Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A characteristic banding pattern can be visualized at the surface of the rat incisor in the maturation zone of amelogenesis by staining with glyoxal bis(2-hydroxyanil) (GBHA). Other banding patterns can be obtained with certain histological and fluorochrome stains and by radioautography following 45Ca injection. In this study, several histochemical reagents known to complex with different states of calcium were used to stain the surface of enamel. Rat incisors were quickly dissected and immediately immersed in solutions containing the following calcium-binding reagents: arsenazo III, calmagite, murexide, N,N-naphthaloylhydroxylamine, and calcein. Routinely, one contralateral lower incisor from each pair was counterstained with GBHA in order to relate each of the staining patterns to the banded distribution of maturation ameloblasts that is reflected by the characteristic GBHA staining pattern in the enamel. Each of the reagents used in this study demonstrated a staining pattern consisting of a series of broad bands running transversely and obliquely across the enamel. In all cases, the dyes stained predominantly that enamel associated with ruffle-ended ameloblasts, i.e. enamel left unstained by GBHA. Some of the reagents also stained enamel in the secretion zone. The appearance and distribution of the staining patterns reflect the banded distribution of maturation ameloblasts and appear to be controlled on a time scale related to the rapid modulation of these cells.
Anat Rec 1989 May
PMID:Banding patterns in rat incisor enamel stained by histochemical complexing methods for calcium. 247 24

Osteocalcin, a major noncollagenous matrix protein of bone, dentin, and cementum, is found in tight association with the calcium phosphate mineral phase of these tissues. This article reviews the structural data for osteocalcin relevant to mineral adsorption. The equilibrium-binding properties for Ca2+ ions and hydroxyapatite are considered, along with the apparent physicochemical effects of osteocalcin on bone mineral dynamics. Several of osteocalcin's possible biological activities (involvement in mineralization, chemoattraction, and leukocyte elastase inhibition) are discussed in relation to the mineral-adsorption characteristics of this protein.
Anat Rec 1989 Jun
PMID:Osteocalcin-hydroxyapatite interaction in the extracellular organic matrix of bone. 254 10

Dentin may be regarded as a mineralized connective tissue. In its composition as well as its mode of formation, dentin exhibits several similarities with bone, but also definite differences. The dentin organic phase, the matrix, determines its morphology and is believed to be instrumental in the formation of the mineral phase. A fibrous web of collagen type I dominates the organic matrix. Also, minor amounts of other collagen types may be present. The noncollagenous proteins (NCPs), which constitute about 10% of the matrix, fall into several categories: phosphoproteins, Gla-proteins of the osteocalcin type as well as matrix Gla-protein, proteoglycans, different acidic glycoproteins, and serum proteins. Some of these NCPs have unique chemical compositions that give them specific properties. Dentinogenesis occurs by two simultaneous processes: the formation of a collagenous web in predentin, which is followed by the formation of the inorganic phase at the mineralization front. The composition of the predentin organic matrix differs from that of dentin, as some NCP components are secreted extracellularly just in advance of the mineralization front. In addition, some constituents of predentin seem to be metabolized. The NCPs may be important to several processes during dentinogenesis. Much evidence indicates that noncollagenous components in the matrix are instrumental in mineral formation. New data show that polyanionic NCPs, such as phosphoprotein and proteoglycans, when immobilized on a solid support, induce apatite formation under physiological conditions. These data indicate that polyanionic NCPs may function as mineral nucleators in vivo. They may also act as size and rate regulators for crystallization and promote calcium ion diffusion in the tissue. In addition, NCPs may regulate collagen fibrillogenesis.
Anat Rec 1989 Jun
PMID:Dentin matrix proteins: composition and possible functions in calcification. 267 82

