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Excessive tensile strain induced the change in chondrocyte phenot

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Języki publikacji
EN
Abstrakty
EN
Chondrocyte extracellular matrix type II collagen and proteoglycans ensure an important compression-bearing structure in synovial joint. However, much more type I collagen is generated in osteoarthritis, which implies the presence of abnormal tensile strain in cartilage. We hypothesize that tensile stress influences chondrocyte phenotype at the cellular level, leading to potential osteoarthritis. Methods: Chondrocytes were stimulated with cyclic excessive tensile (10%) or mild tensile or compressive strain (5%) at 0.5 Hz, 3 h per day for 3 days. Chondrocyte morphology and matrix proteoglycans level was separately determined by Rhodamine phalloidin and toluidine blue staining. The expression of cartilage marker molecules was measured using quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assays. Results: Chondrocytes demonstrated significant fibroblastic morphology, reduced proliferation and increased apoptosis following exposure to 10% tensile strain. The 10% tensile strain group induced the lowest matrix proteoglycans level. It observably reduced the expression of COL2A1, Acan and SOX9, and increased COL1A1 expression level. The 5% tensile (5% compression) group, maintained the chondrocyte phenotype. Conclusions: The findings identified the effects of different magnitudes of tensile stress on chondrocyte phenotype compared to compressive strain. Further studies on cartilage biomechanical micro-environment might benefit from this study.
Rocznik
Strony
3--10
Opis fizyczny
Bibliogr. 26 poz., rys., tab., wykr.
Twórcy
autor
  • Orthopedic Institute, Medical College, Soochow University, Suzhou, Jiangsu, China
autor
  • Orthopedic Institute, Medical College, Soochow University, Suzhou, Jiangsu, China
autor
  • Orthopedic Institute, Medical College, Soochow University, Suzhou, Jiangsu, China
Bibliografia
  • [1] ALMONTE-BECERRIL M., NAVARRO-GARCIA F., GONZALEZ- -ROBLES A., VEGA-LOPEZ M.A., LAVALLE C., KOURI J.B., Cell death of chondrocytes is a combination between apoptosis and autophagy during the pathogenesis of Osteoarthritis within an experimental model, Apoptosis., 2010, 15(5), 631–638.
  • [2] CHEN C., TAMBE D.T., DENG L., YANG L., Biomechanical properties and mechanobiology of the articular chondrocyte, Am. J. Physiol. Cell. Physiol., 2013, 305(12), C1202–1208.
  • [3] D’LIMA D.D., HASHIMOTO S., CHEN P.C., COLWELL C.W., Jr., LOTZ M.K., Human chondrocyte apoptosis in response to mechanical injury, Osteoarthritis Cartilage, 2001, 9(8), 712–719.
  • [4] D’LIMA D.D., HASHIMOTO S., CHEN P.C., COLWELL C.W., Jr., LOTZ M.K., Impact of mechanical trauma on matrix and cells, Clin. Orthop. Relat. Res., 2001, (391 Suppl), S90–99.
  • [5] DVIR-GINZBERG M., GAGARINA V., LEE E.J., HALL D.J., Regulation of cartilage-specific gene expression in human chondrocytes by SirT1 and nicotinamide phosphoribosyltransferase, J. Biol. Chem., 2008, 283(52), 36300–36310.
  • [6] EYRE D., Collagen cross-linking amino acids, Methods Enzymol., 1987, 144, 115–139.
  • [7] GAGARINA V., GABAY O., DVIR-GINZBERG M. et al., SirT1 enhances survival of human osteoarthritic chondrocytes by repressing protein tyrosine phosphatase 1B and activating the insulin-like growth factor receptor pathway, Arthritis Rheum., 2010, 62(5), 1383–1392.
  • [8] HUANG K., YAN Z.Q., ZHAO D. et al., SIRT1 and FOXO Mediate Contractile Differentiation of Vascular Smooth Muscle Cells under Cyclic Stretch, Cell Physiol. Biochem., 2015, 37(5), 1817–1829.
  • [9] KAWAKITA K., NISHIYAMA T., FUJISHIRO T. et al., Akt phosphorylation in human chondrocytes is regulated by p53R2 in response to mechanical stress, Osteoarthritis Cartilage, 2012, 20(12), 1603–1609.
