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Microbiology (Reading, England) Apr 2021Micro-organisms contribute to Earth's mineral deposits through a process known as bacteria-induced mineral precipitation (BIMP). It is a complex phenomenon that can... (Review)
Review
Micro-organisms contribute to Earth's mineral deposits through a process known as bacteria-induced mineral precipitation (BIMP). It is a complex phenomenon that can occur as a result of a variety of physiological activities that influence the supersaturation state and nucleation catalysis of mineral precipitation in the environment. There is a good understanding of BIMP induced by bacterial metabolism through the control of metal redox states and enzyme-mediated reactions such as ureolysis. However, other forms of BIMP often cannot be attributed to a single pathway but rather appear to be a passive result of bacterial activity, where minerals form as a result of metabolic by-products and surface interactions within the surrounding environment. BIMP from such processes has formed the basis of many new innovative biotechnologies, such as soil consolidation, heavy metal remediation, restoration of historic buildings and even self-healing concrete. However, these applications to date have primarily incorporated BIMP-capable bacteria sampled from the environment, while detailed investigations of the underpinning mechanisms have been lagging behind. This review covers our current mechanistic understanding of bacterial activities that indirectly influence BIMP and highlights the complexity and connectivity between the different cellular and metabolic processes involved. Ultimately, detailed insights will facilitate the rational design of application-specific BIMP technologies and deepen our understanding of how bacteria are shaping our world.
Topics: Bacteria; Chemical Precipitation; Minerals; Oxidation-Reduction; Soil
PubMed: 33881981
DOI: 10.1099/mic.0.001049 -
Global Change Biology Jan 2020Hard, or stony, corals make rocks that can, on geological time scales, lead to the formation of massive reefs in shallow tropical and subtropical seas. In both... (Review)
Review
Hard, or stony, corals make rocks that can, on geological time scales, lead to the formation of massive reefs in shallow tropical and subtropical seas. In both historical and contemporary oceans, reef-building corals retain information about the marine environment in their skeletons, which is an organic-inorganic composite material. The elemental and isotopic composition of their skeletons is frequently used to reconstruct the environmental history of Earth's oceans over time, including temperature, pH, and salinity. Interpretation of this information requires knowledge of how the organisms formed their skeletons. The basic mechanism of formation of calcium carbonate skeleton in stony corals has been studied for decades. While some researchers consider coral skeletons as mainly passive recorders of ocean conditions, it has become increasingly clear that biological processes play key roles in the biomineralization mechanism. Understanding the role of the animal in living stony coral biomineralization and how it evolved has profound implications for interpreting environmental signatures in fossil corals to understand past ocean conditions. Here we review historical hypotheses and discuss the present understanding of how corals evolved and how their skeletons changed over geological time. We specifically explain how biological processes, particularly those occurring at the subcellular level, critically control the formation of calcium carbonate structures. We examine the different models that address the current debate including the tissue-skeleton interface, skeletal organic matrix, and biomineralization pathways. Finally, we consider how understanding the biological control of coral biomineralization is critical to informing future models of coral vulnerability to inevitable global change, particularly increasing ocean acidification.
Topics: Animals; Anthozoa; Calcification, Physiologic; Calcium Carbonate; Coral Reefs; Hydrogen-Ion Concentration; Oceans and Seas; Seawater
PubMed: 31696576
DOI: 10.1111/gcb.14912 -
Bone Research Nov 2023Matrix vesicles (MVs) have shown strong effects in diseases such as vascular ectopic calcification and pathological calcified osteoarthritis and in wound repair of the...
Matrix vesicles (MVs) have shown strong effects in diseases such as vascular ectopic calcification and pathological calcified osteoarthritis and in wound repair of the skeletal system due to their membranous vesicle characteristics and abundant calcium and phosphorus content. However, the role of MVs in the progression of osteoporosis is poorly understood. Here, we report that annexin A5, an important component of the matrix vesicle membrane, plays a vital role in bone matrix homeostasis in the deterioration of osteoporosis. We first identified annexin A5 from adherent MVs but not dissociative MVs of osteoblasts and found that it could be sharply decreased in the bone matrix during the occurrence of osteoporosis based on ovariectomized mice. We then confirmed its potential in mediating the mineralization of the precursor osteoblast lineage via its initial binding with collagen type I to achieve MV adhesion and the subsequent activation of cellular autophagy. Finally, we proved its protective role in resisting bone loss by applying it to osteoporotic mice. Taken together, these data revealed the importance of annexin A5, originating from adherent MVs of osteoblasts, in bone matrix remodeling of osteoporosis and provided a new strategy for the treatment and intervention of bone loss.
