Inhibitory effects of tetrandrine on the serum- and platelet-derived growth factor-BB-induced proliferation of rat aortic smooth muscle cells through inhibition of cell cycle progression, DNA synthesis, ERK1/2 activation and c-fos expression

Hyperplasia of airway smooth muscle (ASM) is a feature of the remodelled airway in asthmatics. We examined the antiproliferative effectiveness of the corticosteroid dexamethasone on expression of the key regulator of G1 cell cycle progression—cyclin D1—in ASM cells from nonasthmatics and asthmatics stimulated with the mitogen platelet-derived growth factor BB. While cyclin D1 mRNA and protein expression were repressed in cells from nonasthmatics in contrast, cyclin D1 expression in asthmatics was resistant to inhibition by dexamethasone. This was independent of a repressive effect on glucocorticoid receptor translocation. Our results corroborate evidence demonstrating that corticosteroids inhibit mitogen-induced proliferation only in ASM cells from subjects without asthma and suggest that there are corticosteroid-insensitive proliferative pathways in asthmatics.

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Protein kinase C may regulate cell cycle progression but not cytosolic Catransients, induced by platelet-derived growth factor in vascular smooth muscle cells in primary culture.

The Japanese Journal of Pharmacology ◽

10.1016/s0618-8278(19)31705-0 ◽

1993 ◽

Vol 61 ◽

pp. 323

Author(s):

Sei Kobayashi ◽

Junji Nishimura ◽

Hideo Kanaide

Keyword(s):

Cell Cycle ◽

Smooth Muscle ◽

Protein Kinase C ◽

Growth Factor ◽

Protein Kinase ◽

Cell Cycle Progression ◽

Platelet Derived Growth Factor ◽

Cycle Progression ◽

Kinase C ◽

Regulate Cell Cycle Progression

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Aldose reductase regulates platelet-derived growth factor-induced proliferation through mediating cell cycle progression in rat mesangial cells

International Journal of Molecular Medicine ◽

10.3892/ijmm.2012.997 ◽

2012 ◽

Vol 30 (2) ◽

pp. 409-416 ◽

Cited By ~ 4

Author(s):

LIPING ZOU ◽

WENJUAN WANG ◽

ZUDE XU ◽

NONG ZHANG ◽

TAO JIANG

Keyword(s):

Cell Cycle ◽

Growth Factor ◽

Aldose Reductase ◽

Cell Cycle Progression ◽

Mesangial Cells ◽

Platelet Derived Growth Factor ◽

Cycle Progression

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6-Methylsulfinylhexyl Isothiocyanate Inhibits Cell Cycle Progression in Quiescent Jb6 Cells Stimulated with Epidermal Growth Factor

Annual Research & Review in Biology ◽

10.9734/arrb/2021/v36i630386 ◽

2021 ◽

pp. 19-28

Author(s):

Takashi Hashimoto ◽

Maki Kobayashi ◽

Kazuki Kanazawa

Keyword(s):

Gene Expression ◽

Cell Cycle ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Dna Synthesis ◽

Cell Cycle Progression ◽

Nuclear Antigen ◽

Cycle Progression ◽

Epidermal Growth ◽

Jb6 Cells

Objective: The effects of 6-MSITC on cell cycle progression were investigated in quiescent mouse epidermal JB6 cells. Background: 6-Methylsulfinylhexyl isothiocyanate (6-MSITC) derived from wasabi (Wasabia japonica) has been reported to prevent tumor development in vivo. Material and methods: Treatment with epidermal growth factor (EGF) to quiescent JB6 cells, which were serum-starved for 36 h, promoted cell cycle progression from the G0/G1 phase to the S phase. Effects of pretreatment with 6-MSITC on cell cycle progression were estimated by flowcytometry and real-time RT-PCR. Results: Pretreatment with 6-MSITC at 0.25-1.0 μg/ml prior to the growth stimulation with EGF significantly inhibited cell cycle progression. Pretreatment with 6-MSITC inhibited the gene expression of DNA synthesis-related proteins cyclin A2, dumbbell former 4, and proliferating cell nuclear antigen. Conclusion: These results showed that 6-MSITC inhibits cell cycle progression in quiescent cells, accompanied by the inhibition of gene expression of DNA synthesis proteins.

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Ethanol, Zn2+ and insulin interact as progression factors to enhance DNA synthesis synergistically in the presence of Ca2+ and other cell cycle initiators in fibroblasts

Biochemical Journal ◽

10.1042/bj3460241 ◽

2000 ◽

Vol 346 (1) ◽

pp. 241-247 ◽

Cited By ~ 4

Author(s):

Jin-Sheng HUANG ◽

Qing-Bai SHE ◽

Karan S. CRILLY ◽

Zoltan KISS

Keyword(s):

Cell Cycle ◽

Growth Factor ◽

Dna Synthesis ◽

Cell Cycle Progression ◽

Synergistic Effects ◽

Dependent Manner ◽

Cycle Progression ◽

3T3 Fibroblasts ◽

Igf I ◽

Nih 3T3

In serum-starved NIH 3T3 fibroblasts, ethanol (30-80 mM) promoted the effects of insulin and insulin-like growth factor I (IGF-I) on DNA synthesis in a Zn2+-dependent manner. Ethanol and Zn2+ were most effective when added shortly before or after insulin, indicating that all these agents facilitated cell cycle progression. The synergistic effects of ethanol, Zn2+ and insulin (or IGF-I) on DNA synthesis required 1.1-2.3 mM Ca2+, which seemed to act as the cell cycle initiator. When serum-starved cells were pretreated for 2 h with other cell cycle initiators such as 10% (v/v) serum, 50 ng/ml platelet-derived growth factor or 2 ng/ml fibroblast growth factor, subsequent co-treatments with 60 mM ethanol, Zn2+ and insulin for an 18 h period again synergistically increased DNA synthesis. Of the various signal transducing events examined, ethanol stimulated cellular uptake of 45Ca and it enhanced the stimulatory effects of insulin on p70 S6 kinase activity in a Zn2+-dependent manner. In contrast, ethanol inhibited insulin-induced activating phosphorylation of p42/p44 mitogen-activated protein kinases; these inhibitory ethanol effects were prevented by Zn2+. The results show that, in NIH 3T3 fibroblasts, ethanol can promote cell cycle progression in the presence of a cell cycle initiator as well as Zn2+ and insulin (or IGF-I).

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