| First Author | Shintani N | Year | 2004 |
| Journal | Regul Pept | Volume | 123 |
| Issue | 1-3 | Pages | 155-9 |
| PubMed ID | 15518906 | Mgi Jnum | J:102435 |
| Mgi Id | MGI:3607496 | Doi | 10.1016/j.regpep.2004.04.022 |
| Citation | Shintani N, et al. (2004) Overexpression of PACAP in the pancreas failed to rescue early postnatal mortality in PACAP-null mice. Regul Pept 123(1-3):155-9 |
| abstractText | PACAP exerts multiple activities as a hormone and neurotransmitter, and has been proposed to play vital roles in a variety of neuronal functions. PACAP is also involved in insulin secretion from pancreatic beta-cells. Recently, we and other groups demonstrated that PACAP-deficient mice (PACAP(-/-)) are viable, but suffer from increased postnatal mortality. To ascertain whether this high mortality is rescued by overexpression of PACAP in peripheral tissue (such as pancreas), we performed a genetic cross between PACAP(-/-) and our recently developed transgenic mice overexpressing PACAP in pancreatic beta-cells; and then examined the survival rate of their F2 progeny. PACAP(-/-) mice were segregated into two groups based on mortality as well as body weight gain: PACAP(-/-) that survived >20 days of age with normal weight gain and PACAP(-/-) that died before 20 days with a marked weight loss. Kaplan-Meier survival analysis demonstrated that PACAP(-/-) mice and those carrying the PACAP transgene have similarly lower survival probability compared with their heterozygous littermates that served as positive controls. Further study using additional tissue-specific transgenic or knockout mouse models will be required to determine the causative defects underlying the high mortality of PACAP(-/-) mice. |
