The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Endothelin-1 down-regulates the expression of vascular endothelial growth factor-A associated with osteoprogenitor proliferation and differentiation.

Endothelin-1 (ET-1) is implicated in the signaling between vascular endothelial cells (VECs) and osteoblasts during bone development, remodeling and repair. Vascular endothelial growth factor (VEGF) also plays an important role in these intercellular interactions. Our objectives were to identify which specific VEGF isoforms were produced during osteoblastic proliferation and differentiation and to determine the effects of ET-1 on VEGF mRNA and protein production by osteoblastic cells. Semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and ELISA were used to evaluate VEGF mRNA isoform expression and protein synthesis at different stages of ET-1-induced osteoblastic differentiation in fetal rat calvaria (FRC) osteoblastic cells. Three VEGF mRNA isoforms were identified corresponding to VEGF(120), VEGF(164) and VEGF(188). Predominant isoforms VEGF(120) and VEGF(164) had a bimodal expression that increased in the early proliferation and late mineralization phases. ET-1 stimulated osteoblastic proliferation and differentiation, but surprisingly, ET-1 down-regulated VEGF mRNA and protein expression and sustained the down-regulation over time in long-term cultures. Time course studies showed that ET-1 inhibited VEGF mRNA expression after incubation for 3 h in 7- and 14-day FRC cell cultures. Similarly, ET-1 inhibited VEGF protein secretion by 5.8- and 2.8-fold in 7- and 14-day FRC cells, respectively. VEGF-A protein secretion was inhibited by ET-1 in a dose-dependent manner with a maximal effect at 10(-7) M. This study supports a novel inhibitory role for ET-1 on VEGF synthesis in osteoblastic cells as a feedback mechanism in the temporal and spatial coupling of angiogenesis to bone formation and resorption.[1]

References

 
WikiGenes - Universities