Histology and histopathology Vol.28, nº 1 (2013)
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- PublicationOpen AccessInbred wild type mouse strains have distinct spontaneous morphological phenotypes(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Serpi, Raisa; Klein-Rodewald, Tanja; Calzada-Wack, Julia; Neff, Frauke; Schuster, Tibor; Gailus-Durner, Valérie; Fuchs, Helmut; Poutanen, Matti; Hrabé de Angelis, Martin; Esposito, IreneThe mouse is the most commonly used animal for modelling human disease. New approaches for generating genetically manipulated mouse models to represent human disease, as well as target the function of specific genes, has increased the importance of mice in biomedical science. For the correct interpretation of alterations in mouse phenotype the basic morphology of background mouse strains must be known. Despite ongoing efforts to create publicly available baseline phenotypic data, the information concerning spontaneous lesions in wild-type mice is incomplete and scattered so far, and further studies are needed. We addressed this problem by screening haematoxylin-eosin stained sections of brain, reproductive organs, urinary bladder, kidney, thyroid, parathyroid, heart, lung, spleen, thymus, lymph nodes, adrenal glands, stomach, intestine, liver, skin and pancreas of six commonly used inbred mouse strains (C57BL6/J, C57BL6/NTac, C3HeB/FeJ, BALB/cByJ, 129P2/OlaHsd and FVB/N) for inherent spontaneous morphological lesions. Interesting spontaneous phenotypes were seen in morphology of the liver, pancreas, adrenal glands, lungs, intestines and heart. In conclusion, care should be taken when choosing the background mouse strain for genetic manipulations, since different mouse strains harbour different inherent lesions that can affect the function of targeted genes, interpretation of results and translation of results to model human disease.
- PublicationOpen AccessExpression pattern of the endoplasmic reticulum stress protein GP96 in monophasic and chronic relapsing form of experimental autoimmune encephalomyelitis in rats(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Jakovac, Hrvoje; Grebić, Damir; Barac-Latas, Vesna; Mrakovčić-Šutić, Ines; Radošević-Stašić, BiserkaGp96 is the endoplasmic reticulum (ER)- resident molecular chaperone, which is involved in the correction of unfolded proteins, in the activation of proteasome-dependent ER-associated degradation of the misfolded proteins, and in activation of the protein translation that modulates polypeptide traffic into the ER. Furthermore, owing to its peptide chaperone capacity and ability to interact with professional antigenpresenting cells, as well as with growth factors, integrins and Toll-like receptors, it is also endowed with crucial immunological functions acting as a “danger signal” to the innate and adaptive immunity. Considering these properties, in the present study the tissue expression of gp96 was examined during the monophasic and chronic relapsing form of experimental autoimmune encephalomyelitis (CR-EAE), induced in genetically susceptible DA rats by subcutaneous injection of myelin basic protein (MBP) or bovine brain homogenate in complete Freund's adjuvant (CFA). Immunohistochemical analyses were done in periods of attacks and remissions of EAE, and the results were compared with findings in intact rats and those treated only with CFA. The data revealed that the constitutive gp96 expression, found in several neurons and glial cells in the brain and spinal cord of intact animals, significantly diminished during the attacks of CR-EAE. On the contrary, the remission of disease was followed by high upregulation of gp96, mainly in the oligodendrocytes within the white matter, in the neurons of the hippocampal area, as well as in the motoneurons of lumbar spinal cord, suggesting that gp96 might be involved in proteostasis and immune-related pathways linked with the reparative processes in the CNS.
