| First Author | Sandgren EP | Year | 1991 |
| Journal | Cell | Volume | 66 |
| Issue | 2 | Pages | 245-56 |
| PubMed ID | 1713128 | Mgi Jnum | J:135418 |
| Mgi Id | MGI:3793573 | Doi | 10.1016/0092-8674(91)90615-6 |
| Citation | Sandgren EP, et al. (1991) Complete hepatic regeneration after somatic deletion of an albumin-plasminogen activator transgene. Cell 66(2):245-56 |
| abstractText | We previously demonstrated that expression of an albumin-urokinase-type plasminogen activator (Alb-uPA) fusion construct in transgenic mice resulted in elevated plasma uPA concentration, hypofibrinogenemia, and neonatal hemorrhaging. Two lines of Alb-uPA mice were established in which only one half of the transgenic pups died at birth; surprisingly, plasma uPA concentrations in survivors gradually returned to normal by 2 months of age. The basis for this phenomenon is DNA rearrangement within hepatocytes that affects the transgene tandem array and abolishes transgene expression. Transgene-deficient cells selectively proliferate relative to surrounding liver, and this process culminates in replacement of the entire liver by clonal hepatic nodules derived from transgene-deficient progenitor cells. In some cases as few as two nodules can reconstitute over 90% of liver mass, highlighting the remarkable regenerative capacity of individual liver cells. |
