipvTryBB0LfW5JI0jW8y3BQGis7nkjbJVuna2rS6fS0_iJ_JFifey3HH7_4Ph9AFJSElSl4TGj49v4SkL0qoABVySSIIGT9A42EOOHA4RGNCGASUCBihE-_fei5ZJI7RiHIpYgAxRutZYbdVg1tbmqrEn1VXGry2usjLFc5L_JG3TXWDFzprdWtxVweNXXWFbvNeVw4v57Pg-wvbbd1Y74el7gNcV2aD0AXuD_M-ZHeKjpwuvD3b9wl6nd0tp_fB4nH-ML1dBBko3gaWgVbcWSVinrI0Mko6Kg0IBSyOwUoCWoKDlGTOOiOk4U5zk0mnjIuBsAm6-s2tm-q9s75NNrnPbFHo0ladT2JCGZBogOd72KUba5K6yTe62SV_v-nB5R5on-nCNbrMcv_vBBcxUYr9ACzhdxo</recordid><startdate>20040201</startdate><enddate>20040201</enddate><creator>YALAMANCHI, Naveen</creator><creator>KLEIN, Matthew B</creator><creator>PHAM, Hung M</creator><creator>LONGAKER, Michael T</creator><creator>CHANG, James</creator><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>7X8</scope></search><sort><creationdate>20040201</creationdate><title>Flexor tendon wound healing in vitro: Lactate up-regulation of TGF-β expression and functional activity</title><author>YALAMANCHI, Naveen ; KLEIN, Matthew B ; PHAM, Hung M ; LONGAKER, Michael T ; CHANG, James</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c294t-e32a94fe9584b3b6d97f17d25923882e702a72f2b0cfefd57d4fa4dc7f9df8203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Assay</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Forelimb</topic><topic>Lactic Acid - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Rabbits</topic><topic>Receptors, Transforming Growth Factor beta - biosynthesis</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Tendon Injuries - metabolism</topic><topic>Tendons - cytology</topic><topic>Tendons - metabolism</topic><topic>Transforming Growth Factor beta - biosynthesis</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Up-Regulation</topic><topic>Wound Healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YALAMANCHI, Naveen</creatorcontrib><creatorcontrib>KLEIN, Matthew B</creatorcontrib><creatorcontrib>PHAM, Hung M</creatorcontrib><creatorcontrib>LONGAKER, Michael T</creatorcontrib><creatorcontrib>CHANG, James</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>MEDLINE - Academic</collection><jtitle>Plastic and reconstructive surgery (1963)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YALAMANCHI, Naveen</au><au>KLEIN, Matthew B</au><au>PHAM, Hung M</au><au>LONGAKER, Michael T</au><au>CHANG, James</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Flexor tendon wound healing in vitro: Lactate up-regulation of TGF-β expression and functional activity</atitle><jtitle>Plastic and reconstructive surgery (1963)</jtitle><addtitle>Plast Reconstr Surg</addtitle><date>2004-02-01</date><risdate>2004</risdate><volume>113</volume><issue>2</issue><spage>625</spage><epage>632</epage><pages>625-632</pages><issn>0032-1052</issn><eissn>1529-4242</eissn><abstract>Flexor tendon wound healing in zone II is complicated by adhesions to the surrounding fibro-osseous sheath. These adhesions can significantly alter tendon gliding and ultimately hand function. Lactate and transforming growth factor-beta (TGF-beta) are two important mediators of wound healing that have been demonstrated to independently increase collagen production by cells of the tendon sheath, epitenon, and endotenon. This study examined the effects of lactate on TGF-beta peptide and receptor production by flexor tendon cells. Tendon sheath fibroblasts, epitenon tenocytes, and endotenon tenocytes were isolated from rabbit flexor tendons and cultured separately. Cell cultures were supplemented with 50 mM lactate, and the expression of three TGF-beta peptide isoforms (beta1, beta2, and beta3) and three receptor isoforms (R1, R2, and R3) was quantified with enzyme-linked immunosorbent assays. TGF-beta functional activity was also assessed with the addition of tendon cell conditioned media to mink lung epithelial cells transfected with a luciferase reporter gene expression construct responsive to TGF-beta. Supplementation of the cell culture medium with lactate significantly (p < 0.05) increased the expression of all TGF-beta peptide and receptor isoforms in all three cell lines. Tendon sheath fibroblasts exhibited the greatest increases in beta1 and beta2 peptide isoform expression (30 and 23 percent, respectively), whereas endotenon tenocytes demonstrated the greatest increase in beta3 peptide expression (32 percent). Epitenon tenocytes exhibited the greatest increases in receptor isoform R1 and R2 expression (17 and 19 percent, respectively). All three tendon cell types demonstrated significant (p < 0.05) increases in TGF-beta functional activity when exposed to lactate. Epitenon tenocytes demonstrated the greatest increase in activity (>4 times control values), whereas tendon sheath fibroblasts demonstrated the highest overall levels of total TGF-beta functional activity. Lactate significantly increased TGF-beta peptide (beta1, beta2, and beta3) expression, receptor (R1, R2, and R3) expression, and functional activity, suggesting a common pathway regulating tendon cell collagen production. Modulation of lactate and TGF-beta levels may provide a means of modulating the effects of TGF-beta on adhesion formation in flexor tendon wound healing.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>14758225</pmid><doi>10.1097/01.PRS.0000101529.47062.34</doi><tpages>8</tpages></addata></record> |
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| ispartof | Plastic and reconstructive surgery (1963), 2004-02, Vol.113 (2), p.625-632 |
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| subjects | Animals Biological and medical sciences Biological Assay Cell Line Cells, Cultured Enzyme-Linked Immunosorbent Assay Forelimb Lactic Acid - pharmacology Male Medical sciences Rabbits Receptors, Transforming Growth Factor beta - biosynthesis Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Tendon Injuries - metabolism Tendons - cytology Tendons - metabolism Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - pharmacology Up-Regulation Wound Healing |
| title | Flexor tendon wound healing in vitro: Lactate up-regulation of TGF-β expression and functional activity |
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