Mechanisms of magnesium‐stimulated adhesion of osteoblastic cells to commonly used orthopaedic implants

Wiley - Tập 62 Số 2 - Trang 175-184 - 2002
Hala Zreiqat1, C. R. Howlett1, Andrew C.W. Zannettino2, Peter Evans3, Gundula Schulze‐Tanzil4, Christine Knabe5, Mehdi Shakibaei4
1School of Pathology, UNSW, Sydney 2052, Australia.
2Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science, Adelaide, Australia
3ANSTO, Lucas Heights, Australia
4Institute for Anatomy, Benjamin Franklin Medical Center, Free University of Berlin, Berlin, Germany
5Department of Experimental Dentistry, University Hospital Benjamin Franklin, Free Univesity of Berlin, Berlin, Germany

Tóm tắt

AbstractPoor cell adhesion to orthopaedic and dental implants may result in implant failure. Cellular adhesion to biomaterial surfaces primarily is mediated by integrins, which act as signal transduction and adhesion proteins. Because integrin function depends on divalent cations, we investigated the effect of magnesium ions modified bioceramic substrata (Al2O3‐Mg2+) on human bone‐derived cell (HBDC) adhesion, integrin expression, and activation of intracellular signalling molecules. Immunohistochemistry, flow cytometry, cell adhesion, cell adhesion blocking, and Western blotting assays were used. Our findings demonstrated that adhesion of HBDC to Al2O3‐Mg2+ was increased compared to on the Mg2+‐free Al2O3. Furthermore, HBDC adhesion decreased significantly when the fibronectin receptor α5β1‐ and β1‐integrins were blocked by functional blocking antibodies. HBDC grown on the Mg2+‐modified bioceramic expressed significantly enhanced levels of β1‐, α5β1‐, and α3β1‐integrins receptors compared to those grown on the native unmodified Al2O3. Tyrosine phosphorylation of intracellular integrin‐dependent signalling proteins as well as the expression of key signalling protein Shc isoforms (p46, p52, p66), focal adhesion kinase, and extracellular matrix protein collagen type I were significantly enhanced when HBDC were grown on Al2O3‐Mg2+ compared to the native Al2O3. We conclude that cell adhesion to biomaterial surfaces is probably mediated by α5β1‐ and β1‐integrin. Cation‐promoted cell adhesion depends on 5β1‐ and β1‐integrins associated signal transduction pathways involving the key signalling protein Shc and results also in enhanced gene expression of extracellular matrix proteins. Therefore, Mg2+ supplementation of bioceramic substrata may be a promising way to improve integration of implants in orthopaedic and dental surgery. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 62: 175–184, 2002

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Tài liệu tham khảo

10.1002/(SICI)1097-4636(19990615)45:4<345::AID-JBM9>3.0.CO;2-J

10.1002/(SICI)1097-4636(19990315)44:4<389::AID-JBM4>3.0.CO;2-O

10.1063/1.373052

Howlett CR, 2000, Bone tissue engineering, 240

10.1126/science.177.4049.606

10.1016/S0140-6736(96)90072-0

10.1002/jor.1100140606

10.1002/jor.1100170423

10.1096/fasebj.4.11.2199285

10.1016/0092-8674(92)90115-S

10.1016/S0021-9258(18)37650-6

10.1074/jbc.270.43.25570

10.1074/jbc.270.44.26270

10.1074/jbc.273.12.6670

10.1083/jcb.133.2.391

10.1016/S0167-4889(01)00072-6

10.1007/s000180050180

10.1016/S8756-3282(99)00106-4

10.1091/mbc.6.6.637

10.1002/1097-4636(20001215)52:4<738::AID-JBM19>3.0.CO;2-F

10.1002/1097-4636(20001215)52:4<725::AID-JBM18>3.0.CO;2-O

10.1016/S0092-8674(00)81392-6

Shakibaei M, 1999, Signal transduction by beta1 integrin receptors in human chondrocytes in vitro: collaboration with the insulin‐like growth factor‐I receptor, Biochem J, 342, 615, 10.1042/bj3420615

10.1083/jcb.124.6.1047

10.1083/jcb.131.3.791

10.1146/annurev.cb.11.110195.003001

10.1063/1.1138660

10.1002/(SICI)1097-4636(199624)33:4<217::AID-JBM2>3.0.CO;2-S

10.1359/jbmr.1997.12.8.1189

10.1016/0076-6879(82)82103-4

10.1182/blood.V84.12.4164.bloodjournal84124164

10.1007/s004410051318

10.1007/s002040000203

10.1007/BF00690290

10.1038/ki.1997.193

10.1007/s002040050272

10.1007/s002040050010

10.1074/jbc.273.14.7981

10.1083/jcb.105.3.1175

10.1242/jcs.110.18.2187

10.3109/15419069809010781

10.1002/jbmr.5650080503

10.1002/jbmr.5650090408

10.1002/jor.1100120311

10.1006/excr.2000.5099

10.1242/dev.119.4.1079

10.1038/377539a0

10.1074/jbc.272.12.7892

10.1038/372786a0

10.1074/jbc.M010859200

10.1128/AAC.39.9.2013

10.1006/excr.1994.1053

10.1016/0014-4827(88)90191-7

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Wiley

Tập 62 Số 2

175-184

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