Clark Richard A F
Department of Biomedical Engineering, Dermatology, and Medicine, Stony Brook University, Stony Brook, New York 11794, USA.
J Invest Dermatol. 2008 Jun;128(6):1354-5. doi: 10.1038/jid.2008.75.
Investigations on extracellular matrix (ECM) and growth factor (GF) complexes have revealed an underappreciated phenomenon: they can either negate GF activity or generate synergistic signals for cell function, in particular mitogenesis. ECM and pericellular matrix molecules were first recognized to complex with GFs and regulate GF activity by the seminal observations that basic fibroblast growth factor (bFGF or FGF-2) required binding to a cell-surface heparin sulfate proteoglycan and to its authentic cell-surface receptor for biological activity (Klagsbrun and Baird, 1991; Yayon et al., 1991). Subsequently, numerous ECM-GF interactions that modulate GF activity were discovered; we have reviewed many of these findings (Macri et al., 2007).
对细胞外基质（ECM）和生长因子（GF）复合物的研究揭示了一个未被充分认识的现象：它们既可以抵消GF活性，也可以为细胞功能，特别是有丝分裂产生协同信号。ECM和细胞周围基质分子首次被认为与GF形成复合物并调节GF活性，这是基于一些开创性的观察结果，即碱性成纤维细胞生长因子（bFGF或FGF-2）需要与细胞表面硫酸乙酰肝素蛋白聚糖及其真正的细胞表面受体结合才能发挥生物活性（Klagsbrun和Baird，1991；Yayon等人，1991）。随后，发现了许多调节GF活性的ECM-GF相互作用；我们已经回顾了其中的许多发现（Macri等人，2007）。
