Induction of A- and D-type cyclins and cdc2 kinase activity during recovery from short-term XXXX .

@entity1603 @entity871 @entity26 @entity651 @entity1975 @entity35
@entity871 causes a reproducible pattern of @entity651 and repair in rodents, in which proliferation of alveolar epithelial cells (AEC) and fibroblasts is observed during recovery. We postulated that if quiescent cells are stimulated to reenter the cell cycle, then @entity1975 expression and @entity1975 -dependent protein kinase activity would be reactivated in AEC during the repair process after @entity651 . To test this hypothesis, we exposed adult @entity35 to short-term @entity871 , followed by recovery for various times in room air. Cellular proliferation in vivo was confirmed by 1) flow cytometric analysis of DNA content (FACS) of freshly isolated AEC and 2) immunohistochemistry of @entity1975 ( @entity1975 ) and @entity1603 ( @entity1603 ) incorporation into DNA on lung sections. The percentage of freshly isolated AEC in S phase and G2/M phase on FACS analysis increased twofold to a maximum of 16.5%, after 48 h in 100% @entity26 and 48 h recovery in air. Cyclins A and D and p34cdc2 protein expression were also increased during the recovery period; while p33cdk2 and p34cdk4 increased only slightly. p34cdc2 histone H1 kinase activity, both in whole lung and in AEC, decreased initially after 48 h in @entity26 . However, a marked increase in p34cdc2 kinase activity was observed at 48 h recovery in whole lung and returned to baseline by 72 h. In isolated and cultured AEC, p34cdc2 kinase activity was maximal at 24 h of recovery in air. We conclude that cyclins A and D and p34cdc2 protein expression and p34cdc2 kinase activity are increased in vivo during recovery from @entity651 in both adult @entity35 lungs and in AEC isolated from these lungs. We speculate that the induction of @entity1975 -dependent protein kinase activity is a key event in mediating the proliferative cellular repair response to @entity651 .
