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The bone induction principle identified important cues for tissue engineering of bone, namely, osteogenic soluble molecular signals, the bone morphogenetic and osteogenic proteins, and insoluble signals or substrata including biomimetic bioactive matrices and responding stem cells.

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The addition of minced fragments of autogenous rectus abdominis muscle significantly enhances cementogenesis. The recruitment of myoendothelial cells is also discussed in the light of the intrinsic and spontaneous induction of bone formation by smart biomaterial matrices that induce bone differentiation in heterotopic extraskeletal sites of P. Alternate Sources. Save to Library. Create Alert. Share This Paper. Figures, Tables, and Topics from this paper.

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Transforming growth factor-β in stem cells and tissue homeostasis

Citations Publications citing this paper. References Publications referenced by this paper. The induction of bone formation by transforming growth factor-b3: Experimental studies in the non-human primate Papio ursinus. The evolution of a multicellular organism into ever more complex life forms needs the establishment of communication and control among individual cells to maintain order in the organism. The basic physiological processes, including proliferation, differentiation, metabolism, and apoptosis, are intricately regulated by a dense signaling network that is elicited by cytokines, growth factors or polypeptide hormones.

They are pleiotropic, regulate cell proliferation, migration, and differentiation during embryonic development, and have an essential role in maintaining tissue homeostasis in adults. It has an essential role in the development of the palate and lungs, mainly through the regulation of epithelial—mesenchymal interactions during embryonic, fetal, and neonatal development. Therefore, the temporal and spatial activation of this growth factor is critical for its context-dependent physiological effects in vivo.

However, for BMP-4, -5, and -7, although LAP and the mature growth factor is also non-covalently associated, the complex is still active. Most of these activators are also indicators of ECM perturbations. Many proteases including plasmin and matrix metalloproteinases e.

Introduction

Proteases can also target the protease-sensitive hinge region of LTBP to liberate the LLC, which can then be further processed for activation. Thrombospondin-1 TSP-1 is a complex multi-functional glycoprotein which mediates cell-to-cell and cell-to-matrix interactions during multiple cellular events in a temporally regulated manner. In addition, wild-type mice treated with the LSKL blocking peptide in the perinatal period showed similar features to the TSP-1 knockout phenotype in both the airways and pancreas.

Moreover, the expression of TSP-1 is induced by factors such as reactive oxygen species, high glucose, and angiotensin II which are closely associated with systemic diseases that have fibrotic end-organ involvement. However, how to modulate TSP-1 activity to avoid either defective or excessive wound repair processes in vivo remains to be determined.

The first proposed mechanism is MMP-dependent. The second mechanism is proteolytic action-independent, but more closely associated with cell traction forces that are directly transmitted to the LLC via integrin binding.

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It should be noted that both mechanisms are not mutually exclusive, and it is conceivable that cells can use either or both mechanisms at the same time depending on the specific organs or conditions. We suggest that fibrosis is the result of a failure to interrupt this feed-forward loop that is perpetuated by persistent ECM perturbation after injury or inflammation. Conversely, in carbon tetrachloride-induced hepatic fibrosis, excessive proteases are released due to extensive cytotoxic damage.

In vivo, osteoclasts generate a similar pH during bone resorption when an integrin-dependent sealing zone is generated between the bone and the cell. By inhibiting osteoclast bone resorption with alendronate, osteoblast recruitment is uncoupled from PTH-induced bone resorption. Upon ligand activation, a type II receptor phosphorylates its type I receptor partner, which then transmits the signal by phosphorylation of intracellular downstream substrates, i.

Eight Smads Smad1 to Smad8 have been identified in vertebrates. Upon ligand stimulation and subsequent activation by type II receptors, type I receptors transmit intracellular signaling through phosphorylation of downstream effector Smads.

Review ARTICLE

The DNA-binding affinity of Smad complexes is not strong. Hence, they need to interact and cooperate with other DNA sequence-specific transcription factors to target the specific downstream genes. Smad-mediated assembly of basal transcription machinery is also dependent on chromatin conformation, and thus Smads interact with and recruit various chromatin-modifying enzymes to DNA.

This increased nuclear retention is mediated by transcriptional co-factors such as TAZ and YAP, which are the downstream effectors of the Hippo pathway. R-Smads are subsequently degraded by the proteasome and the transcriptional activity is terminated. The Smad-mediated downstream gene expression may also activate non-Smad pathways. Wnt is implicated in stimulation of cell proliferation during embryonal development and tumorigenesis. Parathyroid hormone regulates calcium homeostasis and bone metabolism by binding to and activating a G protein-coupled receptor.

The Notch pathway specifies cell fate determination during development. However, there are reports that in certain cell types, e. A major pathway induced by tyrosine kinase receptors is the Ras pathway. The normal adult bone undergoes continual remodeling by precisely coordinating the activities of osteoblasts and osteoclasts.

Owing to the inadequate recruitment of BMSC to sites of resorption, poor-quality bone is formed with unfilled resorbed areas and haphazard sclerotic areas. The aberrant bone formation in the subchondral bone in turn causes uneven distribution of stress on the articular cartilage, and in a feed-forward manner leads to cartilage degeneration. The MSCs were noted to differentiate into endothelial cells for re-endothelialization and myofibroblastic cells to form thick neointima.

Ugo Ripamonti (Author of Induction of Bone Formation in Primates)

It mediates the mobilization of MSCs to the circulation and further recruits these cells to the perturbed airways in asthma, likely to participate in tissue repair. It should be noted the that the lineage of the recruited endogenous cells was not delineated. Stem cells are long-lived cells functioning to make and replenish the differentiated cells that are lost through normal stress and injury.

