| First Author | Genetos DC | Year | 2011 |
| Journal | Exp Cell Res | Volume | 317 |
| Issue | 6 | Pages | 737-44 |
| PubMed ID | 21237152 | Mgi Jnum | J:170716 |
| Mgi Id | MGI:4947178 | Doi | 10.1016/j.yexcr.2011.01.007 |
| Citation | Genetos DC, et al. (2011) Purinergic signaling is required for fluid shear stress-induced NF-kappaB translocation in osteoblasts. Exp Cell Res 317(6):737-44 |
| abstractText | Fluid shear stress regulates gene expression in osteoblasts, in part by activation of the transcription factor NF-kappaB. We examined whether this process was under the control of purinoceptor activation. MC3T3-E1 osteoblasts under static conditions expressed the NF-kappaB inhibitory protein IkappaBalpha and exhibited cytosolic localization of NF-kappaB. Under fluid shear stress, IkappaBalpha levels decreased, and concomitant nuclear localization of NF-kappaB was observed. Cells exposed to fluid shear stress in ATP-depleted medium exhibited no significant reduction in IkappaBalpha, and NF-kappaB remained within the cytosol. Similar results were found using oxidized ATP or Brilliant Blue G, P2X(7) receptor antagonists, indicating that the P2X(7) receptor is responsible for fluid shear-stress-induced IkappaBalpha degradation and nuclear accumulation of NF-kappaB. Pharmacologic blockage of the P2Y6 receptor also prevented shear-induced IkappaBalpha degradation. These phenomena involved neither ERK1/2 signaling nor autocrine activation by P2X(7)-generated lysophosphatidic acid. Our results suggest that fluid shear stress regulates NF-kappaB activity through the P2Y(6) and P2X(7) receptor. |