Topics: Animals; Mice; Annexin A5; Calcification, Physiologic; Bone Matrix; Vascular Calcification; Bone Diseases, Metabolic; Osteoporosis
PubMed: 37940665
DOI: 10.1038/s41413-023-00290-9 -
International Journal of Molecular... Mar 2020Calcification of the vessel wall contributes to high cardiovascular morbidity and mortality. Vascular calcification (VC) is a systemic disease with multifaceted... (Review)
Review
Calcification of the vessel wall contributes to high cardiovascular morbidity and mortality. Vascular calcification (VC) is a systemic disease with multifaceted contributing and inhibiting factors in an actively regulated process. The exact underlying mechanisms are not fully elucidated and reliable treatment options are lacking. Due to the complex pathophysiology, various research models exist evaluating different aspects of VC. This review aims to give an overview of the cell and animal models used so far to study the molecular processes of VC. Here, in vitro cell culture models of different origins, ex vivo settings using aortic tissue and various in vivo disease-induced animal models are summarized. They reflect different aspects and depict the (patho)physiologic mechanisms within the VC process.
Topics: Animals; Calcification, Physiologic; Disease Models, Animal; Disease Susceptibility; Humans; Models, Biological; Vascular Calcification
PubMed: 32210002
DOI: 10.3390/ijms21062204 -
JCI Insight Dec 2023Fibroblast growth factor 23 (FGF23) is a phosphate-regulating (Pi-regulating) hormone produced by bone. Hereditary hypophosphatemic disorders are associated with FGF23...
Fibroblast growth factor 23 (FGF23) is a phosphate-regulating (Pi-regulating) hormone produced by bone. Hereditary hypophosphatemic disorders are associated with FGF23 excess, impaired skeletal growth, and osteomalacia. Blocking FGF23 became an effective therapeutic strategy in X-linked hypophosphatemia, but testing remains limited in autosomal recessive hypophosphatemic rickets (ARHR). This study investigates the effects of Pi repletion and bone-specific deletion of Fgf23 on bone and mineral metabolism in the dentin matrix protein 1-knockout (Dmp1KO) mouse model of ARHR. At 12 weeks, Dmp1KO mice showed increased serum FGF23 and parathyroid hormone levels, hypophosphatemia, impaired growth, rickets, and osteomalacia. Six weeks of dietary Pi supplementation exacerbated FGF23 production, hyperparathyroidism, renal Pi excretion, and osteomalacia. In contrast, osteocyte-specific deletion of Fgf23 resulted in a partial correction of FGF23 excess, which was sufficient to fully restore serum Pi levels but only partially corrected the bone phenotype. In vitro, we show that FGF23 directly impaired osteoprogenitors' differentiation and that DMP1 deficiency contributed to impaired mineralization independent of FGF23 or Pi levels. In conclusion, FGF23-induced hypophosphatemia is only partially responsible for the bone defects observed in Dmp1KO mice. Our data suggest that combined DMP1 repletion and FGF23 blockade could effectively correct ARHR-associated mineral and bone disorders.
Topics: Animals; Mice; Calcification, Physiologic; Extracellular Matrix Proteins; Familial Hypophosphatemic Rickets; Fibroblast Growth Factors; Hypophosphatemia; Mice, Knockout; Minerals; Osteomalacia
PubMed: 37943605
DOI: 10.1172/jci.insight.156850 -
Bone Dec 2020Three physiologically mineralizing tissues - teeth, cartilage and bone - have critical common elements and important evolutionary relationships. Phylogenetically the... (Review)
Review
Three physiologically mineralizing tissues - teeth, cartilage and bone - have critical common elements and important evolutionary relationships. Phylogenetically the most ancient densely mineralized tissue is teeth. In jawless fishes without skeletons, tooth formation included epithelial transport of phosphates, a process echoed later in bone physiology. Cartilage and mineralized cartilage are skeletal elements separate from bone, but with metabolic features common to bone. Cartilage mineralization is coordinated with high expression of tissue nonspecific alkaline phosphatase and PHOSPHO1 to harvest available phosphate esters and support mineralization of collagen secreted locally. Mineralization in true bone results from stochastic nucleation of hydroxyapatite crystals within the cross-linked collagen fibrils. Mineral accumulation in dense collagen is, at least in major part, mediated by amorphous aggregates - often called Posner clusters - of calcium and phosphate that are small enough to diffuse into collagen fibrils. Mineral accumulation in membrane vesicles is widely suggested, but does not correlate with a definitive stage of mineralization. Conversely mineral deposition at non-physiologic sites where calcium and phosphate are adequate has been shown to be regulated in large part by pyrophosphate. All of these elements are present in vertebrate bone metabolism. A key biological element of bone formation is an epithelial-like cellular organization which allows control of phosphate, calcium and pH during mineralization.
