Histology and histopathology Vol.19, nº 3 (2004)
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- PublicationOpen AccessImmuno-histochemical expression of a1, a2 and a3 integrin subunits during angiogenesis in vitro(Murcia: F. Hernández, 2004) Suda, H.; Asami, Y.; Murata, E.; Fujita, K.; Akita, M.Aortic explants were obtained from mouse fetuses and cultured in collagen gels. Immuno-fluorescence microscopy, antibodies (anti a1, a2 and a3 integrin subunits) were used. Fibroblastic cells migrated from the aortic explant after one day of cultivation. The migrating cells located in the peripheral part of the aortic explant were positive for a1 and a2 integrin subunit antibodies. Immuno-fluorescence-positive staining for the a3 integrin subunit antibody was clearly seen in the migrating cells located near the aortic explant and surrounding tube-like structures. In an immuno-electron microscope study performed by pre-embedding immuno labeling, gold particles associated with the a3 integrin subunit were found to reside on the membranes of the cells surrounding the capillary-like tubes. Two synthetic peptides, GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) and KDGEA (Lys-Asp-Gly-Glu-Ala), were added to the growth medium to study their effects on cell migration. KDGEA, a compound containing the recognition sequence for a2ß1 integrin, decreased cell migration, while GRGDSP exhibited no effect. The migration of fibroblastic cells is an important phenomenon for tube formation. The present study suggested that the a1 and a2 integrin subunits are both involved in the cell migration, and more specifically, that the a2 integrin subunit participates in cell migration through the KDGEA sequence. The a3 integrin subunit played a role in tube formation.
- PublicationOpen AccessIntra- and extracellular Aß and PHF in clinically evaluated cases of Alzheimer’s disease(Murcia : F. Hernández, 2004) Fernández-Vizarra, P.; Fernández, A.P.; Castro-Blanco, S.; Serrano, J.; Bentura, M.L.; Martínez Murillo, R.; Martínez, A.; Rodrigo, J.Temporal cortical sections from postmortem brains of individuals without any dementing condition and with different degrees of severity of Alzheimer’s disease (AD) evaluated by the Clinical Dementia Rating scale (CDR 0-CDR 3) were analyzed using immunohistochemical procedures. To demonstrate the amyloid-ß-peptide (Aß) deposition and the neurofibrillary pathology, two monoclonal antibodies were used, a human CERAD Aß (10D5) antibody raised against the N-terminal region of the Aß-peptide, and an antibody raised against paired helical filaments (PHF-1). The neuron cell bodies and the glial cells were also recognized by two polyclonal antibodies raised, respectively, against the protein gene peptide (PGP 9.5) and glial fibrillary acidic protein (GFAP). Directly related to severity of AD, progressive deposits of Aßpeptide were found within cortical pyramidal-like neurons and forming senile plaques. Ultrastructurally, Aß-peptide deposits were related to neuronal intracytoplasmic organelles, such as the ER, the mitochondria, the Nissl bodies and lipofuscin. We have also found that the intracellular deposition of the Aß peptide is a neuropathological finding prior to the appearance of PHF-immunoreactive structures. We suggest that the intracellular Aß deposition in cortical pyramidal neurons is a first neurodegenerative event in AD development and that it is involved in cell dysfunction, neuronal death, and plaque formation
- PublicationOpen AccessUltrastructural changes in bones of the senescence-accelerated mouse (SAMP6): a murine model for senile osteoporosis(Murcia : F. Hernández, 2004) chen, H.; Shoumura, S.; Emura, S.SAMP6, a substrain of senescenceaccelerated mice, was developed as an animal model for senile osteoporosis. In the present study, we investigated the bone morphology, together with serum calcium and bone mineral density (BMD) in SAMP6 and agematched normal mice SAMR1. We did not find any significant differences between SAMR1 and SAMP6 at 1 month of age with regard to the serum compositions and bone morphology. As compared with SAMR1, BMD, the femoral weight, femoral calcium and phosphorus levels were significantly reduced in SAMP6 at 2 and 5 months of age. The number of osteoblasts in trabecular bones was also significantly reduced. Swollen mitochondria and myelin-like structures were found in osteoblasts and osteocytes of SAMP6 mice at 2 and 5 months of age. There was a greater proportion of resting surface and less forming surface in the femoral endosteal surfaces of SAMP6 mice. The amount of trabecular bone in the lumbar vertebra and the distal metaphysis of the femur was reduced. The number of the mast cells in bone marrow of the tibia significantly increased in SAMP6 mice. These findings indicate that the lower bone mass in SAMP6 was due to the reduction in osteoblast formation and suggested that mast cells in bone marrows play a role in the pathogenesis of senile osteoporosis.
- PublicationOpen AccessAnimal models of pheochromocytoma(Murcia : F. Hernández, 2004) Tischler, A.S.; Powers, J.F.; Alroy, J.Pheochromocytomas are neuroendocrine tumors of adrenal chromaffin cells. They are rare in all species except rats but occur with increased frequency in several human familial tumor syndromes. Concurrence of pheochromocytoma with other tumors sometimes parallels these human syndromes in rats, bovines, horses and dogs but a shared genetic basis for human and spontaneously occurring animal pheochromocytomas has thus far not been established. Pheochromocytomas are inducible in rats by a variety of non-genotoxic substances that may act indirectly by stimulating chromaffin cell proliferation. They are not known to be similarly inducible in other species but arise with increased frequency in transgenic and knockout mice that to varying degrees recapitulate human tumor syndromes. Preliminary evidence suggests that homologous somatic genetic changes might contribute to pheochromocytoma development in humans and some mouse models. The nerve growth factor-responsive PC12 cell line, established from a rat pheochromocytoma, has for almost 30 years served as a research tool for many aspects of neurobiology involving normal and neoplastic conditions. Recently developed pheochromocytoma cell lines from neurofibromatosis knockout mice supplement the PC12 line and have generated additional applications. Advantages of the mouse lines include expression of substantial levels of the epinephrine-synthesizing enzyme, phenylethanolamine N-methyltransferase and expression of high levels of the receptor tyrosine kinase, Ret, which is characteristic of sporadic and familial human pheochromocytomas but not of PC12 cells. Disadvantages include an apparently less stable phenotype. It is difficult to establish pheochromocytoma cell lines from any species, although the tumor cells persist in culture for many months. Understanding of factors that permit pheochromocytoma cells to proliferate might itself provide important insights for tumor biology.
- PublicationOpen AccessImmune signals in the context of secondary osteoporosis(Murcia : F. Hernández, 2004) Okada, Y.; Tanaka, Y.Bone homeostasis is maintained by a balance between bone resorption by osteoclasts and bone formation by osteoblasts, and alterations in bone metabolism can lead to diseases such as osteoporosis. Inter-cellular and intra-cellular signaling, originating from the immune system, the largest source of cellderived regulatory signals, are involved in these processes. Immune-competent cells such as macrophages and lymphocytes deliver cell-cell signaling through soluble factors such as cytokines and through direct contact with the cells. Such immunological signals to the bone are transmitted primarily through osteoblasts or direct stimulation of osteoclasts to induce osteoclast maturation or bone resorption, which may in turn lead to the disequilibrium of bone metabolism. Inflammatory diseases such as rheumatoid arthritis are good examples of such a process, in which immunological signals play a central role in the pathogenesis of the accompanying secondary osteoporosis. We will achieve a better understanding of the pathogenesis of bone metabolism in osteoporosis through immune signaling, and thereby develop improved therapeutic strategies for these conditions.