- PublicationOpen AccessThe pathophysiology of triose phosphate isomerase dysfunction in Alzheimer’s disease(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Tajes, Marta; Guivernau, Biuse; Ramos Fernández, Eva; Bosch Morató, Mónica; Palomer, Ernest; Guix, Francesc X.; Muñoz, Francisco J.Alzheimer’s disease (AD), the most prevalent neurodegenerative disease worldwide, has two main hallmarks: extracellular deposits of amyloid ß- peptide (Aß) and intracellular neurofibrillary tangles composed by tau protein. Most AD cases are sporadic and are not dependent on known genetic causes; aging is the major risk factor for AD. Therefore, the oxidative stress has been proposed to initiate the uncontrolled increase in Aß production and also to mediate the Aß’s deleterious effects on brain cells, especially on neurons from the cortex and hippocampus. The production of free radicals in the presence of nitric oxide (NO) yields to the peroxynitrite generation, a very reactive agent that nitrotyrosinates the proteins irreversibly. The nitrotyrosination produces a loss of protein physiological functions, contributing to accelerate AD progression. One of the most nitrotyrosinated proteins in AD is the enzyme triosephosphate isomerase (TPI) that isomerises trioses, regulating glucose consumption by both phosphate pentose and glycolytic pathways and thereby pyruvate production. Hence, any disturbance in the glucose supply could affect the proper brain function, considering that the brain has a high rate of glucose consumption. Besides this directly affecting to the energetic metabolism of the neurons, TPI modifications, such as mutation or nitrotyrosination, increase methylglyoxal production, a toxic precursor of advanced glycated end-products (AGEs) and responsible for protein glycation. Moreover, nitro-TPI aggregates interact with tau protein inducing the intraneuronal aggregation of tau. Here we review the relationship between modified TPI and AD, highlighting the relevance of this protein in AD pathology and the consequences of protein nitro-oxidative modifications.
- PublicationOpen AccessRole of skeletal muscle in palate development(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2013) Rot, Irena; Kablar, BorisThe involvement of skeletal muscle in the process of palatal development in mammals is an example of Waddingtonian epigenetics. Our earlier study showed that the cleft palate develops in the complete absence of skeletal musculature during embryonic development in mice. This contrasts with previous beliefs that tongue obstruction prevents the elevation and fusion of the palatal shelves. We argue that the complete absence of mechanical stimuli from the adjacent muscle, i.e., the lack of both static and dynamic loading, results in disordered palatogenesis. We further suggest that proper fusion of the palatal shelves depends not only on mechanical but also on paracrine contributions from the muscle. The muscle’s paracrine role in the process of palatal fusion is achieved through its being a source of certain secreted and/or circulatory proteins. A cDNA microarray analysis revealed differentially expressed genes in the cleft palate of amyogenic mouse fetuses and suggested candidate molecules with a novel function in palatogenesis (e.g., Tgfbr2, Bmp7, Trim71, E2f5, Ddx5, Gfap, Sema3f). In particular, we report on Gdf11 mutant mouse that has cleft palate, and on several genes whose distribution is normally restricted to the muscle (completely absent in our amyogenic mouse model), but which are found down-regulated in amyogenic mouse cleft palate. These molecules probably present a subset of paracrine cues that influence palatogenesis from the adjacent muscle. Future studies will elucidate the role of these genes in muscle-palate crosstalk, connecting the cues produced by the muscle with the cartilage and bone tissue’s responses to these cues, through various degrees of cell p
- PublicationOpen AccessNew serum-derived albumin scaffold seeded with adipose-derived stem cells and olfactory ensheathing cells used to treat spinal cord injured rats(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Ferrero Gutiérrez, Amaia; Menéndez Menéndez, Yolanda; Álvarez Viejo, Maria; Meana, Álvaro; Otero, JesúsRecent advances in spinal cord injury (SCI) research and cell culture techniques and biomaterials predict promising new treatments for patients with SCI or other nerve injuries. Biomaterial scaffolds form a substrate within which cells are instructed to form a tissue in a controlled manner. This study was designed to assess axon regeneration and locomotor recovery in rats with spinal cord injury treated with a novel serumderived albumin scaffold seeded with adipose derived stem cells (ADSCs) and olfactory ensheathing cells (OECs). OECs are considered promising candidates for the treatment of SCI, and ADSCs have the ability to differentiate into neural lineages. In vitro experiments revealed that ADSCs and OECs adhered to the scaffold, remained viable and expressed specific markers of their cell types when cultured in the scaffold. Rats treated with scaffold plus cells showed locomotor skills at several time points from 45 days post-injury that were improved over those recorded in control injured, untreated animals. Astrocytic scars and tissue regeneration, identified using histological and immunohistochemical techniques, revealed that although the scaffold itself appeared to play a significant role in reducing glial scar formation and filling of the lesion cavity with cells, the presence of ADSCs and OECs in the scaffold led to the appearance of cells expressing markers of neurons and axons at the injury site. Our findings point to the clinical feasibility of an albumin scaffold seeded with ADSCs and OECs as a treatment candidate for use in spinal cord injury repair studies.
