Histology and histopathology Vol.24, nº5 (2009)

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https://hdl.handle.net/10201/35888

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Open Access
The role of vascular adhesion molecules PECAM-1 (CD 31), VCAM-1 (CD 106), E-Selectin (CD62E) and P-Selectin (CD62P) in severe porcine pancreatitis
(Murcia: F. Hernández, 2009) Kleinhans, Helge; Kaifi, Jussuf T.; Mann, Oliver; Reinknecht, Felix; Freitag, Marc; Hansen, Bente; Schurr, Paulus G.; Izbicki, Jacob R.; Strate, Tim G.
Inflammatory cytokines have been shown to mediate organ damage by their action on vascular endothelia and leukocytes, in part by upregulating the expression of adhesion molecules, which in turn convey transmigration of leukocytes into tissue. The upregulation and activation of vascular cell adhesion molecules on the endothelial cells avail firm leukocyte adhesion to the vascular endothelium and enhance their transmigration and consecutive tissue injury. The aim of this study was to evaluate the expresion of vascular adhesion molecules CD 31 (PECAM-1), CD 106 (VCAM-1), CD 62E (E-Selectin) and CD 62P (P-Selectin) in the pancreas and distant organs of pigs suffering from acute necrotizing pancreatitis (AP). AP was induced in 13 pigs by a combination of intravenous cerulein and intraductal glycodeoxycholic acid. For immunostaining of vascular adhesion molecules slides of porcine pancreas, lung, kidney and liver tissue were stained with monoclonal antibodies (Ab) against PECAM-1-1, VCAM-1 E- and PSELECTIN. The endothelial cell expression of CD 31 (PECAM- 1), CD 106 (VCAM), CD 62E (E-Selectin) and CD 62P (P-SELECTIN) in severe porcine pancreatitis is detectable and upregulation is partly significantly.
Open Access
Ultrastructure of myotendinous junctions in tendon-skeletal muscle constructs engineered in vitro
(Murcia: F. Hernández, 2009) Kostrominova, Tatiana Y.; Calve, Sarah; Arruda, Hellen M.; Larkin, Lisa M.
During development, the interaction between tenocytes and myotubes leads to the formation of highly specialized muscle-tendon structural interfaces: myotendinous junctions (MTJs). Structural integrity of MTJs is critical for force transmission from contracting muscle through tendon to bone. We recently developed an in vitro model of three-dimensional (3-D) skeletal muscle-tendon constructs to address mechanisms of the MTJs development. We hypothesized that engineered in vitro 3-D skeletal muscle-tendon constructs would develop MTJs ultrastructurally resembling those found during fetal development in vivo. To test this hypothesis we compared MTJs structures in vivo to those developed in 3-D skeletal muscle constructs co-cultured with engineered self-organized tendon constructs (SOT), or segments of adult (ART) or fetal rat tail (FRT) by means of electron microscopy. Our study showed that at sites of termination some of the myofibers of the engineered 3-D skeletal muscle-FRT and -SOT constructs displayed emerging finger-like sarcolemmal projections surrounded by collagen fibers. These structures resemble fetal MTJs in vivo. Muscle-ART constructs did not develop MTJs. Muscle-FRT constructs in addition to muscle and tendon also demonstrated well developed cartilage, possessing high potential for development into bone. The muscle-FRT construct model could be used for studies of developmental mechanisms involved in the establishment of interfaces among all four muscularskeletal tissues: muscle, tendon and cartilage/bone.
Open Access
Diabetes enhances the expression of H-ras and suppresses the expression of EGFR leading to increased cell proliferation
(Murcia : F. Hernández, 2009) Vairaktaris, Eleftherios; Goutzanis, Lampros; Yapijakis, Christos; Vassiliou, Stavros; Spyridonidou, Sofia; Vylliotis, Antonis; Nkenke, Emeka; Lazaris, A. Ch.; Strantzias, Pashalis; Patsouris, Efstratios
