The rate of protein synthesis per cell in cultured hamster embryo fibroblasts in the stationary growth phase falls to about one third of the rate in the exponential growth phase. This reduction can be entirely accounted for by the following observations: (1) the average cell in stationary phase contains about one-half the number of ribosomes per cell compared to the average cell in exponential phase; (2) only two thirds of the ribosomes are bound to polysomes in stationary phase, while nearly all of the ribosomes are polysome-bound in exponential phase.In stationary phase, ribosomes which are polysome-bound function with the same efficiency and produce proteins of approximately the same average length as in exponential phase. Experimental findings are presented which suggest that the generation of a higher proportion of free ribosomes in stationary phase is not due to a limitation in messenger RNA, but to a decreased attachment probability of ribosomes to messenger RNA.

No abstract

Regions of the normal arterial intima predisposed to atherosclerosis are sites of ongoing monocyte trafficking and also contain resident myeloid cells with features of dendritic cells. However, the pathophysiological roles of these cells are poorly understood. Here we found that intimal myeloid cells underwent reverse transendothelial migration (RTM) into the arterial circulation after systemic stimulation of pattern-recognition receptors (PRRs). This process was dependent on expression of the chemokine receptor CCR7 and its ligand CCL19 by intimal myeloid cells. In mice infected with the intracellular pathogen Chlamydia muridarum, blood monocytes disseminated infection to the intima. Subsequent CCL19-CCR7-dependent RTM was critical for the clearance of intimal C. muridarum. This process was inhibited by hypercholesterolemia. Thus, RTM protects the normal arterial intima, and compromised RTM during atherogenesis might contribute to the intracellular retention of pathogens in atherosclerotic lesions.