Histology and histopathology Vol.26, nº8 (2011)
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- PublicationOpen AccessInsights into iron and nuclear factor-kappa B (NF-κB) involvement in chronic inflammatory processes in peritoneal endometriosis(Murcia: F. Hernández y J.F. Madrid, Universidad de Murcia, Departamento de Biología Celular e Histología, 2011) Defrère, Sylvie; González-Ramos, Reinaldo; Lousse, Jean-Christophe; Colette, Sébastien; Donnez, Olivier; Donnez, Jacques; Van Langendonckt, AnneEndometriosis is a chronic pelvic inflammatory process. Local inflammation is known to play a role in pain and infertility associated with the disease, and may be extensively involved in molecular and cellular processes leading to endometriosis development. In this review, we focus on two inflammatory mediators clearly implicated in the pathogenesis of endometriosis, iron and NF-κB, and their potential association. Iron is essential for all living organisms, but excess iron results in toxicity and is linked to pathological disorders. In endometriosis patients, iron overload has been demonstrated in the different compartments of the peritoneal cavity (peritoneal fluid, endometriotic lesions, peritoneum and macrophages). This iron overload affects numerous mechanisms involved in endometriosis development. Moreover, iron can generate free radical species able to react with a wide range of cellular constituents, inducing cellular damage. Overproduction of reactive oxygen species also impairs cellular function by altering gene expression via regulation of redox-sensitive transcription factors such as NF-κB, which is clearly implicated in endometriosis. Indeed, NF-κB is activated in endometriotic lesions and peritoneal macrophages of endometriosis patients, which stimulates synthesis of proinflammatory cytokines, generating a positive feedback loop in the NF-κB pathway. NF-κB-mediated gene transcription promotes a variety of processes, including endometriotic lesion establishment, maintenance and development. In conclusion, iron and NF-κB appear to be linked and both are clearly involved in endometriosis development, making these pathways an attractive target for future treatment and prevention of this disease.
- PublicationOpen AccessOvarian pluripotent/multipotent stem cells and in vitro oogenesis in mammals(Murcia: F. Hernández y J.F. Madrid, Universidad de Murcia, Departamento de Biología Celular e Histología, 2011) Virant-Klun, Irma; Stimpfel, Martin; Skutella, ThomasThere has been a long persisting dilemma about potential ovarian stem cells in adult mammalian ovaries, including human, and now there is steadily increasing experimental evidence on their existence. After some previous indirect evidence about the presence of stem cells in adult mouse ovaries, an important breakthrough was made by Zou and his coworkers who successfully established long-persisting pluripotent/multipotent ovarian stem cell lines in neonatal and adult mice, and were followed by some other important studies in mouse and human. Moreover, oocyte-like cells can be developed in vitro from pluripotent stem cells of different origins (embryonic stem cells, induced pluripotent stem cells, fetal skin stem cells, pancreatic stem cells). The aim of this article is to elucidate the fast growing new knowledge on the ovarian stem cells and potential in vitro oogenesis in mammals.
- PublicationOpen AccessParafibromin expression in lung normal tissue and carcinoma: its comparison with clinicopathological parameters of carcinoma(Murcia: F. Hernández y Juan F. Madrid, Universidad de Murcia, Departamento de Biología Celular e Histología, 2011) Xia, Pu; Wang, Wei; Xu, Xiao-yan; Wang, Jian-ping; Takano, Yasuo; Zheng, Hua-ChuanParafibromin is a protein encoded by the hyperparathyroidism 2 oncosuppressor gene and its down-regulated expression is involved in the pathogenesis of parathyroid, gastric and colorectal carcinomas. To clarify the roles of parafibromin expression in lung carcinomas, it was examined by immunohistochemistry and in situ hybridization on tissue microarray containing lung carcinomas (n=144) and normal lung tissue (n=20), with a comparison to clinicopathological parameters of carcinomas. Lung carcinoma cell lines and tissues were studied for parafibromin expression by Western blot and RT-PCR. Down-regulated expression of parafibromin mRNA was found in lung carcinoma in comparison with matched normal tissue (p<0.05). Parafibromin protein was found in the cilia and nuclei of pseudo-stratified columnar epithelium, and the nuclei of lung carcinoma. According to immunostaining and in situ hybridization, there was no difference in parafibromin expression between histological subtypes of lung carcinoma (p>0.05). The Kaplan-Meier method indicated that nuclear parafibromin expression was positively correlated with adenocarcinoma patients (p<0.05). Down-regulated parafibromin mRNA expression might play an important role in lung carcinogenesis, but not in its histogenesis. Strong parafibromin expression in cilia of the pseudostratified columnar epithelium indicated its possible involvement in cell mobility. Parafibromin expression could be employed to indicate the favorable prognosis of patients with adenocarcinoma.
