It has been shown that MMPs are temporally regulated to perform specific functions during pregnancy. For HEPES example, MMP-9 is selectively expressed in the decidua and fetal membranes with the onset of labor, but barely detectable before labor. Furthermore, it would be interesting to evaluate whether MMP:TIMP ratios differ between patients with preterm labor who delivered preterm and those delivering at term. A preliminary evaluation showed no significant differences, but the number of patients with preterm labor and term delivery was rather low. Finally, we only evaluated immunoreactive forms of MMP-3 and -9 with a MMP 3�Cplex detecting all circulating MMPs. An alternative would be to evaluate the enzymatic activity of MMPs, because the mere presence of MMP does not necessarily establish their catalytic capacity. Fortunato et al demonstrated that only a small amount of total amniotic fluid MMP-9 and -2 were active. However, it has been shown that the immunoreactivity of MMP-9 in amniotic fluid correlates well with its enzymatic activity. In conclusion, this study showed that MMP-9:TIMP-1 and MMP-9:TIMP-2 balances in maternal serum are tilting in favor of gelatinolysis in women with preterm labor. All four TIMPs were expressed in maternal serum. While TIMP-1 and -2 concentrations were lower during gestation, irrespective of labor, TIMP-4 levels were elevated during labor. The observations in the present study indicate that circulating MMPs and TIMPs may also play a role in the pathogenesis of preterm labor at systemic level or at least reflect Gue 1654 pregnancy and labor status. Our findings provide the possibility to develop a far less invasive approach for measurement of enzymes essential for ECM remodeling during pregnancy and parturition. However, a great deal still remains to be learned about MMPs and in particular TIMPs during various stages of normal pregnancy and labor as well as in pathological conditions such as preterm labor. Cell cycle progression is balanced by the activation and inhibition of cyclin-dependent kinases. A variety of mechanisms have been identified that interfere with CDK activities, amongst them binding of INK4 and CIP/KIP inhibitors. Whereas INK4 proteins specifically impede G1/S transition by binding to CDK4 and CDK6, inhibitors of the CIP/ KIP family are capable of interfering with the activity of a variety of CDKs. The cell cycle regulator p21 becomes activated within several stress response pathways contributing to cellular fate decisions like cell cycle arrest, differentiation, senescence or apoptosis. p21 exerts its function predominantly through inhibition of CDKs and of DNA synthesis. Despite its main characterization as a mediator of p53-dependent tumor suppressor activity several observations suggest an oncogenic potential of p21, presumably through its anti-apoptotic function and its ability to promote the assembly of cyclinD-CDK4 and CDK6 complexes. However, to date only a few direct transcriptional targets of PRMT6 have been described, amongst them the HoxA2 and TSP-12 genes.