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Density‐ and proliferation status‐dependent expression of T‐cadherin, a novel lipoprotein‐binding glycoprotein: a function in negative regulation of smooth muscle cell growth?
Author(s) -
Kuzmenko Yelena S,
Kern Frances,
Bochkov Valery N,
Tkachuk Vsevolod A,
Resink Thérèse J
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00977-6
Subject(s) - microbiology and biotechnology , cadherin , cell growth , function (biology) , chemistry , glycoprotein , cell , biology , biochemistry
The atypical low density lipoprotein (LDL) binding proteins ( M r 105 and 130 kDa; p105 and p130) in human aortic medial membranes and cultured human and rat aortic smooth muscle cells (SMC) have recently been identified as the cell adhesion glycoprotein T‐cadherin. Although cadherins are generally recognized to be important regulators of morphogenesis, the function of T‐cadherin in the vasculature is poorly understood. This study has examined the relationship between expression of T‐cadherin and the density and proliferation status of SMC. T‐cadherin (p105 and p130) levels in SMC lysates were measured on Western blots using ligand‐binding techniques. T‐cadherin expression was dependent upon cell density, and maximal levels were achieved at confluency. T‐cadherin levels were reversibly modulated by switching cultures between serum‐free (upmodulation) and serum‐containing (downmodulation) conditions. Platelet‐derived growth factor (PDGF)‐BB, epidermal growth factor (EGF) or insulin‐like growth factor (IGF) elicited a dose‐ and time‐dependent downmodulation that was reversible after transfer of SMC to growth factor‐free medium. Our results support the hypothesis that T‐cadherin may function as a negative determinant of cell growth.