DigitalUM :: Browsing by Subject "Osteoblast"

Browsing by Subject "Osteoblast"

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Open Access
Bone biology in postnatal Wistar rats following hypoxia-reoxygenation
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Hameister, Rita; Lohmann, Christoph H.; Dheen, Thameem; Singh, Gurpal; Kaur, Charanjit
Hypoxia response pathways have a central role in normal and abnormal bone biology but the effect of systemic hypoxia-reoxygenation on bone is not clear. Following hypoxic exposure, aberrant synthesis, folding and trafficking of proteins has been reported to occur, which can result in endoplasmic reticulum (ER) stress and may finally cause cell death. This study aimed to examine the effect of systemic hypoxia-reoxygenation injury on bone biology in postnatal rats. Immunoexpression of HIF-1α and VEGF was upregulated in femurs of newborn Wistar rats in response to systemic hypoxia-reoxygenation. Along with that, increased apoptosis of osteoblast precursors, osteoblasts, osteocytes and endothelial cells was observed in comparison to femurs of control animals by transmission electron microscopy, TUNEL staining and immunoexpression of cleaved caspase-3. The viability of osteoclasts was not affected. After hypoxia- reoxygenation, ER stress was observed in the osteoblasts and osteocytes as indicated by dilatation of the ER and enhanced immunoexpression of the ER stress marker GRP78. Localisation of collagen α1 immunoreaction was widespread in the bone matrix of control femurs but was confined to the osteoblasts and osteocytes in response to hypoxia-reoxygenation. In support of these findings, in vitro work showed reduced viability of osteoblast-like SaOs-2 cells and upregulation of GRP78 protein expression in them by western blotting following exposure to hypoxia. This suggests that systemic hypoxia-reoxygenation may disturb bone biology in postnatal Wistar rats by inducing ER stress and apoptosis in osteoblasts and osteocytes, without affecting the viability of osteoclasts. More in-depth research is needed to confirm causality between ER stress and apoptosis of osteoblasts and osteocytes
Open Access
Cell adhesion molecules in human osteoblasts: structure and function
(Murcia : F. Hernández, 2001) Bennett, J.H.; Moffatt, S.; Horton, M.
Osteoblasts and bone lining cells form a near continuous layer covering the bone surface and interactions between these cells and the organic matrix of bone are important determinants of osteoblast proliferation and differentiation. In addition, cells of the osteoblast-lineage form functional cornrnunications with each other, with the extra-cellular matrix and with osteocytes through cytoplasmic processes extending through canaliculi in the bone. Together, these cells form a network of putative importance in the regulation of skeletal homeostasis. Cell-cell and cell-matrix interactions are mediated by members of severa1 families of cell adhesion molecules, and knowledge of their interactions will be of fundamental importance in understanding the role of osteoblast in skeletal turnover . Here, the expression pattern of members of the major families of cell adhesion molecules by cells of the osteoblast lineage is reviewed. Special emphasis has been placed on human tissues. In addition, the possibility that cells at progressive stages of the osteoblast lineage have different profiles of cell adhesion molecule expression is explored, and the putative significance of cell-matrix interactions in human skeletal disease briefly discussed.
Open Access
Cellular and molecular alterations of osteoblasts in human disorders of bone formation
(Murcia : F. Hernández, 1999) Marie, P.J.
Osteogenesis is a complex process characterized sequentially by the committment of precursor cells, the proliferation of osteoprogenitor cells, the differentiation of pre-osteoblasts into mature osteoblasts and the apposition of a calcified bone matrix. Recent advances in cell and molecular biology have improved our knowledge of the cellular and molecular mechanisms controlling the different steps of bone formation in humans. Using ex vivolin vitro studies of disorders of bone formation, we showed that the recruitment of osteoprogenitor cells is the most important step controlling the rate of bone formation in both rodents and humans. Accordingly, treatments stimulating osteoblast recruitment were found to increase bone formation in experimental models of osteopenic disorders. Using models of human osteoblastic cells, we identified the profile of phenotypic markers expressed during osteoblast differentiation, and found that hormones and growth factors control osteoblastic cell proliferation and differentiation in a sequential and coordinate manner during osteogenesis in vitro. Our recent evaluation of the phenotypic osteoblast abnormalities induced by genetic mutations in the G,a and FGFR-2 genes led to the characterization of the role of these genes in the alterations of osteoblast proliferation and differentiation in humans. These studies at the histological, cellular and molecular levels provided new insight into the mechanisms that are involved in pathological bone formation in humans. It is expected that further determination of the pathogenic pathways in metabolic and genetic abnormalities in human osteoblasts will help to identify novel target genes and to conceive new therapeutic tools to stimulate bone formation in osteopenic disorders.
