Histology and histopathology Vol.26,nº11 (2011)
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- PublicationOpen AccessNovel therapeutic strategies to target RCAS1, which induces apoptosis via ectodomain shedding(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Sonoda, KenzoThe expression of receptor-binding cancer antigen expressed on SiSo cells (RCAS1) is associated with aggressive characteristics and poor overall survival for 15 different human malignancies. The correlation between RCAS1 expression and several clinicopathological variables, including tumor size, clinical stage, invasion depth and lymph node metastasis highlights this molecule’s clinical significance. RCAS1 is a biomarker because: (1) its concentration in serum or pleural effusion is significantly higher in cancer patients; (2) its level is associated with treatment response; and (3) high RCAS1-valued serum from cancer patients inhibits growth of RCAS1 putative receptor-expressing K562 cells. RCAS1 is secreted by ectodomain shedding and induces apoptosis in peripheral lymphocytes and natural killer (NK) cells. Although its putative receptor and mechanism of apoptosis induction remain undefined, RCAS1 is believed to help tumor cells evade immune surveillance. RCAS1 expression is also related to changes in extracellular matrix characteristics, reduction of vimentin-positive stromal cells, and increased microvessel density (MVD), all suggesting that RCAS1 may induce connective tissue remodeling. Further exploration of RCAS1 biological function will facilitate development of novel therapeutic strategies that target RCAS1.
- PublicationOpen AccessNuclear relocation of DGKζ in cardiomyocytes under conditions of ischemia/reperfusion(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Akiyama, Hideyuki; Hozumi, Yasukazu; Nakano, Tomoyuki; Kubota, Isao; Goto, KaoruDiacylglycerol (DG) and phosphatidic acid (PA) are generated under various conditions, such as ligand stimulation and several stresses. They serve as second messengers to respond to pathophysiological conditions. DG kinase (DGK) catalyzes DG to produce PA. It is regarded as a regulator of these lipid messengers. Previous studies show that DGKζ, a nuclear isozyme, translocates from the nucleus to the cytoplasm in hippocampal neurons under transient ischemia and never relocates to the nucleus after reperfusion. This study examined whether a similar phenomenon is observed in cardiomyocytes, which represent another type of postmitotic, terminally differentiated cell. We performed immunostaining on ischemic hearts induced by occlusion of the left anterior descending coronary artery and on primary cultured cardiomyocytes under oxygen-glucose deprivation (OGD). In the animal model, 10 min ischemia is sufficient to cause DGKζ to disappear from the nucleus in cardiomyocytes. However, DGKζ is observed again in the nucleus at 10 min following reperfusion after 10 min ischemia, which contrasts sharply with ischemic hippocampal neurons. Similar results were obtained from experiments using primary cultured cardiomyocytes under OGD conditions, except that DGKζ relocates autonomously, if at all, to the nucleus, even under continuous OGD conditions. Results suggest that DGKζ is involved in the acute phase of cellular response to ischemic stress in cardiomyocytes in a similar, but not identical, manner to that of neurons.
