Most commercial markets require growers of poinsettia (Euphorbia pulcherrima Willd. ex Klotzsch.) to produce plants within strict height specifications. Plant growthretarding chemicals (PGRs) are commonly used to limit internode extension, but in some countries, growers are being pressured to reduce chemical use. Recently, a photoselective film was developed that specifically reduces the transmission of far-red light [(FR), 700 to 800 nm], offering an alternative strategy for height control. Two complementary trials, one in the United Kingdom and one in the United States, showed that plants grown under the FR film for 10 to 12 weeks were ≈20% shorter than control plants growing under neutral density (ND) films transmitting a similar photosynthetic photon flux as the FR film. In the United Kingdom trial, the FR filter delayed time to 50% bract color and first visible cyathia by 6.0 and 3.5 days, respectively, but did not influence time to final harvest. In the United States trial, plants under the FR film had an average of 25% more axillary branches than those under the ND film. In addition, the effects of reduced red [(R), 600 to 700 nm] and blue [(B), 400 to 500 nm] light on internode length, plant biomass, and axillary branching were determined using other photoselective plastics. Compared with plants under the ND film, internode length was 9% or 71% greater in plants grown under environments deficient in B or R, respectively. Our results indicate that poinsettia is highly sensitive to the R: FR ratio, and that spectral manipulation has potential for height control of commercial poinsettia crops.
The role of matrix metalloproteinases in parathyroid hormone (PTH)-induced bone resorption was assayed using a fetal rat limb bone culture system. Cotreatment of bones with PTH and recombinant inhibitor of metalloproteinases, TIMP-1, in vitro, inhibited the PTH-stimulated 45Ca release from the limb bones without affecting beta-glucuronidase release. TIMP-1 was fully effective when added during only the final 24 h of a 72 h culture with PTH but was ineffective when added for only the first 24 h of the 72 h culture. In contrast, calcitonin (CT) was effective when added for either the first 24 or the final 24 h of the culture. Using in situ hybridization, the mRNA for collagenase was detected in mononuclear cells of cultured bone. Treatment of the bones with PTH resulted in an increase in the number of cells producing collagenase mRNA, some of which had osteoclastic morphology, PTH also caused a dramatic induction of the mRNA for the 92-kD gelatinase B metalloproteinase in both mononuclear and osteoclastic cells. There was no detectable mRNA for the metalloproteinases stromelysin-1, stromelysin-2, or matrilysin in PTH-treated or control cultures. These results suggest that PTH-induced bone resorption is mediated, at least in part, by the induction of collagenase and gelatinase B mRNA in bone cells.
The effects of endothelin-1 (ET) on several tissues are mediated by prostaglandins. In this study, we investigated the actions of ET on bone and determined whether they are mediated through prostaglandin-dependent pathways. Bone resorption, collagen, and non-collagen protein synthesis and inositol phosphate (IP) production were studied in neonatal mouse calvaria and fetal rat limb bone cultures. The effects of ET in the calvaria model were examined in the presence or absence of the cyclooxygenase inhibitor indomethacin (INDO). Bone resorption was stimulated by ET in the neonatal mouse calvaria, and this effect was inhibited by INDO. 45Ca release in the fetal rat limb bones was not affected by ET. ET stimulated collagen and noncollagen protein synthesis significantly in the calvaria model in the presence but not in the absence of INDO, suggesting that the anabolic effects of ET were masked by endogenous prostaglandin production. ET increased phosphatidylinositol turnover in both bone organ cultures. Although the addition of INDO reduced IP production slightly in the mouse calvaria, it was still significantly stimulated by ET. Our results demonstrate that ET has marked effects on bone tissue in vitro. Effects on resorption appear to be prostaglandin dependent, whereas the anabolic effects were not prostaglandin mediated. The stimulatory effects of ET on protein synthesis could be mediated through the IP signaling pathway. Since ET stimulates both bone resorption and anabolism, this peptide may have a role in the coupling of bone remodeling.
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