Hypoxia-inducible factor-1α

Effects of autologous SCF- and G-CSF-mobilized bone marrow stem cells on hypoxia-inducible factor-1 in rats with ischemia-reperfusion renal injury

L. Y. Bi, Zhao, D. A., Yang, D. S., Guo, J. G., Liang, B., Zhang, R. X., Zhao, J. L., Bai, H. T., and Li, S. J., Effects of autologous SCF- and G-CSF-mobilized bone marrow stem cells on hypoxia-inducible factor-1 in rats with ischemia-reperfusion renal injury, vol. 14, pp. 4102-4112, 2015.

To explore the mechanism whereby stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) jointly mobilize bone marrow stem cells (BMSCs) and promote kidney repair, male Sprague-Dawley rats were randomly assigned into 4 groups. In the treatment control group, rats were administered SCF (200 μg·kg-1·day-1) and G-CSF (50 μg·kg-1·day-1) for 5 days. In the treatment group, RIRI models were established, and 6 h later, SCF (200 μg·kg-1·day-1) and G-CSF (50 μg·kg-1·day-1) were administered for 5 days.

Expression of hypoxia-inducible factor-1α during ovarian follicular growth and development in Sprague-Dawley rats

Z. H. Zhang, Chen, L. Y., Wang, F., Wu, Y. Q., Su, J. Q., Huang, X. H., Cheng, Y., and Wang, Z. C., Expression of hypoxia-inducible factor-1α during ovarian follicular growth and development in Sprague-Dawley rats, vol. 14, pp. 5896-5909, 2015.

Hypoxia-inducible factor-1α (HIF-1α) has been identified as a transcription factor that is involved in diverse physiological and pathological processes in the ovary. In this study, we examined whether HIF-1α is expressed in a cell- and stage-specific manner during follicular growth and development in the mammalian ovaries. Using immunohistochemistry and Western blot analysis, HIF-1α expression was observed in granulosa cells specifically and was significantly increased during the follicular growth and development of postnatal rats.

Nerve growth factor regulates the expression of vascular endothelial growth factor in human HaCaT keratinocytes via PI3K/mTOR pathway

J. Zhang and Ma, W. Y., Nerve growth factor regulates the expression of vascular endothelial growth factor in human HaCaT keratinocytes via PI3K/mTOR pathway, vol. 13, pp. 9324-9335, 2014.

Decades of research have provided the data to confirm the hypothesis that there is bidirectional communication between the central nervous system and the immune system in psoriasis pathogenesis, but the contribution of the cutaneous neural system remains underexplored. In this study, we evaluated the molecular mechanisms by which nerve growth factor (NGF) regulates hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) production. The mRNA and protein levels of VEGF secretion from HaCaT cells by NGF were increased in a concentration-dependent manner.

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