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Effects of 25‐hydroxycholesterol, cholesterol, and isoprenoid derivatives on the G 1 progression in Swiss 3T3 cells
Author(s) -
Larsson Olle,
Zetterberg Anders
Publication year - 1986
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041290114
Subject(s) - dolichol , reductase , hmg coa reductase , coenzyme a , cholesterol , cell cycle , hydroxymethylglutaryl coa reductase , biochemistry , cell , 3t3 cells , chemistry , biology , endocrinology , enzyme , biosynthesis , transfection , gene
The effect of inhibition of 3‐Hydroxy‐3‐methylglutaryl Coenzyme A reductase (HMG CoA reductase) on cell cycle progression in proliferating 3T3 cells was studied. It was found that short transient exposures to the HMG CoA reductase inhibitor 25‐hydroxycholesterol temporarily blocked the cell cycle traverse in the postmitotic half of G 1 (G 1 pm), whereas cells in the subsequent cell cycle phases were unaffected. The kinetics of the cell cycle delay, induced by 25‐hydroxycholesterol, resembled the kinetics of the delay induced by serum depletion, which also inhibited the activity of HMG CoA reductase. In contrast to the case of serum depletion, platelet derived growth factor (PDGF), which efficiently prevented the decrease of HMG CoA reductase in serum‐free medium, was not capable of preventing the growth inhibitory effect following treatment by 25‐hydroxycholesterol. However, cholesterol and two isoprenoids, dolichol and coenzyme Q, were effective in this respect. In addition, dolichol counteracted the cell cycle delay following short periods of serum starvation.