Stem cells are also capable of replenishing themselves, a process known as self-renewal. Extensive efforts have been made to identify factors that determine the self-renewal and differentiation of stem cells. Stem cells receive signals from their surrounding environment niche and galvanize intracellular transduction pathways, which deliver information to its genome via activated transcription factors. These transcription factors cooperate with co-activators and chromatin remodelers, intricately balancing the proliferation and cell fate of stem cells. Embryonic stem cells ESCs are pluripotent stem cells derived from the inner cell mass of the blastocyst.

In addition, ESCs are capable of proliferating indefinitely. Smads cooperate with master regulators of cell differentiation or pluripotency. Nodal signaling modulates cell homeostasis e. Nodal signal-driven Smad complexes, with the assistance of other DNA-binding cofactors, readily bind to the Smad binding sites, thus upregulating or downregulating the basal activity of these genes.


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A typical model explaining how Smad complexes gain access to the AREs of poised master regulator genes has been proposed recently. In addition, TRIM33 has been observed to mediate Smad4 ubiquitination, , thus probably providing a negative feedback activity for the inactivation of Smad4 and signal turnover.

In the process, ubiquitin ligases recognize the phosphorylated linker, leading to proteasome-mediated turnover of Smad proteins and signaling attenuation.

In response to Nodal, the OCT4 complex also activates Nanog and the Nodal negative feedback regulators, Smad7 and Lefty1, Lefty2, by directing Smad3 to neighboring sites, and thus maintains the self-renewal and pluripotency of ESCs. In the absence of the pluripotency enforcing factor LIF, ESCs respond to autocrine signals and differentiate into mesendodermal cells of the primitive streak and ectodermal cells.

When contextual self-renewal signals attenuate, the poised chromatin marks provide an entry point for Smad3 complexes to activate differentiation genes. The concept may be especially pertinent in explaining why stem cells at distinct developmental stages may respond differently to a collection of extracellular cues. In addition, some master regulators may themselves be targets of a signaling pathway, the order in which a cell receives a series of signals also matters. Hence, a spatial and temporal profiling of signaling at the single-cell level is necessary and will lead to promising findings.


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Adult stem cells are undifferentiated cells found throughout the body after development. Some adult stem cells are perpetually active, such as intestinal stem cells, whereas others are quiescent, such as stem cells of the hematopoietic system, hair follicles, and mammary gland. Upon specific environmental stimulations, quiescent stem cells can re-enter the cell cycle in response to specific environmental cues, and give rise to lineage-specific progenitors which then differentiate to make functional tissue. Mesenchymal stem cells are multipotent cells existing in various adult tissues including muscle, adipose tissue, connective tissue, bone marrow and teeth, blood, placenta and umbilical cord.

Increased expression of these genes is Smad3- and Rho kinase-dependent. HSCs are stem cells found in bone marrow, being able to differentiate into all blood cell types. Neural stem cells NSCs are stem cells giving rise to neural progenitor cells and eventually to neurons, astrocytes and oligodendrocytes. In the adult central neural system, NSCs reside in the sub-granular zone of the dentate gyrus and in the sub-ventricular zone adjacent to the lateral ventricles. Epithelial hair follicle stem cells HFSCs are stem cells residing in a specific niche of the hair follicle, referred to as the bulge.

Throughout the telogen phase, HFSCs are quiescent. Their quiescence is maintained in part by BMPs provided from the inner layer of non-stem niche cells and from surrounding dermal fibroblasts and adipocytes. Muscle stem cells MuSCs are stem cells isolated from skeletal muscle with myogenic potential in response to environmental cues. BMP4 signals from emerging tendons impact the behavior of a subpopulation of dividing MuSCs at the tips of fetal skeletal muscle. Adult somatic cells can be forced to reprogram into induced pluripotent stem cells iPSCs by ectopically expressing certain transcription factors.

The musculoskeletal system is dynamic in that it undergoes continual adaptations during vertebrate life to attain and preserve skeletal size, shape, microstructure and to regulate mineral homeostasis.

volunteerparks.org/wp-content/tobejyry/2383.php Skeletal homeostasis is maintained by intricate regulation of the bone remodeling process. A typical bone remodeling cycle consists of three distinct phases: a initiation phase, during which osteoclasts are formed and resorb damaged bone; b reversal phase, the transition of osteoclast to osteoblast activity; and c formation phase, when osteoblasts rebuild an equivalent amount of bone to that resorbed.

Multiple adaptations were needed for animals to evolve from aquatic to terrestrial life, and a coupled bone remodeling is critical for this process. Osteoblastic bone formation exists in all vertebrates. A lighter skeleton affords a quick, efficient ability to enhance survival. Bone remodeling, with the evolutionary development of osteoclasts, therefore solved the issues of skeletal weight and a mechanism to regulate mineral metabolism through bone resorption. Quite a few cells have been identified to participate in the highly coordinated bone remodeling process. The osteocyte is the most abundant cell population in mineralized bone tissue.

Osteocytes are cocooned in fluid-filled cavities lacunae within the mineralized bone, and possess long dendrite-like processes that extend throughout canaliculi tunnels within the mineralized matrix. Osteocytes interact with each other and osteoblasts via these dendrite-like processes, functioning as a mechanosensor to coordinate activities of other bone cells. Other cells present in the bone marrow also dynamically cross talk with osteoblast and osteoclast via either direct cell contact or soluble signals, thus modulating bone homeostasis during normal physiology.