- PublicationOpen AccessOvarian function of the algerian wild Libyan jird, Meriones libycus during seasonal reproductive cycle: histological and immunohistochemical expression(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Smaï-Hamdidouche, Souaâd; Gernigon-Spychalowicz, Thérèse; Khammar, Farida; Exbrayat, Jean MarieMeriones libycus (Libyan jird), a nocturnal Saharan rodent, is characterized by a seasonal reproductive cycle with a short active phase (spring and early summer) and a long resting period (late summer, autumn, winter). Histological and immunohistochemical techniques were performed in order to study the seasonal variations in mature ovaries. During the breeding season, the ovary showed a continuous cyclical activity, the various stages of folliculogenesis from primordial to preovulatory follicles were observed; broken follicles and corpora lutea were also observed. During sexual quiescence, the ovarian cycle was interrupted; anovulation was observed without any corpus luteum. Non mature antral follicles entered the atretic process. Steroid and steroidogenic enzyme activities were studied using indirect immunohistochemistry. 17ß-estradiol, progesterone, testosterone hormones and P450 aromatase (P450 arom) were detected in the different components of the ovary and in various stages of healthy and atretic follicles during the seasonal reproductive cycle. Our results indicate that during ovarian folliculogenesis in breeding season steroids hormone and P450 arom present important activities. In comparison with the resting period, steroidogenesis and steroidogenic enzyme activity became less pronounced in the healthy preantral follicle; it seemed that steroid biosynthesis was reduced and could be involved in the stimulation and maintenance of the ovarian structural integrity in early follicle development. In conclusion, the histological and immunohistochemical seasonal variations of ovaries in Meriones libycus support the hypothesis that seasonal fluctuations are indirectly involved in regulating reproduction, inducing significant changes in both ovarian morphology and its hormonal function.
- PublicationOpen AccessProduction and significance of CCAAT enhancer binding proteins alpha and beta in sinonasal inverted papilloma(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Shabana, El-Hassan; Depondt, Joel; Hourseau, Muriel; Walker, Francine; Berdal, ArianeSinonasal inverted papilloma (SIP) is a rare benign tumor featuring increased cell proliferation, a tendency toward squamous differentiation, recurrence and malignant transformation. The CCAAT enhancer binding proteins, C/EBPs, are transcription factors regulating the proliferation and differentiation of various types of cells, including epithelial cells. We prospectively investigated the production of these transcription factors and the related proliferation and differentiation targets, keratin-10, keratin-15 and cyclinD1, in 26 SIP patients and 8 sinonasal polyposis cases suspected for SIP. Ten of these patients had one or more recurrences over follow-up periods of one to eight years. C/EBP-alpha and C/EBP-beta proteins were not found in normal-looking sinonasal epithelial cells. The proteins and RNAs were detected in SIP and, occasionally, in polyposis tissues. The production of these factors was not significantly correlated with age, sex, site, tumor size or medical history. By contrast, correlations were found between the levels of C/EBP-alpha and keratin-10 levels and between those of C/EBP-beta and keratin-15. C/EBP-alpha levels were also significantly correlated with cyclin-D1 levels. These data suggested that the C/EBPs are implicated in the regulation of cell proliferation and differentiation in SIP. Finally, recurrent SIP produced significantly larger amounts of C/EBPalpha than non- recurrent tumors. These results implicate CCAAT enhancer binding proteins in the pathogenesis of SIP and highlight the role of C/EBP-alpha as a candidate marker for tumor recurrence.