The calcification of cartilage matrix in endochondral bone formation occurs in an extracellular matrix composed of fibrils of type II collagen with which type X collagen is closely associated. Also present within this matrix are the large proteoglycans containing chondroitin sulfate which aggregate with hyaluronic acid. In addition, the matrix contains matrix vesicles containing alkaline phosphatase. There is probably a concentration of calcium as a result of its binding to the many chondroitin sulfate chains. At the time of calcification, these proteoglycans become focally concentrated in sites where mineral is deposited. This would result in an even greater focal concentration of calcium. Release of inorganic phosphate, as a result of the activity of alkaline phosphatase, can lead to the displacement of proteoglycan bound calcium and its precipitation. The C-propeptide of type II collagen becomes concentrated in the mineralizing sites, prior to which it is mainly associated with type II collagen fibrils and is present in dilated cisternae of the enlarged hypertrophic chondrocytes. The synthesis of type II collagen and the C-propeptide, together with alkaline phosphatase, are regulated by the vitamin D metabolites 24,25(OH)2 cholecalciferol and 1,25 (OH)2 cholecalciferol. At the time of calcification, type X collagen remains associated with type II collagen fibrils. It may play a role in preventing the initial calcification of these fibrils focusing mineral formation in focal interfibrillar sites. This process of calcification is clearly very complex, and involves different interacting matrix molecules and is carefully regulated at the cellular level.
Anat Rec 1989 Jun
PMID:Cartilage macromolecules and the calcification of cartilage matrix. 267 83

This review addresses the role of lipids and membranes in biologic calcification and examines their regulation during endochondral ossification. The close association of lipids with mineral deposition has been well established. Early observations indicated that lipids, particularly phospholipids, can not be totally extracted from calcified tissues until the tissues are decalcified. Phospholipids associated with mineral are also enriched in extracellular membrane vesicles, called matrix vesicles. Numerous studies indicate that mineral deposits in calcifying cartilage are first seen in these phosphatidylserine and alkaline phosphatase enriched vesicles and that the process of endochondral calcification of epiphyseal growth plate is possibly mediated by them. Matrix vesicles, and the phospholipids present in them, appear to be involved in initial formation of calcium hydroxyapatite crystals via the interaction of calcium and phosphate ions with phosphatidylserine to form phospholipid:Ca:Pi complexes (CPLX). CPLX is present in tissues which are undergoing initial mineral deposition but are absent from nonmineralizing tissues. Evidence suggests that CPLX resides in the interior of matrix vesicles where the earliest mineral crystals are formed in association with the vesicle membrane. More recently, it has been determined that specific membrane proteins, called proteolipids, participate in CPLX formation and hydroxyapatite deposition, in part by structuring phosphatidylserine in an appropriate conformation. Phosphatidylserine involvement in the initiation of mineralization has been extensively investigated because of its extremely high binding affinity for Ca2+. In addition to structuring a specific phospholipid environment, proteolipids may also act as ionophores, promoting export of protons and import of calcium and phosphate, both requirements of biologic calcification.(ABSTRACT TRUNCATED AT 250 WORDS)
Anat Rec 1989 Jun
PMID:Role of lipids in calcification of cartilage. 267 85

The present paper reviews the use of liposomes as synthetic models for studying various biophysical aspects of matrix vesicle calcification, especially the involvement of acidic phospholipids in the nucleation and growth processes which occur during the initial stages of mineral formation in and around these membrane-bound structures. Recent results showed that acidic phospholipids incorporated into phosphatidylcholine-rich anionic liposome membranes were ineffective in initiating extraliposomal calcium phosphate precipitation from metastable solutions at physiological pH. On the contrary, certain acidic phospholipids such as phosphatidic acid and phosphatidylserine retarded the development of such precipitation when the latter was endogenously induced. The extent of inhibition correlated with the strength of the electrostatic interaction between the polar head group of the acidic phospholipid and the surface of the mineral phase. The results suggest that acidic phospholipids may play an important role in controlling the rate of early mineral development in matrix vesicle calcification.
Anat Rec 1989 Jun
PMID:Biophysical aspects of lipid interaction with mineral: liposome model studies. 267 86

The translocation of calcium from the extracellular fluid compartment into the mineralizing matrix during hard tissue formation is not well understood. There are two general means by which such calcium movement may occur: 1) diffusion through the pericellular space, or 2) transcellular transport. Cementum and bone are difficult tissues in which to study the system and little is known about the mechanisms involved. Dentin offers certain advantages for study and it appears that calcium movement into the mineralizing matrix is by transcellular transport. Information concerning the transport mechanism is meager. Enamel is more easily explored. The apparent existence of intercellular junctions tight to calcium in the ameloblast layer at all stages of enamel formation indicates that calcium movement occurs by transcellular transport. Based on published findings, a hypothesis concerning mechanisms of transcellular transport may be advanced. It is proposed that the relatively low level of calcium transport through secretory ameloblasts occurs without direct involvement of a calcium binding protein. During the maturation stage, when calcium influx to the matrix is greatly increased, a calcium binding protein (9 kd) appears and facilitates transport while preventing unphysiologic increases in the cytosolic free calcium ion concentration. Differences in the calcium ion concentrations of extracellular fluid and enamel matrix fluid appear to be critical to the influx of calcium across the proximal cell membrane and the efflux of calcium across the distal cell membrane.
Anat Rec 1989 Jun
PMID:Calcium transport during mineralization. 267 87