  • [10] KEMPSON G.E., MUIR H., POLLARD C., TUKE M., The tensile properties of the cartilage of human femoral condyles related to the content of collagen and glycosaminoglycans, Biochim. Biophys. Acta, 1973, 297(2), 456–472.
  • [11] KIM H.A., BLANCO F.J., Cell death and apoptosis in osteoarthritic cartilage, Curr. Drug. Targets, 2007, 8(2), 333–345.
  • [12] LAHM A., MROSEK E., SPANK H. et al., Changes in content and synthesis of collagen types and proteoglycans in osteoarthritis of the knee joint and comparison of quantitative analysis with Photoshop-based image analysis, Arch. Orthop. Trauma Surg., 2010, 130(4), 557–564.
  • [13] LEFEBVRE V., BEHRINGER R.R., DE CROMBRUGGHE B., L-Sox5, Sox6 and Sox9 control essential steps of the chondrocyte differentiation pathway, Osteoarthritis Cartilage, 2001, 9, S69–S75.
  • [14] LIU S.H., YANG R.S., AL-SHAIKH R., LANE J.M., Collagen in tendon, ligament, and bone healing. A current review, Clin. Orthop. Relat. Res., 1995, (318), 265–278.
  • [15] LOENING A.M., JAMES I.E., LEVENSTON M.E. et al., Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis, Arch. Biochem. Biophys., 2000, 381(2), 205–212.
  • [16] MCILWAIN D.R., BERGER T., MAK T.W., Caspase functions in cell death and disease, Cold Spring Harb. Perspect. Biol., 2015, 7(4).
  • [17] MIOSGE N., HARTMANN M., MAELICKE C., HERKEN R., Expression of collagen type I and type II in consecutive stages of human osteoarthritis, Histochem. Cell Biol., 2004, 122(3),229–236.
  • [18] PEI M., YU C., QU M., Expression of collagen type I, II and III in loose body of osteoarthritis, J. Orthop. Sci., 2000, 5(3), 288–293.
  • [19] RAMAGE L., NUKI G., SALTER D.M., Signalling cascades in mechanotransduction: cell-matrix interactions and mechanical loading, Scand. J. Med. Sci. Sports, 2009, 19(4), 457–469.
  • [20] SMITH R.L., CARTER D.R., SCHURMAN D.J., Pressure and shear differentially alter human articular chondrocyte metabolism: a review, Clin. Orthop. Relat. Res., 2004, (427 Suppl), S89–95.
  • [21] SOPHIA FOX A.J., BEDI A., RODEO S.A., The basic science of articular cartilage: structure, composition, and function, Sports Health, 2009, 1(6), 461–468.
  • [22] TEW S.R., KWAN A.P., HANN A., THOMSON B.M., ARCHER C.W., The reactions of articular cartilage to experimental wounding: role of apoptosis, Arthritis Rheum., 2000, 43(1), 215–225.
  • [23] THOMAS C.M., FULLER C.J., WHITTLES C.E., SHARIF M., Chondrocyte death by apoptosis is associated with cartilage matrix degradation, Osteoarthritis Cartilage, 2007, 15(1), 27–34.
  • [24] THOMAS R.S., CLARKE A.R., DUANCE V.C., BLAIN E.J., Effects of Wnt3A and mechanical load on cartilage chondrocyte homeostasis, Arthritis Res. Ther., 2011, 13(6), R203.
  • [25] UEKI M., TANAKA N., TANIMOTO K. et al., The effect of mechanical loading on the metabolism of growth plate chondrocytes, Ann. Biomed. Eng., 2008, 36(5), 793–800.
  • [26] XU Z., BUCKLEY M.J., EVANS C.H., AGARWAL S., Cyclic tensile strain acts as an antagonist of IL-1 beta actions in chondrocytes, J. Immunol., 2000, 165(1), 453–460.
Uwagi
This project is funded by the National Natural Science Foundation of China (81320108018, 31570943 and 31270995), Innovation and Entrepreneurship Program of Jiangsu Province, and the Priority Academic Program Development of Jiangsu Higher Education Institutions.
Opracowanie rekordu w ramach umowy 509/P-DUN/2018 ze środków MNiSW przeznaczonych na działalność upowszechniającą naukę (2019).
Typ dokumentu
Bibliografia
Identyfikator YADDA
bwmeta1.element.baztech-a8683053-da10-44e1-adbe-608c4fae3963
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