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 AccessAngiogenesis and the role of bone marrow endothelial cells in haematological malignancies(Murcia : F. Hernández, 2004) De Raeve, H.; Van Marck, E.; Van Camp, B.; Vanderkerken, K.Increased microvessel density (MVD) has been observed in the bone marrow (BM) of patients with multiple myeloma (MM), acute lymphoblastic leukaemia, acute myeloid leukaemia, and myelodysplastic and myeloproliferative syndrome. The MVD is the net result of cumulative phases of angiogenesis and angio-regression and is as such not an indicator of the ongoing angiogenesis at the time of biopsy. There is, therefore, a need for additional methods that allow the estimation of ongoing angiogenesis. Double immunostainings for CD34 and Ki-67 can be used on paraffin-embedded tissue to determine the endothelial proliferation fraction. The BM endothelial cells, as a component of the BM stroma, have a close interaction with the malignant cells. In MM, for example, they are involved in the specific homing and are a source of paracrine growth factors. Targeting the BM microvessels will not only influence the nutrient and oxygen supply, but will in addition reduce the growth stimuli provided by the EC.
- 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.
- PublicationOpen AccessPulmonary lymphoid lesions in an experimental model of collapsing glomerulopathy in rats(Murcia : F. Hernández, 2004) Ávila-Casado, M.C.; Pérez-Torres, I.; Aurón, A.; Zepeda Rodríguez, A.; Soto, V.; Soria, E.; Hernández, S.; Chávez-Rentería, B.; Mussali-Galante, Patricia; Ávila-Costa, M.R.; Fortoul, T.I.The characterization of lung damage in an experimental model of collapsing glomerulopathy (CG) in rats is described. Methods: 12 rats were divided into two groups and injected intravenously (iv) with 1 mg/ saline in a final volume of 1 ml/ day in the tail vein for 5 days, with fractionated serum from control and CG subjects. Proteinuria was quantified, and the Glomerular filtration rate was calculated based on creatinine clearance (CC). Rats were sacrificed by perfusion fixation at day 5. Results: Rats injected with serum from CG patients developed proteinuria (p<0.001). A decrease in CC (0.68±0.19) in these rats was also observed. Glomerular tuft retraction and mesangial proliferation was observed in all rats receiving serum from the CG patients. Peribronchiolar infiltrate integrated mainly by lymphocytes, was identified in all CG rats. In some areas this infiltration disrupted the basement membrane and damaged the epithelium. No histopathological abnormalities in the kidney or lungs were found in rats receiving control serum. Conclusion: Patchy pulmonary lymphoid infiltrates were found in the CG model. Up to now there was no information about pulmonary lymphoid infiltration in CG patients. Besides fluid overload due to renal insufficiency or a nephrotic syndrome, other causes of pulmonary involvement in CG patients should be explored.
- PublicationOpen AccessOn the role of the islets of Langerhans in pancreatic cancer(Murcia : F. Hernández, 2004) Hennig, R.; Ding, X.Z.; Adrian, T.E.Pancreatic cancer is a devastating disease characterized by a dismal prognosis with most patients dying within six months after diagnosis. Surgery is an option in less than one in five of these patients, and even with tumor resection the majority of patients succumb to the disease. Other effective treatment options are not available. Common features of pancreatic cancer are severe cachexia, marked insulin resistance and diabetes mellitus. Several studies have demonstrated connections between pancreatic cancers and the endocrine pancreas and this has raised questions regarding the role of the islets of Langerhans in pancreatic adenocarcinoma. This manuscript reviews the recent literature in this field and addresses several questions regarding the interaction between the islets of Langerhans and pancreatic cancer. This review considers the histological findings in pancreatic cancer, cell culture and animal experiments, the four islet cell types and the hormones they secrete, as well as the influence of the arachidonic acid pathways on islet cell function and pancreatic cancer. While pancreatic adenocarcinomas are ductal in nature, the cell of origin has not been identified and there is even some evidence that the islets may harbor the precursor cell. Considerable evidence suggests that the diabetes is caused by the tumor, while other studies have identified diabetes as a risk factor. Clearly, the islets are important in many aspects of this disease. However, even though progress has been made, some questions regarding the interaction of pancreatic cancer and the endocrine pancreas remain unanswered.