A dual approach consisting of cultivation and molecular retrieval of actinobacterial 16S rRNA genes was used to characterize the diversity of actinobacterial community inhabiting interior of rice stems and roots. Streptomyces is the most frequently isolated genus from rice stems and roots. Forty-five clones chosen randomly among 250 clones in the 16S rRNA gene clone library from roots were affiliated with nine genera of actinobacteria and uncultured actinobacteria (Mycobacterium, Streptomyces, Micromonospora, Actinoplanes, Frankia, Dactylosporangium, Amycolatopsis, Corynebacterium, Rhodococcus, and uncultured actinobacterium). However, 33 clones from stems were affiliated with four genera and uncultured actinobacteria (Streptomyces, Mycobacterium, Nocardiodies, Janibacter, uncultured earthworm cast bacterium, uncultured earthworm intestine bacterium, and uncultured actinobacterium). Species similar to S. cyaneus were isolated from surface-sterilized roots and stems of rice and detected inside rice roots by culture-independent methods. Species similar to S. caviscabies, S. scabies, and S. turgidiscabies were simultaneously detected from the interior of rice stems by the culture-dependent and culture-independent methods. S. galilaeus was detected from the interior of rice stems and roots. These results indicated that some actinobacterial populations in rice stems were correlated with those in roots.
Electrical stimulation (ES) is able to enhance angiogenesis by stimulating fibroblasts. Fibroblast growth factor 2 (FGF2) is an independent angiogenesis inducer. The present study aimed to evaluate the role of ES-induced FGF2 secretion in affecting angiogenesis during wound healing via the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling pathway. Fibroblasts and human umbilical vein endothelial cells (HUVECs) were exposed to ES, and the HUVECs were cocultured with ES-treated fibroblast culture solution. ES exposure showed no toxic effects on fibroblasts or HUVECs. ES led to enhanced growth of fibroblasts and HUVECs as well as FGF2 secretion, which is induced through the NOS pathway. ES-induced FGF2 secretion was shown to increase vascular endothelial growth factor (VEGF) protein and enhance migration, invasion, and angiogenesis of HUVECs. Also, ES-induced FGF2 secretion activated the MAPK/ERK signaling pathway. However, inhibition of the MAPK/ERK signaling pathway reversed the positive effects of ES-induced FGF2 secretion. In vitro experiments showed positive effects of ES on wound healing. Taken together, the findings suggested that ES promoted FGF2 secretion and then activated the MAPK/ERK signaling pathway by facilitating angiogenesis and promoting wound healing.
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