Open Access
Distribution and expression of mRNAs for the proto-oncogenes c-fos and c-jun in bone cells in vivo
(Murcia : F. Hernández, 1998) Oyama, M.; Chiba, J.; Kato, Y.; Igarashi, N.; Yoshida, M.; Ishigami, M.; Sugawara, S.; Kobayashi, M.
In this study we assessed the expression and localization of the proto-oncogenes c-fos and c-jun in normal bone so as to gain more insight into the role of these proto-oncogenes in bone tissue. Femurs of 4-weekold rats were examined by non-radioactive in situ hybridization. cDNA probes for c-fos- and c-jun-labeled digoxygenin were produced by Polymerase Chain Reaction (PCR). C-fos and c-jun exhibited similar distribution in growth plate and bone tissue. Expression of c-fos and cjun mRNAs in growth plate was observed in the proliferative zone and partly in the upper layer of the hypertrophic zone. In spongy bone, high expression of cfos and c-jun mRNAs was observed in the osteoblast cytoplasm. However, there was little expression in bone lining cells. In the bony trabeculae, slight expression of c-fos and c-jun was observed in the premature osteocytes situated close to the bone surface, but no expression was detected in osteocytes that possessed relatively large lacunae in the center of the trabeculae. C-fos and c-jun were also slightly expressed in osteoclasts. These data strongly suggest that c-fos and c-jun are involved in regulating chondrocyte proliferation as immediate early genes, and may also be involved in the gene expression of bone matrix proteins as transcription factor (M-1) in vivo. In addition, the fact that strong expression was observed in osteoblasts but hardly any expression at all in bone lining cells seems to suggest that these genes are also involved in osteoblast activation.
Open Access
Histological assessment for femora of ovariectomized obesity (db/db) mice carrying mutated leptin receptor
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Tanaka, Yusuke; Hasegawa, Tomoka; Yamada, Tamaki; Yamamoto, Tomomaya; Sasaki, Muneteru; Hongo, Hiromi; Tsuboi, Kanako; Haraguchi, Mai; Luiz de Freitas, Paulo Henrique; Li, Minqi; Oda, Kimimitsu; Totsuka, Yasunori; Tei, Kanchu; Amizuka, Norio
In order to provide a clue to understand the interplay between leptin and estrogen, we have examined femoral metaphyses of ovariectomized db/db mice carrying a mutated leptin receptor. We performed ovariectomy (OVX) or sham-operation (sham) on 12- week old female wild-type and db/db mice, and then, after 8 weeks, divided the animals into four groups: wild-type sham, wild-type OVX, db/db sham and db/db OVX. Samples from all groups were prepared for histochemical and ultrastructural examinations. As a result, db/db sham mice showed a reduced number and thickness of metaphyseal trabeculae and excessive adipose tissue when compared to wild-type sham mice. The wild-type OVX group exhibited markedly diminished trabecular number, as well as lower populations of osteoblasts and osteoclasts in comparison to wild-type sham group. On the other hand, trabecular numbers were similar for the two db/db groups, suggesting that the effect of the ovariectomy, i.e., estrogen deficiency may be lessened in this animal model. Leptin receptor was mainly found in osteoblasts and in bone marrow stromal cells including adipocytes. In addition, the expression of estrogen receptor did not seem to change after OVX in wild-type mice and in db/db mice. Both db/db sham and OVX mice featured many adipocytes close to the metaphyseal chondroosseous junction, while osteoblasts accumulated glycogen granules and lipid droplets. Therefore, it seems likely that the disruption of leptin signaling in db/db mice shifts the cell differentiation cascade towards the adipocyte lineage, resulting in an osteoporotic bone independently of estrogen deficiency.
Open Access
Interaction between osteoblast and osteoclast: impact in bone disease
(Murcia : F. Hernández, 2004) Phan, T.C.A.; Xu, J.; Zheng, M.H.
The intercellular communication between osteoblasts and osteoclasts is crucial to bone homeostasis. Since Rodan and Martin proposed the control of osteoclasts by osteoblasts in the 1980s, many factors have been isolated from osteoblasts and shown to regulate the differentiation and function of osteoclasts. However, the mechanism by which osteoblasts regulate osteoclasts during bone remodelling is still unclear. On the other hand, it is well accepted that many metabolic bone diseases are associated with the disruption of the communication between osteoblast and osteoclasts. Thus, this review focuses on the cross-talk between osteoblasts and osteoclasts and its impact in bone disease.
Open Access
Plasticity and regulation of human bone marrow stromal osteoprogenitor cells: potential implication in the treatment of age-related bone loss
(Murcia : F. Hernández, 2004) Ahdjoudj, S.; Fromigué, O.; Marie, P.J.