- PublicationOpen AccessMaternal diabetes affects cell proliferation in developing rat placenta(Editores F. Hernandez y Juan F. Madrid. Murcia, Universidad de Murcia, Departamento de Biologia Celular e Histologia, 2011) Zorn, T.M.T.; Zúñiga, M.; Madrid, E.; Tostes, R.; Fortes, Z.; Giachini, F.; San Martín, S.Placentation starts with the formation of a spheroidal trophoblastic shell surrounding the embryo, thus facilitating both implantation into the uterine stroma and contact with maternal blood. Although it is known that diabetes increases the placental size and weight, the mechanisms responsible for this alteration are still poorly understood. In mammals, cellular proliferation occurs in parallel to placental development and it is possible that diabetes induces abnormal uncontrolled cell proliferation in the placenta similar to that seen in other organs (e.g. retina). To test this hypothesis, the objective of this work was to determine cell proliferation in different regions of the placenta during its development in a diabetic rat model. Accordingly, diabetes was induced on day 2 of pregnancy in Wistar rats by a single injection of alloxan (40 mg/kg i.v.). Placentas were collected on days 14, 17, and 20 postcoitum. Immunoperoxidase was used to identify Ki67 nuclear antigen in placental sections. The number of proliferating cells was determined in the total placental area as well as in the labyrinth, spongiotrophoblast and giant trophoblast cell regions. During the course of pregnancy, the number of Ki67 positive cells decreased in both control and diabetic rat placentas. However, starting from day 17 of pregnancy, the number of Ki67 positive cells in the labyrinth and spongiotrophoblast regions was higher in diabetic rat placentas as compared to control. The present results demonstrate that placentas from the diabetic rat model have a significantly higher number of proliferating cells in specific regions of the placenta and at defined developmental stages. It is possible that this increased cell proliferation promotes thickness of the placental barrier consequently affecting the normal maternal-fetal exchanges.
- PublicationOpen AccessNeural stem cell-mediated therapy for rare brain diseases: perspectives in the near future for LSDs and MNDs(Murcia: F. Hernández y J.F. Madrid, Universidad de Murcia, Departamento de Biología Celular e Histología, 2011) Filippis, Lidia deLysosomal storage diseases (LSDs) are genetically inherited disorders affecting most patients in pediatric age and progressively lead to severe, even lethal, multiorgan dysfunction and brain neurodegeneration. Motor neuron diseases (MNDs) or Amyotrophic Lateral Sclerosis (ALS)-related syndromes are neurodegenerative disorders occurring in the majority of cases sporadically and affect adult middleaged patients. Despite being divergent in most pathological and physiological hallmarks, both MNDs and LSDs are characterized by tremendous clinical heterogeneity due to poor prognosis and variable onset of the symptoms. Moreover, both LSDs and MNDs are characterized by the concurrence of multiple pathogenetic processes, such as the development of inflammatory and excitotoxic environments. Furthermore, pharmacological, enzyme or genetic therapies have proven to be ineffective and no cure is currently available for the neurodegeneration in either LSD or ALS affected patients. Recent studies have identified non-neuronal cell types, such as astrocytes and microglia, as being involved in non cell-autonomous effects on MND or LSD progression. These findings have prompted the use of neural stem cells for the replacement of non-neuronal cells rather than neuronal cells, which may result in neuroprotection and immunomodulation. The choice of an appropriate tissue source and the establishment of standardized paradigms to culture human neural stem cells (hNSC) will allow their use for future clinical trials on both ALS and LSD affected patients and parallel drug screening studies with novel breakthroughs in the knowledge of neurodegenerative diseases.
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