| First Author | Armstrong BD | Year | 2006 |
| Journal | Neuroreport | Volume | 17 |
| Issue | 3 | Pages | 309-12 |
| PubMed ID | 16462603 | Mgi Jnum | J:106085 |
| Mgi Id | MGI:3617436 | Doi | 10.1097/01.wnr.0000199465.54907.74 |
| Citation | Armstrong BD, et al. (2006) Impairment of axotomy-induced pituitary adenylyl cyclase-activating peptide gene expression in T helper 2 lymphocyte-deficient mice. Neuroreport 17(3):309-12 |
| abstractText | CD4+ (T helper) lymphocytes appear to play important roles in neuron survival and regeneration after injury, although their functions in regulating gene expression in injured neurons are unknown. Mice with targeted mutations in the STAT4 and STAT6 genes are deficient in T helper (Th)1 and Th2 responses, respectively, and have been used to determine the relative importance of T helper subsets in a variety of inflammatory processes. As pituitary adenylyl cyclase-activating peptide mRNA is normally strongly induced in facial motor neurons after axotomy, we examined this induction in Th1 and Th2 lymphocyte-deficient and control Balb/C wild-type mice. As previously reported, pituitary adenylyl cyclase-activating peptide gene expression was strongly induced in ipsilateral but not contralateral motor neurons in the facial motor nucleus of wild-type mice. The mean number of hybridizing motor neurons in STAT4-deficient mice did not differ from that in wild-type mice, whereas the number in STAT6 mice was reduced by more than 50%. The results indicate that STAT6 plays a key role in the upregulation of pituitary adenylyl cyclase-activating peptide gene expression in facial motor neurons after injury, possibly through its role in regulating T helper cell differentiation to the type 2 phenotype. |