Topics: Bone and Bones; Calcification, Physiologic; Minerals; Osteogenesis; Phylogeny
PubMed: 32858255
DOI: 10.1016/j.bone.2020.115621 -
International Journal of Molecular... Jun 2021Vascular calcification is defined as an inappropriate accumulation of calcium depots occurring in soft tissues, including the vascular wall. Growing evidence suggests... (Review)
Review
Vascular calcification is defined as an inappropriate accumulation of calcium depots occurring in soft tissues, including the vascular wall. Growing evidence suggests that vascular calcification is an actively regulated process, sharing similar mechanisms with bone formation, implicating both inhibitory and inducible factors, mediated by osteoclast-like and osteoblast-like cells, respectively. This process, which occurs in nearly all the arterial beds and in both the medial and intimal layers, mainly involves vascular smooth muscle cells. In the vascular wall, calcification can have different clinical consequences, depending on the pattern, localization and nature of calcium deposition. Nuclear receptors are transcription factors widely expressed, activated by specific ligands that control the expression of target genes involved in a multitude of pathophysiological processes, including metabolism, cancer, inflammation and cell differentiation. Some of them act as drug targets. In this review we describe and discuss the role of different nuclear receptors in the control of vascular calcification.
Topics: Animals; Biomarkers; Calcification, Physiologic; Disease Susceptibility; Gene Expression Regulation; Humans; Protein Binding; Receptors, Cytoplasmic and Nuclear; Signal Transduction; Vascular Calcification
PubMed: 34204304
DOI: 10.3390/ijms22126491 -
Molecular Biology and Evolution Aug 2021Mollusc shells are a result of the deposition of crystalline and amorphous calcite catalyzed by enzymes and shell matrix proteins (SMP). Developing a detailed...
Mollusc shells are a result of the deposition of crystalline and amorphous calcite catalyzed by enzymes and shell matrix proteins (SMP). Developing a detailed understanding of bivalve mollusc biomineralization pathways is complicated not only by the multiplicity of shell forms and microstructures in this class, but also by the evolution of associated proteins by domain co-option and domain shuffling. In spite of this, a minimal biomineralization toolbox comprising proteins and protein domains critical for shell production across species has been identified. Using a matched pair design to reduce experimental noise from inter-individual variation, combined with damage-repair experiments and a database of biomineralization SMPs derived from published works, proteins were identified that are likely to be involved in shell calcification. Eighteen new, shared proteins likely to be involved in the processes related to the calcification of shells were identified by the analysis of genes expressed during repair in Crassostrea gigas, Mytilus edulis, and Pecten maximus. Genes involved in ion transport were also identified as potentially involved in calcification either via the maintenance of cell acid-base balance or transport of critical ions to the extrapallial space, the site of shell assembly. These data expand the number of candidate biomineralization proteins in bivalve molluscs for future functional studies and define a minimal functional protein domain set required to produce solid microstructures from soluble calcium carbonate. This is important for understanding molluscan shell evolution, the likely impacts of environmental change on biomineralization processes, materials science, and biomimicry research.
Topics: Animal Shells; Animals; Biomineralization; Calcification, Physiologic; Crassostrea; Mytilus edulis
PubMed: 34014311
DOI: 10.1093/molbev/msab153 -
Applied and Environmental Microbiology Jun 2023The Fe content and the morphometry of asbestos are two major factors linked to its toxicity. This study explored the use of microbe-mineral interactions between asbestos...