EGFR kinase activity triggers numerous signaling pathways, such as the Ras/Raf/MAPK cascade, leading to the activation of various mitogen activated protein kinases, which are implicated in cell proliferation through induction of several genes, including c-fos. The possible effect of diabetes on the expression of the oncogenes EGFR, H-ras and c-fos was investigated in an experimental model of chemically induced oral oncogenesis in normal and diabetic (type I) Sprague- Dawley rats. Thirteen diabetic and twelve normal rats developed cancer after 4NQO treatment, while six diabetic and six normal animals were used as controls. The biopsies were classified pathologically (ranging from dysplasia to moderately differentiated oral squamous cell carcinoma) and were studied immunohistochemically. Several representative histological regions from each biopsy were analysed in regard to EGFR, H-ras and c-fos expression, and a comparison between normal and diabetic rats was effected. A trend of decreased EGFR expression in diabetic compared to normal rats was revealed throughout oncogenesis, which was significant in the stage of dysplasia (P<0.05). On the contrary, a trend of increased H-ras expression was observed in diabetic compared to normal rats during oncogenesis, which rose significantly in early invasion and well differentiated OSCC (P<0.001 and P<0.01 respectively). Finally, no statistical differences concerning c-fos expression were detected between diabetic and normal animals. In conclusion, it seems that diabetes reduces the expression of EGFR and initiates the Ras/Raf/MAPK signal transduction pathway by enhancing activation of other signalling molecules, such as the diabetes-associated Insulin Receptor Substrate-1, leading to increased cell proliferation without c-fos involvement.
Open Access
c-KIT signaling as the driving oncogenic event in sub-groups of melanomas
(Murcia : F. Hernández, 2009) Smalley, Keiran S.M.; Sondak, Vernon K.; Weber, Jeffrey S.
As we enter the era of targeted therapy for melanoma, attempts are being made to sub-group tumors on the basis of their driving oncogenic mutations, with the hope of developing truly personalized therapeutic regimens. c-KIT is a receptor tyrosine kinase whose aberrant activation is implicated in the progression of gastrointestinal stromal tumors and some acute myeloid leukemias. The role of c-KIT signaling in melanoma has been controversial; although c-KIT activity is critical to melanocyte development, its expression tends to be lost in most melanomas. Some reports have even shown that the re-expression of c-KIT induces apoptosis in melanoma cell lines. The recent publication of work showing the presence of activating c-KIT mutations in acral and mucosal melanomas, as well as melanomas arising on skin with chronic sun damage, has renewed interest in c-KIT signaling in melanoma. Recent work from our own laboratory has further identified melanomas with constitutive c-KIT signaling activity resulting from c- KIT receptor overexpression. Although the initial clinical trials of the c-KIT inhibitor imatinib mesylate in melanoma were negative, some dramatic responses have been seen in patients with very high c-KIT expression and/or documented activating mutations, fostering the belief that focused studies in patients selected on the basis of c-KIT mutational status will yield more encouraging results. The current review discusses the role of c-KIT signaling in melanoma progression and how this new information can be applied to the targeted therapy of melanoma.
Open Access
Golgi apparatus localization of ZNT7 in the mouse cerebellum
(Murcia : F. Hernández, 2009) Gao, Hui-Ling; Feng, Wan-Yu; Li, Xiao-Ling; Xu, He; Huang, Liping; Wang, Zhan-You
We have recently reported that four members of the zinc transporter (ZNT) family, ZNT1, ZNT3, ZNT4, and ZNT6, are abundantly expressed in the mouse cerebellum. In the present study, we reported that ZNT7 was present throughout the cerebellar cortex. ZNT7 immunoreactivity was predominately present in the somas and primary dendrites of the Purkinje cells. ZNT7 was also present in the Bergmann glial cell bodies as well as their radial processes, which extended into the molecular cell layer. Confocal immunofluorescence results demonstrated that the expression of ZNT7 overlapped with that of TGN38 in the somas of the Purkinje cells and granule cells. Immuno-electron microscopic study showed that ZNT7 was localized to the membrane of the Golgi apparatus in the somas of the Purkinje cells, Bergmann glial cells, and granule cells. Western blot analysis demonstrated that a considerable amount of ZNT7 was expressed in the cerebellum. These findings suggest a significant role of ZNT7 in zinc homeostasis in the mouse cerebellum.

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