- PublicationOpen AccessAlterations of the perivascular dystrophin-dystroglycan complex following brain lesions. An immunohistochemical study in rats(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Kálmán, Mihály; Mahalek, J.; Adorján, A.; Pócsai, Károly; Bagyura, Zsolt; Sadeghian, S.Dystroglycan is a laminin receptor, which with dystrophins and other components forms the dystrophin-dystroglycan complex. It has an important role in the formation of gliovascular connections, cerebral vascularisation and blood-brain barrier. Dystroglycan consists of two sub-units, α and ß. Previous studies demonstrated that the ß-dystroglycan immunoreactivity of cerebral vessels temporarily disappeared in the area adjacent to the lesion, whereas the vascular laminin which is not immunoreactive in the intact brain became detectable. The present study extends these investigations over other components of the complex: utrophin, α1-syntrophin and α1-dystrobrevin. The experiments were performed on adult rats. The lesions were stab wounds or cryogenic lesions in deep ketamine-xylasine narcosis. Following survival periods 2 to 30 days, the animals were perfused and floating brain sections were processed for fluorescent immunohistochemistry. The α1-dystrobrevin, like ß-dystroglycan, vanished temporarily around the lesion. The immunoreactivity of utrophin changed in a similar way to that of laminin. In intact brains they were confined to the entering segments of the vessels and to the circumventricular organs. Following lesions their immunoreactivity manifested in the vessels around the lesions. However, utrophin followed laminin with a delay: their peaks were about POD (postoperative days) 21 and 7, respectively. Only immunoreactivity of α1-syntrophin appeared in the reactive astrocytes, peaking at POD 14. Double-labeling proved its co-localization with GFAP. Cryogenic lesions had similar immunohistochemical effects, but provided more suitable samples for Western blot analysis, which proved the altered levels of α1-dystrobrevin and α1-syntrophin. The phenomena may help to monitor the post-lesion vascular processes and the alterations of the gliovascular connections.
- PublicationOpen AccessTransglutaminase 2 expression is significantly increased in cyclosporine-induced gingival overgrowth(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Asioli, Sofia; Righi, Alberto; Cardone, Pietro; Aimetti, Mario; Maletta, Francesca; Coda, Renato; Carossa, Stefano; Navone, Roberto; Cassoni, PaolaCyclosporine A is a potent immunosuppressant used to prevent organ transplant rejection and treat various autoimmune diseases. However, cyclosporine A can also induce gingival overgrowth, which is characterized by increased extracellular matrix due to an altered balance between collagen synthesis and degradation. This study proposed to verify whether trans-glutaminase 2, an enzyme thought to be responsible for the assembly and remodelling of extracellular matrix, plays any role in the pathogenesis of cyclosporine A-induced gingival overgrowth. Cyclosporine A-induced gingival overgrowths were collected from 21 liver transplant patients and case-controlled with 20 non-hyperplastic gingival biopsies from healthy patients who had previous periodontal treatment. In both groups, the presence and tissue distribution of transglutaminase 2 were determined by immunohistochemistry and analyzed in comparison with the tissue morphology and expression of lymphocyte-related antigens (CD3 and CD20) and a vessel-related marker (CD34). Transglutaminase 2 expression showed a significant increase (2.6-fold) in the stromal component of cyclosporine A-treated patients compared with controls (p<0.001), which suggested that transglutaminase 2 had a role in the pathogenesis of the disease. Further studies should investigate the therapeutic effect of anti-transglutaminase 2 drugs (putrescine or 1,4-diamino-butane) in these patients.
- PublicationOpen AccessInhibin beta B: a useful tumor marker in uterine endometrioid adenocarcinomas?(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Mylonas, IoannisInhibins, dimeric peptide hormones composed of an alpha-subunit and one of two possible beta-subunits (betaA or betaB), exhibit substantial roles in human reproduction and in endocrine-responsive tumours. However, the prognostic significance and clinical implications of the inhibin-betaB subunit in uterine endometrioid adenocarcinomas is still not defined yet. A series of 227 uterine endometrioid adenocarcinomas of a previous well-characterized cohort were re-evaluated for the expression of the inhibin-betaB subunit and correlated with several clinicopathological characteristics and the clinical outcome. In this re-analysis, the betaB-subunit expression demonstrated a significant association with the patients' age and cervical involvement. However, inhibin-betaB did not significantly affect the patients survival in this large cohort group. However, patients with a higher intensity of betaB-subunit immunolabelling had a slightly worse survival expectation, although without any significant association, suggesting that this subunit might have a substantial role in the carcinogenesis and pathology of endometrioid adenocarcinomas. Thus, the inhibin-betaB subunit appears not to be a useful prognostic marker regarding endometrioid adenocarcinomas. However, further research is warranted in elucidating the possible implications of inhibin-ßB and endometrial carcinogenesis.
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