Human bone marrow stroma contains pluripotent mesenchymal progenitor cells that can give rise to many mesenchymal lineages, including chondroblasts, adipocytes or osteoblasts. The differentiation of these cells towards a specific lineage is dependent on hormonal and local factors activating specific transcription factors. Attempts have been recently made to identify osteoprogenitor cells in the human bone marrow and to identify the molecular mechanisms responsible for lineage-specific differentiation of human bone marrow stromal cells. Using a clonal pluripotent human bone marrow stromal cell line with tri-potential characteristics, we have provided evidence for a controlled reciprocal regulation of osteoblast/chondroblast and osteoblast/adipocyte differentiation of human bone marrow stromal cells. We have also shown that administration of TGFß that regulates the expression of specific osteoblast and adipocyte transcription factors can promote osteoblast differentiation and inhibit adipocyte conversion of rat marrow stromal cells in vivo. This indicates that the reciprocal relationship between osteoblastogenesis and adipogenesis can be manipulated in vivo in order to improve bone formation. Future studies will have to identify key signals for lineage-specific differentiation of human marrow stromal cells. This may result in the development of therapeutic strategies to promote the differentiation of these cells towards the osteoblast lineage and to inhibit excessive bone marrow adipogenesis associated with aging.
Open Access
Role of angiogenesis on bone formation
(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2012) Portal Núñez, Sergio; Lozano, Daniel; Esbrit, Pedro
Angiogenesis and bone formation are coupled during skeletal development and fracture healing. This relationship, although known for some time, has not been properly explored. Advances in the discovery of how angiogenesis is regulated in physiological processes like embryogenesis, endometrial regeneration and wound healing or in pathologies such as cancer have provided a deeper understanding of how angiogenic factors may interact with bone cells to improve bone formation and bone regeneration. The lack of oxygen (hypoxia) and the subsequent generation of angiogenic factors have been shown to be critical in the development of a regular skeleton and achieving successful bone regeneration and fracture healing. Given that vascular status is important for a proper bone homeostasis, defining the roles of osteoblasts, osteoclasts, endothelial cells and angiogenic factors and their interactions in bone is a key issue for the development of new strategies to manage bone pathologies and nonfused fractures
Open Access
Signaling pathways governing osteoblast proliferation, differentiation and function
(Murcia : F. Hernández, 2009) Fung Ling Chau, Jenny; Fook Leong, Wai; Li, Baojie
Osteoblasts are bone forming cells that are responsible for bone growth and remodeling. They are derived from bone marrow mesenchymal stem cells through a series of processes including commitment, osteoprogenitor expansion, terminal differentiation and cell death. Osteoblastogenesis and bone formation are regulated by hormones, growth factors, cytokines, mechanical loading and aging. Osteoblasts can sense these external cues, transduce the signals through various signaling pathways and regulate the expression of specific genes, to determine the cell fate. In this review, we aim to update our current understanding of the signaling pathways that control different steps of osteoblast homeostasis, with special focus on how signaling events control cell fate through regulating gene expression.
Open Access
The hypertrophic chondrocyte: To be or not to be
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Hallett, Shawn A.; Ono, Wanida; Ono, Noriaki
Hypertrophic chondrocytes are the master regulators of endochondral ossification; however, their ultimate cell fates cells remain largely elusive due to their transient nature. Historically, hypertrophic chondrocytes have been considered as the terminal state of growth plate chondrocytes, which are destined to meet their inevitable demise at the primary spongiosa. Chondrocyte hypertrophy is accompanied by increased organelle synthesis and rapid intracellular water uptake, which serve as the major drivers of longitudinal bone growth. This process is delicately regulated by major signaling pathways and their target genes, including growth hormone (GH), insulin growth factor-1 (IGF-1), indian hedgehog (Ihh), parathyroid hormone-related protein (PTHrP), bone morphogenetic proteins (BMPs), sex determining region Y-box 9 (Sox9), runt-related transcription factors (Runx) and fibroblast growth factor receptors (FGFRs). Hypertrophic chondrocytes orchestrate endochondral ossification by regulating osteogenic-angiogenic and osteogenic-osteoclastic coupling through the production of vascular endothelial growth factor (VEGF), receptor activator of nuclear factor kappa-B ligand (RANKL) and matrix metallopeptidases-9/13 (MMP-9/13). Hypertrophic chondrocytes also indirectly regulate resorption of the cartilaginous extracellular matrix, by controlling formation of a special subtype of osteoclasts termed "chondroclasts". Notably, hypertrophic chondrocytes may possess innate potential for plasticity, reentering the cell cycle and differentiating into osteoblasts and other types of mesenchymal cells in the marrow space. We may be able to harness this unique plasticity for therapeutic purposes, for a variety of skeletal abnormalities and injuries. In this review, we discuss the morphological and molecular properties of hypertrophic chondrocytes, which carry out important functions during skeletal growth and regeneration.

Browsing by Subject "Osteoblast"

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