- PublicationOpen AccessReview of renal carcinoid tumor with focus on clinical and pathobiological aspects(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Kuroda, Naoto; Tanaka, Azusa; Ohe, Chisato; Mikami, Shuji; Nagashima, Yoji; Inoue, Keiji; Shuin, Taro; Taguchi, Takahiro; Tominaga, Akira; Alvarado-Cabrero, Isabel; Petersson, Fredrik; Brunelli, Matteo; Michal, Michal; Hes, OndrejRenal carcinoid tumor is a rare neoplasm. In this article, we review this neoplasm with a focus on clinical and pathobiological aspects. The majority of patients present in the fourth to seventh decades, but there is no gender predilection. Clinically, patients with renal carcinoid tumor frequently present with abdominal, back or flank pain. This tumor is occassionally associated with horseshoe kidney and/or mature cystic teratoma located in the kidney. Macroscopically, these tumors are well demarcated with a lobulated appearance and yellow or tan-brown color cut surface. Microscopically, these tumors are composed of monomorphic round to polygonal cells with granular amphophilic to eosinophilic cytoplasm. Tumor cells are arranged in trabecular, ribbon-like, gyriform, insular, glandular and solid patterns. The nuclei are round to oval and with evenly distributed nuclear chromatin, frequently with a “salt and pepper”-pattern. Immunohistochemically, tumor cells demonstrate immunolabeling for chromogranin A and synaptophysin. Ultrastructurally, the neoplastic cells contain abundant dense core neurosecretory granules. In previous genetic studies, abnormalities of chromosomes 3 or 13 have been reported. The clinical behavior of renal carcinoid tumors is variable, but is more indolent than most renal cell carcinomas. Further investigations are warranted in order to elucidate the critical genetic abnormalities responsible for the pathogenesis of this rare entity in renal neoplastic pathology.
- PublicationOpen AccessChondrogenesis of mesenchymal stem cells for cartilage tissue engineering(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Gardner, Oliver F.W.; Archer, Charles W.; Alini, Mauro; Stoddart, Martin J.Despite its remarkable ability to resist mechanical loading, articular cartilage is not capable of mounting a useful reparative reaction in response to damage caused by trauma or disease. As a result numerous surgical and medical approaches have been developed to aid the healing of articular cartilage. Despite the success of surgical techniques such as microfracture, recently attentions have been turned to cell based therapies such as autologous chondrocyte implantation (ACI). ACI has produced encouraging results, however better results may be achievable through an evolution of this surgical approach. Since the first generation of ACI techniques changes have been made in the technique e.g. the introduction of collagen membranes instead of periosteal flaps, and more recently the use of collagen scaffolds for cellular delivery. The procedure has also moved on from being performed as an open operation and can now be performed arthroscopically. Despite these advances the procedure still uses chondrocytes harvested from the joint being repaired. These cells are vulnerable to dedifferentiation during the required in vitro expansion, and as a result may not be capable of producing repair tissue once implanted back into the joint. Mesenchymal stem cells (MSCs) may provide a dedifferentiation resistant alternative to chondrocytes. MSCs would also allow for the use of one arthroscopic operation on the affected joint, as opposed to the two operations that are currently required for ACI.
- PublicationOpen AccessAssociations of intrauterine growth restriction with placental pathological factors, maternal factors and fetal factors; clinicopathological findings of 257 Japanese cases(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Sato, Yuichiro; Benirschke, Kurt; Marutsuka, Kousuke; Yano, Yuichiro; Hatakeyama, Kinta; Iwakiri, Takashi; Yamada, Naoshi; Kodama, Yuki; Sameshima, Hiroshi; Ikenoue, Tsuyomu; Asada, YujiroIntrauterine growth restriction (IUGR) is the leading cause of fetal mortality and morbidity. As an etiology, each of placental findings, maternal factors and fetal factors has been reported to be associated with IUGR, although a comprehensive approach to examine all of these parameters as a cause of IUGR has not been reported. In the present study, therefore, we comprehensively examined the placental findings and maternal and fetal factors in the cases of IUGR (n=257, mean maternal age, 30 years; gestational weeks, 34 weeks) and normal growth pregnancies (n=258, mean maternal age, 30 years; gestational weeks, 33 weeks), and determined risk factors for IUGR. The prevalence of pregnancy hypertension (PHT) (19% vs. 8%, P<0.01), smoking habit (3% vs. 0.7%, P<0.05) and fetal anomaly (3.5% vs. 0.8%, P<0.05) were higher in IUGR cases than normal growth pregnancies. Pathologically, the prevalence of infarction (33% vs. 14%, P<0.05), fetal vessel thrombosis (22% vs. 6%, P<0.001) and chronic villitis (11% vs. 3%, P<0.001) were higher in IUGR cases than those in normal growth pregnancies. A multivariable regression analysis revealed that maternal factors (PHT), fetal factors (anomaly), and placental findings (infarction, fetal vessel thrombosis, and chronic villitis) are independently associated with increased risk of IUGR (all P<0.01).
