题名：INS-1 cell glucose-stimulated insulin secretion is reduced by the downregulation of the 67 kDa laminin receptor.
作者：SABRA G; DUBIEL EA; KUEHN C; KHALFAOUI T; BEAULIEU JF; VERMETTE P;
来源：J Tissue Eng Regen Med. 2013 Jan 30. doi: 10.1002/term.1689. [ IF= 0.00 ] ]
摘要：Understanding beta cell-extracellular matrix (ECM) interactions can advance our
knowledge of the mechanisms that control glucose homeostasis and improve culture
methods used in islet transplantation for the treatment of diabetes. Laminin is
the main constituent of the basement membrane and is involved in pancreatic beta
cell survival and function, even enhancing glucose-stimulated insulin secretion.
Most of the studies on cell responses towards laminin have focused on
integrin-mediated interactions, while much less attention has been paid on
non-integrin receptors, such as the 67 kDa laminin receptor (67LR). The
specificity of the receptor-ligand interaction through the adhesion of INS-1
cells (a rat insulinoma cell line) to CDPGYIGSR-, GRGDSPC- or CDPGYIGSR +
GRGDSPC-covered surfaces was evaluated. Also, the effects of the 67LR knocking
down over glucose-stimulated insulin secretion were investigated. Culture of the
INS-1 cells on the bioactive surfaces was improved compared to the low-fouling
carboxymethyl dextran (CMD) surfaces, while downregulation of the 67LR resulted
in reduced cell adhesion to surfaces bearing the CDPGYIGSR peptide.
Glucose-stimulated insulin secretion was hindered by downregulation of the 67LR,
regardless of the biological motif available on the biomimetic surfaces on which
the cells were cultured. This finding illustrates the importance of the 67LR in
glucose-stimulated insulin secretion and points to a possible role of the 67LR in
the mechanisms of insulin secretion. Copyright (c) 2013 John Wiley & Sons, Ltd.