Many studies of calcium phosphate precipitation have been made using relaxation techniques in which the concentrations of the lattice ions are allowed to decrease as equilibrium is approached. Since the nature of the phases that form depend markedly on the solution composition, this decrease can lead to concomitant phase transformations during the crystallization experiments. The results of the present constant composition (CC) studies show that defect apatites may be formed under conditions of sustained supersaturation with a non-stoichiometric coefficient dependent on the pH of the growth medium. An important factor in analyzing these experiments is the initial surface modification and ion-exchange processes involving H+ and Ca2+ ions after inoculation of the supersaturated solutions. Thereafter, active growth sites may be eliminated as the crystals undergo lattice perfection. Transformation of dicalcium phosphate dihydrate to octacalcium phosphate, involving dissolution and subsequent nucleation and growth of the new phase, is also influenced by surface roughening of the initial phase. Typical inhibitors that reduce the rate of growth of seed crystals in supersaturated solutions may actually induce the nucleation of calcium phosphate phases when immobilized on inert surfaces. This may be a factor in the modulation of crystal growth in many biological systems.
Anat Rec 1989 Jun
PMID:Mineral phases of calcium phosphate. 267 88

The application of high resolution electron microscopy, computer image processing, and image simulation techniques to the investigation of synthetic nonstoichiometric apatites has provided new details of apatite crystal growth mechanisms. Under certain precipitation conditions, calcium-deficient apatites with distinct octacalcium phosphate (OCP)-apatite intergrowths have been observed. Apatite crystals with unit-cell thick overgrowths of OCP on their surfaces confirmed the stepwise hydrolysis crystal growth mechanism initially proposed by Brown (Nature 196:1048-1050). However, many crystals also contained a central two-dimensional OCP inclusion one to two unit cells thick, embedded in an apatite matrix. Similar planar defects have been observed in dental enamel, dentin, and bone crystals. We have developed a modified version of Brown's stepwise OCP hydrolysis apatite crystal growth mechanism to explain the formation of crystals with OCP central planar defects. The mechanism involves the nucleation of an OCP seed that grows until it reaches a critical size, rh, before OCP hydrolysis occurs. Apatite subsequently grows epitaxially on the OCP seed, thereby embedding it in the center of an apatite crystal. Apatite growth is facilitated by partial screw dislocations emanating from the planar defect.
Anat Rec 1989 Jun
PMID:High resolution electron microscopy of nonstoichiometric apatite crystals. 267 90

The new calcium antagonist Rec 15/2375, supposed to be selective for the vascular tissue, was compared to nifedipine, a non-selective agent that reduces blood pressure and impairs cardiac inotropism as well. Six rabbits, chronically catheterized and continuously monitored for systemic blood pressure, heart rate and the isovolumic contractility index dP/Tmax, were alternatively treated with Rec 15/2375 and nifedipine, according to a randomized cross-over design. Both drugs were given under either autonomically intact (AI) or suppressed (AS) heart function control, induced by cholinergic and beta-adrenoceptor blockade. The two agents reduced mean arterial blood pressure comparably and dose-dependently (P less than 0.01) under both experimental conditions (from 10 to 40%), thus causing heart rate to increase reflexly (P less than 0.01), similarly between drugs in AI rabbits, whereas the AS manoeuvre totally abolished such a response. Cardiac contractility, on the other hand, displayed opposing behaviour between the two drugs. Rec 15/2375 caused mild but significant (P less than 0.01) increases, which were similar at all doses (+10, +15%) and insensitive to the AS intervention, whereas nifedipine caused dose-dependent reductions (from -10 to -60%; P less than 0.01) of comparable intensity as mean blood pressure decrease in both protocols. We conclude that Rec 15/2375 effectively lowers blood pressure with no impairment, unlike nifedipine, of cardiac inotropism and we discuss the possibility that dP/dTmax may be increased as a result of the haemodynamic rearrangement following after-load reduction.
 ...
PMID:Effects of a new calcium antagonist, Rec 15/2375, on cardiac contractility of conscious rabbits. 274 6


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>