Molla A, Block M R
Laboratoire d'étude de la différenciation et de l'adhérence cellulaires, UMR Centre National de la Recherche Scientifique/UJF 5538, Institut Albert Bonniot, Faculté de Médecine Domaine de la Merci, La Tronche, France.
Cell Growth Differ. 2000 Feb;11(2):83-90.
To investigate the effect of extracellular matrix molecules in the megakaryocytic lineage, we studied the role of integrin engagement in the proliferation and differentiation of human erythroleukemia (HEL) cells. HEL cells grew in suspension, but their adherence depended upon the presence of matrix proteins or protein kinase C signaling. Adherence by itself did not trigger commitment of these cells but accelerated phorbol 12-myristate 13-acetate-induced differentiation. HEL cells adhered to fibronectin mainly through alpha5beta1, and this receptor acted synergetically with alpha4beta1. Integrin engagement induced cell growth arrest through mitogen-activated protein kinase inactivation. Such down-regulation of the mitogen-activated protein kinase pathway by integrin engagement was suggested as a megakaryocytic-platelet lineage specificity. This signaling was not restricted to a peculiar integrin but was proposed as a general mechanism in these cells.
为了研究细胞外基质分子在巨核细胞系中的作用，我们研究了整合素结合在人红白血病（HEL）细胞增殖和分化中的作用。HEL细胞悬浮生长，但其黏附依赖于基质蛋白或蛋白激酶C信号的存在。黏附本身不会触发这些细胞的定向分化，但会加速佛波酯12-肉豆蔻酸酯13-乙酸酯诱导的分化。HEL细胞主要通过α5β1黏附于纤连蛋白，且该受体与α4β1协同作用。整合素结合通过丝裂原活化蛋白激酶失活诱导细胞生长停滞。整合素结合对丝裂原活化蛋白激酶途径的这种下调被认为是巨核细胞-血小板系的特异性表现。这种信号传导并不局限于特定的整合素，而是被认为是这些细胞中的一种普遍机制。