The Fe content and the morphometry of asbestos are two major factors linked to its toxicity. This study explored the use of microbe-mineral interactions between asbestos (and asbestos-like) minerals and thermophilic chemolithoautotrophic microorganisms as possible mineral dissolution treatments targeting their toxic properties. The removal of Fe from crocidolite was tested through chemolithoautotrophic Fe(III) reduction activities at 60°C. Chrysotile and tremolite-actinolite were tested for dissolution and potential release of elements like Si and Mg through biosilicification processes at 75°C. Our results show that chemolithoautotrophic Fe(III) reduction activities by Deferrisoma palaeochoriense were supported with crocidolite as the sole source of Fe(III) used as a terminal electron acceptor during respiration. Microbial Fe(III) reduction activities resulted in higher Fe release rates from crocidolite in comparison to previous studies on Fe leaching from crocidolite through Fe assimilation activities by soil fungi. Evidence of biosilicification in Thermovibrio ammonificans did not correspond with increased Si and Mg release from chrysotile or tremolite-actinolite dissolution. However, overall Si and Mg release from chrysotile into our experimental medium outmatched previously reported capabilities for Si and Mg release from chrysotile by fungi. Differences in the profiles of elements released from chrysotile and tremolite-actinolite during microbe-mineral experiments with underscored the relevance of underlying crystallochemical differences in driving mineral dissolution and elemental bioavailability. Experimental studies targeting the interactions between chemolithoautotrophs and asbestos (or asbestos-like) minerals offer new access to the mechanisms behind crystallochemical mineral alterations and their role in the development of tailored asbestos treatments. We explored the potential of chemosynthetic microorganisms growing at high temperatures to induce the release of key elements (mainly iron, silicon, and magnesium) involved in the known toxic properties (iron content and fibrous mineral shapes) of asbestos minerals. We show for the first time that the microbial respiration of iron from amphibole asbestos releases some of the iron contained in the mineral while supporting microbial growth. Another microorganism imposed on the two main types of asbestos minerals (serpentines and amphiboles) resulted in distinct elemental release profiles for each type of asbestos during mineral dissolution. Despite evidence of microbially mediated dissolution in all minerals, none of the microorganisms tested disrupted the structure of the asbestos mineral fibers. Further constraints on the relationships between elemental release rates, amount of starting asbestos, reaction volumes, and incubation times will be required to better compare asbestos dissolution treatments studied to date.
Topics: Asbestos, Serpentine; Asbestos, Crocidolite; Ferric Compounds; Asbestos; Minerals; Iron; Bacteria, Anaerobic
PubMed: 37184266
DOI: 10.1128/aem.02048-22 -
International Journal of Molecular... Oct 2022Mineralization-competent cells like osteoblasts and chondrocytes release matrix vesicles (MVs) which accumulate Ca and P, creating an optimal environment for apatite...
Mineralization-competent cells like osteoblasts and chondrocytes release matrix vesicles (MVs) which accumulate Ca and P, creating an optimal environment for apatite formation. The mineralization process requires the involvement of proteins, such as annexins (Anx) and tissue-nonspecific alkaline phosphatase (TNAP), as well as low molecular-weight compounds. Apigenin, a flavonoid compound, has been reported to affect bone metabolism, but there are doubts about its mechanism of action under physiological and pathological conditions. In this report, apigenin potency to modulate annexin A6 (AnxA6)- and TNAP-mediated osteoblast mineralization was explored using three cell lines: human fetal osteoblastic hFOB 1.19, human osteosarcoma Saos-2, and human coronary artery smooth muscle cells HCASMC. We compared the mineralization competence, the morphology and composition of minerals, and the protein distribution in control and apigenin-treated cells and vesicles. The mineralization ability was monitored by AR-S/CPC analysis, and TNAP activity was determined by ELISA assay. Apigenin affected the mineral structure and modulated TNAP activity depending on the concentration. We also observed increased mineralization in Saos-2 cells. Based on TEM-EDX, we found that apigenin influenced the mineral composition. This flavonoid also disturbed the intracellular distribution of AnxA6 and TNAP, especially blocking AnxA6 aggregation and TNAP attachment to the membrane, as examined by FM analysis of cells and TEM-gold analysis of vesicles. In summary, apigenin modulates the mineralization process by regulating AnxA6 and TNAP, as well as through various effects on normal and cancer bone tissues or atherosclerotic soft tissue.
Topics: Humans; Alkaline Phosphatase; Annexin A6; Apigenin; Calcification, Physiologic; Osteoblasts
PubMed: 36361965
DOI: 10.3390/ijms232113179