- PublicationOpen AccessThe angiogenesis promoter, proadrenomedullin Nterminal 20 peptide (PAMP), improves healing in both normoxic and ischemic wounds either alone or in combination with autologous stem/progenitor cells(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) García-Honduvilla, Natalio; Cifuentes, Alberto; Bellón, Juan Manuel; Buján, Julia; Martínez, AlfredoA combination of vascular pathologies and other complicating factors results in chronic wounds which constitute a serious burden for both patients and national health systems, due to prolonged hospital stays, high costs, and prolonged nursing staff dedication. Here we investigate whether proadrenomedullin N-terminal 20 peptide (PAMP), a naturally occurring peptide of the skin with antimicrobial and proangiogenic properties, either alone or in combination with autologous skeletal muscle stem/progenitor cells, acts as a wound healing factor. The rabbit ear was chosen as a test system, since it offers a reliable model for normoxic and ischemic wounds. Topical treatments with PAMP, stem/progenitor cells, or a combination of both, resulted in significant improvements of healing, when compared to untreated wounds. PAMP was very effective in promoting reepithelialization and angiogenesis, whereas treatment with stem/progenitor cells alone resulted in less wound contraction. Interestingly, the combination of PAMP and stem/progenitor cells, while maintaining angiogenic potency, reverted to the contraction levels observed in the untreated controls. Under ischemic conditions, generalized necrosis of the dermis and the underlying cartilage was observed in untreated wounds. Treatments of these wounds with PAMP or stem/progenitor cells allowed a timely recovery. In conclusion, PAMP either alone or in combination with autologous stem/progenitor cells may provide a useful tool for improving wound healing both in normoxic and ischemic conditions.
- PublicationOpen AccessPhenotypic characterization of hereditary epithelial ovarian cancer based on a tissue microarray study(F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Muñoz-Repeto, Iván; García, María José; Kamieniak, María; Ramón y Cajal, Teresa; Domingo, Samuel; Cazorla, Cazorla; García Donas, Jesús; Hernando Polo, Susana; García Sagredo, José Miguel; Hernández, Elena; Lacambra, Carmen; Sáez, Raquel; Robles, Luis; Borrego, Salud; Prat, Jaime; Palacios, José; Benítez, JavierThe pathologic and immunohistochemical features of familial epithelial ovarian cancers are not well understood. We have carried out a comprehensive immunohistochemical study of familial ovarian carcinomas from women with and without BRCA1 or BRCA2 mutations, in order to identify specific and/or common features among these different familial case groups (BRCA1, BRCA2 and non-BRCA1/2) and to identify markers of diagnostic value that might help to select more specific treatments. 73 familial primary ovarian carcinomas were analyzed for the expression of 40 antibodies involved in different genetic pathways using a tissue microarray. Serous carcinomas comprised the majority of all three familial case groups. On the other hand, BRCA1 and BRCA2 carcinomas have similar histopathologic features; i.e. they are often highgrade and are usually diagnosed at a more advanced FIGO stage than non-BRCA1/2 carcinomas. In our series, BRCA1 carcinomas had better clinical evolution and they also more frequently over-expressed PR and P53 than BRCA2 and non-BRCA1/2carcinomas. Unsupervised cluster analysis and survival analysis identified ERCC1 as a potential marker of better clinical outcome for hereditary epithelial ovarian cancer.