DEOXYRIBONUCLEIC-ACID SYNTHESIS IN LUNG-CELLS DURING COMPENSATORY LUNG GROWTH AFTER PNEUMONECTOMY
- 1 January 1978
- journal article
- research article
- Published by Elsevier
- Vol. 117 (2) , 307-316
- https://doi.org/10.1164/arrd.1978.117.2.307
Abstract
To understand the cellular events associated with compensatory lung growth, DNA synthesis and autoradiographs of right lungs from mice killed 1 h after injection of thymidine labeled with 3H were evaluated in studies performed 1-14 days after left pneumonectomy. Total lung DNA synthesis was increased by postoperative day 3, reaching a peak by day 6. DNA synthesis in liver and kidney did not increase during this period, illustrating that the growth stimulus was lung specific. Increased DNA synthesis, as judged by autoradiographs, appeared in pleural mesothelial cells by postpneumonectomy day 1; in interstitium, endothelium and peripheral alveoli by postpneumonectomy day 3; and in the bulk of alveoli by postpneumonectomy day 6. Labeling of pleural, interstitial and endothelial cells was maximal within the 1st postoperative week at 7.8, 5.2 and 1.3% of cells, respectively, and decreased toward control values thereafter. DNA synthesis in alveolar wall cells increased to peak values of 1.6 to 2.0% (3 times the control value), remaining high throughout the period of study. The early increase in labeling of pleura and peripheral alveoli was prevented when the postpneumonectomy space was filled with wax, although DNA synthesis at other sites was not decreased. Alveolar Type II cells accounted for the bulk of alveolar wall labeling, with evidence that some of these cells transformed into alveolar Type I cells. Stretch of the remaining lung apparently accounts for only a small proportion of lung DNA synthesis during compensatory lung growth after pneumonectomy. Alveolar Type II cell proliferation and differentiation into Type I cells seem to characterize this type of lung growth in a fashion apparently similar to early postnatal lung growth and lung repair after injury.This publication has 0 references indexed in Scilit: