Progesterone-Growth Factor Interactions in Uterine Stromal Cells: CELL CYCLE REGULATION(1)

In: Progesterone

4 Feb 2013

Recent progress in understanding the mechanisms involved in cellular differentiation has been possible because of our increased appreciation of the regulation of cell proliferation and cell cycle progression. The convergence of these two fields is critical because differentiation programs are normally initiated as cell proliferation decreases and arrest occurs. This concept, supported by experimental evidence in a variety of cell types, clearly indicates that increased understanding of endocrine control of cell cycle progression is essential before cellular differentiation and apoptosis can be systematically studied in hormone target tissues. Current research in our laboratory is therefore focused on understanding the role of progesterone in regulating stromal cell transit through the cell cycle. ventolin inhaler

Mammalian cells use a small family of related cyclin-dependent kinase (cdk) complexes to regulate progression through the cell cycle. Some of these function during G1 while others are important during the G2 to M transition. Cyclin-dependent kinase complexes are heterodimeric proteins composed of two subunits. One is a catalytic protein that phosphorylates multiple substrates via its kinase activity. The second subunit is a cyclin protein that regulates substrate specificity. The current model for the action of growth factors during G1 of the cell cycle predicts that cyclin D and cyclin E levels increase, resulting in the formation of different cdk complexes that drive cells through the restriction point of G1 into DNA replication. Cy-clins are rapidly degraded once the peak concentration is reached, and this degradation is essential before cells go into the next phase of the cycle. Regulated cyclin destruction via the ubiquitin-mediated degradation pathway is an important regulatory mechanism for cell cycle progression. A large number of growth factors and their receptors have been mapped to the various cell types in the uterus of the human and of rodents and domestic animals, and reviews summarizing their distribution are available. It is clear that some steroidal effects on the endometrium are mediated by endocrine-dependent synthesis of growth factors and their receptors. Newly synthesized growth factors presumably then act on endometrial cells via mechanisms identified in other cell types.

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