W. W. L. Chang

Isoproterenol accelerates the postnatal differentiation of rat submandibular gland

Abstract The incorporation of 14 C-leucine into the soluble proteins of the submandibular gland was studied in rats of different ages. The proteins were separated by ion-exchange chromatography and by electrophoresis on polyacrylamide gels. The pattern of protein synthesis during postnatal development undergoes a considerable change. Certain secretory proteins are not synthesized before 3 wk of age. Isoproterenol, given for 5 days beginning at 6 days of age, accelerates the postnatal differentiation of the submandibular gland. This is manifested not only in a morphological differentiation of acinar cells but in the induction of the synthesis of proteins characteristic for more advanced stages of development.

STIMULATION OF DNA SYNTHESIS BY ISOPROTERENOL IN RAT SUBMANDIBULAR GLAND DURING POSTNATAL GROWTH

The post‐natal growth of rat submandibular gland and the effect of isoproterenol on this process were studied. Between 2 and 42 days of age the DNA content of the gland increased linearly but the increase in RNA and protein content was more rapid after 29 days of age. The RNA: DNA and protein: DNA ratio increased linearly with age. The proliferative activity, measured by the incorporation of tritiated thymidine, was maximum in the gland of 7‐day‐old rats. It declined steadily to a low level in 42‐day‐old rats. A single injection of isoproterenol had no effect on thymidine incorporation in 2‐day‐old rats. The drug, however, stimulated DNA synthesis in older animals and the degree of stimulation was inversely correlated with the proliferative activity in control rats. Small doses of isoproterenol given to rats for 4 days between 2 and 5 days of age produced a hypertrophy of the submandibular gland. The same treatment between 7 and 10 days of age caused both hypertrophy and hyperplasia of the gland. It is concluded that both the regulation of growth and the regulation of induced cell proliferation are a function of cellular differentiation and that cell proliferation can be induced only in cells that reached a certain degree of differentiation.

Effect of estrogen on cell proliferation in colonic mucosa of the mouse

SummaryThe effect of estrogen on cell proliferation in the descending colon of the mouse as an example of a non-target organ was investigated. Ovariectomized mice were given single or multiple injections of 10 ng/g body weight of 17β-estradiol and were killed 1 h after3H-thymidine injection. Estrogen treatments decreased incorporation of3H-thymidine into the DNA of colonic mucosa most markedly at 4 h after the single or the last of multiple injections. The inhibitory effect of estrogen on3H-thymidine incorporation was greater and lasted longer after a single injection than after multiple ones. A similar inhibitory effect was observed in the colonie mucosa of male mice as well as in the mucosa of mice in which colonie epithelial cell proliferation was enhanced by refeeding after 48 h of fasting. However, the colonie mucosa of mice treated with estrogen implants for up to 4 days was not affected. Estrogen treatments caused no significant change in the DNA, RNA and protein contents of the colonie mucosa. The efficacy of estrogen treatments was verified by an increase in both the wet and dry weights of the uterine horns of ovariectomized mice.

Carbon partitioning in green algae (chlorophyta) and the enolase enzyme.

The exact mechanisms underlying the distribution of fixed carbon within photoautotrophic cells, also referred to as carbon partitioning, and the subcellular localization of many enzymes involved in carbon metabolism are still unknown. In contrast to the majority of investigated green algae, higher plants have multiple isoforms of the glycolytic enolase enzyme, which are differentially regulated in higher plants. Here we report on the number of gene copies coding for the enolase in several genomes of species spanning the major classes of green algae. Our genomic analysis of several green algae revealed the presence of only one gene coding for a glycolytic enolase [EC 4.2.1.11]. Our predicted cytosolic localization would require export of organic carbon from the plastid to provide substrate for the enolase and subsequent re-import of organic carbon back into the plastids. Further, our comparative sequence study of the enolase and its 3D-structure prediction may suggest that the N-terminal extension found in green algal enolases could be involved in regulation of the enolase activity. In summary, we propose that the enolase represents one of the crucial regulatory bottlenecks in carbon partitioning in green algae.

Cell Population Kinetics of 1,2-Dimethylhydrazine-Induced Colonic Neoplasms and Their Adjacent Colonic Mucosa in the Mouse

SummaryThe parameters of cell population kinetics of symmetrical 1,2-dimethylhydrazine-induced colonic neoplasms and their adjacent colonic mucosa in the mouse were analyzed using the fraction labeled-mitoses curve method and compared with those of three groups of epithelial cells in the crypt of the descending colon of normal mouse.The analysis of three groups of epithelial cells in the crypt of normal mouse indicates that differentiation of epithelial cells was associated not only with a smaller proliferative pool of cells but also with a shortening of the duration of G2 phase and a prolongation of mitotic time. Other parameters of cell cycle did not change significantly.The mean cell cycle time of neoplastic cells in chemically induced colonic neoplasms was similar to that of epithelial cells in normal colon, but the variance was much greater in neoplastic cells. In neoplastic cells, the proliferative pool was greater, the G1 phase prolonged, and the S phase and the mitotic time became shorter as compared to epithelial cells in normal colon. The duration of G2 phase of neoplastic cells fell between the values of presumptive stem cells and differentiating cells in normal colon, compatible with the hypothesis that neoplastic cells are transformed stem cells defective in cellular differentiation.In the colonic mucosa immediately adjacent to neoplasms, the fractionlabeled-mitoses curve showed a flat second wave, indicating that the group of cells initially labeled by the pulse became a mixture of cells, some continuing the proliferative cycle normally, some going out of cycle, some slowing down in their passage from S through G2 to M, and some being arrested in mitotic phase. Such heterogeneous behavior of cells may be closely related to expansion of neoplasms. With some assumptions, however, cell cycle parameters of those normally cycling cells were estimated: the cell cycle time and the duration of G1 phase and mitotic phase were prolonged as compared to neoplastic cells and epithelial cells of normal colon.