uniform dental biofilm development in vitro for the related biofilm research. Additionally, this micro-mixer is highly compatible with the widely used soft lithography technique, and hence, it can be directly integrated with general microfluidic devices for extended biomedical diagnosis and bio-sample processing applications.
Abstract. It has been reported that RhoA activation and Rho-kinase (ROCK) expression are increased in chronic hypoxic lungs, and the long-term inhibition of ROCK markedly improves the survival of patients with pulmonary arterial hypertension (PAH). However, whether Rho-kinase α (ROCK2) participates in regulation of the growth of pulmonary arterial endothelial cells (PAECs) remains unknown. The aim of the present study was to investigate the effect of hypoxia on the proliferation of PAECs and the role of ROCK2 in the underlying mechanism. The results of western blotting and reverse transcription-quantitative polymerase chain reaction analysis showed that hypoxia increased the activity and expression of ROCK2 in PAECs, and the stimulating effects of hypoxia on the proliferation of PAECs were attenuated by either the ROCK inhibitor Y27632 or transfection with ROCK2 small interfering RNA. Moreover, analysis of cyclin A and cyclin D1 mRNA expression indicated that ROCK2 mediates the cell cycle progression promoted by hypoxia. These results indicate that hypoxia promotes the proliferation of pulmonary arterial endothelial cells via activation of the ROCK2 signaling pathway.
IntroductionPulmonary arterial hypertension (PAH) is a fatal condition characterized by increased pulmonary vascular resistance and finally leading to right heart failure and mortality (1,2). Endothelial injury, prolonged vasoconstriction and the proliferation and migration of vascular smooth muscle cells (VSMCs), are causes of increased pulmonary vascular resistance (3). Multiple pharmacological agents, such as vasodilators and anticoagulants, have been developed for the treatment of PAH; however, the long-term prognosis of patients with severe PAH remains poor (3). Therefore, there is an urgent requirement for the development of more effective treatments for PAH.Rho-kinase (ROCK) is a member of the serine/threonine kinase family that is an important downstream effector of the small GTP-binding protein RhoA. The Rho/ROCK pathway plays an important role in various fundamental cellular functions, including contraction, motility, proliferation and migration (4,5). There are two isoforms of ROCK, namely ROCK1 (Rho-kinase β) and ROCK2 (Rho-kinase α) (6). ROCK1 and ROCK2 are highly homologous with regard to amino acid sequence and kinase domains, sharing ~65% homology in amino acid sequence and 92% homology in their kinase domains (6). Although the two isoforms are ubiquitously expressed in invertebrates and vertebrates, ROCK1 is expressed mainly in circulating inflammatory cells and ROCK2 is expressed in vascular cells (7,8). Homozygous ROCK1-deficient mice show open eyelids at birth and omphalocele, whereas homozygous ROCK2-deficient mice die embryonically because of placental dysfunction, suggesting that ROCK1 and ROCK2 mediate different functions in different types of cells (9,10). To date, to the best of our knowledge, whether ROCK is responsible for the growth of pulmonary arterial endothelial cells (PAECs) has not yet been evaluated.The present ...
Dissolved oxygen is a critical micro-environmental factor to determine the growth characteristics of bacteria, such as cell viability, migration, aggregation and metabolic processes.
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