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Retinoic acid receptor α (RARα), a member of family of the nuclear retinoic acid receptors (RARs), plays an essential role in various chronic kidney diseases (CKD). Renal tubular epithelial to mesenchymal transition (EMT) is a common mechanism of progression of renal interstitial fibrosis (RIF). Hypoxia has been extensively considered as one of major inducers of renal tubular EMT. However, the effects of RARα on hypoxia-induced EMT have not yet been described so far. The aim of the present study was to explore the roles and potential mechanisms of RARα in hypoxia-induced EMT of renal tubular epithelial cells (RTECs). Our results showed that expression of RARα in RTECs subjected to hypoxia significantly was reduced, accompanied by decreased expression level of the epithelial marker E-cadherin, and increased expression levels of the mesenchymal markers α-smooth muscle actin (α-SMA) and vimentin, in accord with EMT. Meanwhile, hypoxia could cause RTECs to obviously express TGF-β and matrix metalloproteinase-9 (MMP-9). Furthermore, using lentivirus-based delivery vectors to overexpress RARα in RTECs, we demonstrated that RARα alleviated hypoxia-induced EMT of RTECs and downregulated the expression levels of TGF-β and MMP-9. In a word, RARα protects RTECs against EMT induced by hypoxia associated with TGF-β/MMP-9 pathway.

Retinoic acid receptor α (RARα), a member of family of the nuclear retinoic acid receptors (RARs), plays an essential role in various chronic kidney diseases (CKD). Renal tubular epithelial to mesenchymal transition (EMT) is a common mechanism of progression of renal interstitial fibrosis (RIF). Hypoxia has been extensively considered as one of major inducers of renal tubular EMT. However, the effects of RARα on hypoxia-induced EMT have not yet been described so far. The aim of the present study was to explore the roles and potential mechanisms of RARα in hypoxia-induced EMT of renal tubular epithelial cells (RTECs). Our results showed that expression of RARα in RTECs subjected to hypoxia significantly was reduced, accompanied by decreased expression level of the epithelial marker E-cadherin, and increased expression levels of the mesenchymal markers α-smooth muscle actin (α-SMA) and vimentin, in accord with EMT. Meanwhile, hypoxia could cause RTECs to obviously express TGF-β and matrix metalloproteinase-9 (MMP-9). Furthermore, using lentivirus-based delivery vectors to overexpress RARα in RTECs, we demonstrated that RARα alleviated hypoxia-induced EMT of RTECs and downregulated the expression levels of TGF-β and MMP-9. In a word, RARα protects RTECs against EMT induced by hypoxia associated with TGF-β/MMP-9 pathway.

In this paper, a hybrid algorithm, combined the adaptive simulated annealing genetic algorithm with the improved bottom-left algorithm, is presented for the optimal layout problem of rectangle pieces which is a NP-complete problem and possesses widespread applications in the industry. Adaptive genetic algorithm is adopted to change the probabilities of crossover and mutation automatically. Simulated annealing algorithm is used to modify the individuals whose fitness value is higher than the average fitness value of the population. The presented algorithm provides with global search capability of adaptive genetic algorithm and local search capability of simulated annealing algorithm. The computation results show that the optimal layout problem of rectangular pieces can be effectively solved by the hybrid algorithm.