Platelet glycoprotein Ia* is the processed form of multimerin--isolation and determination of N-terminal sequences of stored and released forms

Glycoprotein Ia* (GPIa*), a very high molecular mass, platelet alpha-granule protein consisting of 167 kDa subunits disulphide-linked in a multimeric structure, was first described by Bienz and Clemetson in 1989 (J. Biol. Chem. 264, 507-514). In 1991 Hayward et al. (J. Biol. Chem. 266, 7114-7120) independently identified a platelet protein with multimeric structure. Despite strong similarities to GPIa* they concluded that it was a novel multimeric protein and named it first p-155 and later, multimerin. Multimerin has also been found in endothelial cells and has been cloned recently from an endothelial cell cDNA library. This has made it possible for us to clarify the relationship between GPIa* and multimerin. GPIa* was isolated from platelet releasate and the N-terminal sequence of 167 kDa and 155 kDa subunit species were determined. The N-terminal 15 amino acids of GPIa* were identical to the deduced amino acids 184-198 of endothelial multimerin. The N-terminal sequence of the 155 kDa protein was identical to the deduced amino acids 318-326 of multimerin. Thus, platelet GPIa* (167 kDa) is the main processed form of multimerin stored in platelet alpha-granules. The GPIa*/processed multimerin (167 kDa) still contains an RGDS sequence near its N-terminus as well as an EGF domain which may be involved in binding to the platelet surface after release. This sequence and domain are cleaved off in the p-155 form, described earlier as platelet multimerin, which is probably formed after release from alpha-granules.

Effects of various forms of calcium added to chewing gum on initial enamel carious lesions in situ

The purpose of this randomized, cross-over in situ study was to determine the effects of 4 chewing gums on artificial caries-like subsurface lesions. Two chewing gums (1 with zinc citrate and 1 without) contained dicalcium phosphate (3.9%), calcium gluconate (1.8%) and calcium lactate (0.45%), 1 chewing gum contained casein phosphopeptide-amorphous calcium phosphate nanocomplexes (0.7%), and another one contained no calcium. Fifteen subjects without current caries activity (7 male, 8 female; mean age: 27.5 +/- 2.5 years) wore removable buccal appliances in the lower jaw with 4 bovine enamel slabs with subsurface lesions. The appliances were inserted immediately before gum chewing for 20 min and then retained for an additional 20 min. This was performed 4 times per day. Every subject chewed 4 different chewing gums over 4 periods of 14 days each. During a fifth period (control) the subjects only wore the appliances without chewing gum. At completion of each period the enamel slabs were embedded, sectioned and subjected to transversal microradiography. With regard to change of mineral loss and of lesion depth no significant differences could be found between chewing gums containing calcium and calcium-free chewing gums. Moreover, the chewing gum groups and the control group did not differ significantly if adjustments were made for baseline values (p > 0.05; ANCOVA). Under the conditions of the present study it may be concluded that the use of chewing gum offers no additional remineralizing benefit to buccal tooth surfaces, even if the chewing gum contains calcium compounds.