| First Author | Venna VR | Year | 2012 |
| Journal | Acta Neuropathol | Volume | 124 |
| Issue | 3 | Pages | 425-38 |
| PubMed ID | 22562356 | Mgi Jnum | J:336909 |
| Mgi Id | MGI:6867996 | Doi | 10.1007/s00401-012-0990-8 |
| Citation | Venna VR, et al. (2012) NF-kappaB contributes to the detrimental effects of social isolation after experimental stroke. Acta Neuropathol 124(3):425-38 |
| abstractText | Social isolation (SI) is increasingly recognized as a risk factor for stroke. Individuals with lack of social support systems have an increased incidence of stroke, poorer recovery, and greater functional decline after injury compared to individuals with social support. Attesting to the importance of social factors in stroke outcome is that these same effects can be reproducibly demonstrated in animals; social interaction improves behavioral deficits and reduces damage after experimental stroke, whereas SI enhances injury. The mechanism by which SI exacerbates injury is unclear. We investigated the role of nuclear factor-kappaB (NF-kappaB) signaling in male mice that were pair housed (PH) with an ovariectomized female prior to random assignment into continued PH or SI for 7 days prior to middle cerebral artery occlusion. The effects of SI on infarct volume and functional recovery were assessed at 72 h post-stroke. Nuclear NF-kappaB levels and activity were assessed by Western blot and transcriptional assays. SI significantly exacerbated infarct size in both male and female mice compared to PH mice. SI mice had delayed functional recovery compared to PH mice. An elevation of systemic IL-6 levels, increased nuclear NF-kappaB transcriptional activity, and enhanced nuclear translocation of NF-kappaB was seen in SI stroke animals. Interference with NF-kappaB signaling using either a pharmacological inhibitor or genetically engineered NF-kappaB p50 knockout mice abolished the detrimental effects of SI on both infarct size and functional recovery. This suggests that NF-kappaB mediates the detrimental effects of SI. |
