Histology and histopathology Vol.31,nº 11 (2016)
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- PublicationOpen AccessEwing sarcoma and the new emerging Ewing-like sarcomas: (CIC and BCOR-rearranged-sarcomas). A systematic review(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Machado, Isidro; Navarro, Samuel; Llombart Bosch, AntonioEwing-like sarcomas (ELS) are a heterogenous group of tumors that frequently affect pediatric and young adult patients. Accurate classification and distinction from the Ewing sarcoma family of tumor (ESFT) is decisive in patient management. ELS share a significant morphologic, immunohistochemical and clinical overlap with ESFT, thus the differential diagnosis is challenging, especially with atypical ESFT and tumors with unusual immunoprofiles or uncommon clinicoradiological findings. A subset of ELS harboring the CIC-DUX4 or BCORCCNB3 fusions has been described recently. The spectrum of ELS is now expanding, and additional gene fusion partners besides DUX4 or CCNB3 have been detected, and the terms CIC or BCOR-rearranged sarcomas have recently been proposed. We review the clinical, histological, phenotypic and molecular findings of ESFT and these new emerging ELS.
- PublicationOpen AccessHistological and immunohistochemical effects of L-arginine and silymarin on TNBS-induced inflammatory bowel disease in rats(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Al-Drees, Abdul Majeed; Khalil, Mahmoud SalahInflammatory bowel disease (IBD) is a chronic disease that affects quality of life. Various mediators are involved in IBD pathogenesis including inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB), cytochrome c, heat shock protein 70 (HSP70) and tumor necrosis factor (TNF)-α. L-Arginine (L-Arg) can be depleted in IBD, and silymarin inhibits neutrophil infiltration, NF-κB, and TNF-α, which have crucial roles in inducing IBD. This study aimed to investigate whether silymarin and L-Arg supplementation decreases IBD progression in trinitrobenzinesulfonic acid (TNBS)-induced colitis. Fifty adult male albino rats were randomized into five groups (10 animals per group): Group I rats orally received 10 mg silymarin/100 g body weight once daily; Group II rats orally received 2 mg L-Arg/100 g body weight once daily; Group III rats rectally received 0.85 mL TNBS in 50% ethanol to induce colitis; Group IV rats were treated similar to group III and, on recovery from anesthesia, received silymarin as described for group I; and Group V rats were treated similar to group III and, on recovery from anesthesia, received L-Arg as described for group II. On day 7, the rats were anesthetized, and blood samples were collected to determine the serum concentrations of TNF-α. Laparotomy and total colectomy were performed for macroscopic, histological, and immunohistochemical investigations. The results showed that silymarin and L-Arg macroscopically and microscopically ameliorated TNBS-induced colitis; significantly decreased the serum levels of TNFα; inhibited the colonic expression of iNOS, NF-κB, and cytochrome c; and increased expression of HSP70. Our results suggest that these complementary medicines could be used to supplement current treatments for IBD.
- PublicationOpen AccessHistological parameters of the adrenal cortex after testosterone application in a rat model of the andropause(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Ajdžanović, Vladimir Z.; Jarić, Ivana M.; Živanović, Jasmina B.; Filipović, Branko R.; Šošić Jurjević, Branka T.; Ristić, Nataša M.; Stanković, Sanja D.Histological analysis of the adrenal cortex, after testosterone application in a rat model of the andropause, was the main subject of the present study. Middle-aged Wistar rats were divided into shamoperated (SO; n=8), orchidectomized (Orx; n=8) and testosterone treated orchidectomized (Orx+T; n=8) groups. Testosterone propionate (5 mg/kg b.m. /day) was administered for three weeks, while SO and Orx groups received the vehicle alone. Histological objectives were achieved using stereology, histochemistry and steroid receptor immunostaining. The concentrations of testosterone, aldosterone, corticosterone and DHEA were determined by immunoassays. Expectedly, increased (p<0.05) serum concentration of testosterone was observed in Orx+T group. The volume of ZG cells and nuclei increased in Orx+T animals by 50% and 25% (p<0.05) respectively, but the serum concentrations of aldosterone decreased (p<0.05) by 60%, all compared to the same parameters in Orx group. The immunostaining for androgen receptors (ARs) suggested their cytoplasmic localization in ZG cells of Orx+T rats. Volume of the ZF cell nuclei in Orx+T group decreased (p<0.05) by 17%, which was followed by the significant (p<0.05) fall in corticosterone production and secretion, all in comparison with Orx animals. Also, nuclear immunolocalization of ARs of high optical density was observed through the ZF of Orx+T group. In Orx+T rats volume of ZR cells and nuclei, and circulating DHEA concentration increased (p<0.05) by 68%, 22% and about 6.6 times respectively, compared to Orx animals. Besides the extra-receptor actions in adrenal cortex, testosterone supposedly affects some steroidogenesisrelated gene expression, as indicated by centripetal rise in the number of nuclear ARs.
- PublicationOpen AccessRoles of TGF-beta 1 signaling in the development of osteoarthritis(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Fang, Jie; Xu, Lin; Li, Yefu; Zhao, ZhiheOsteoarthritis (OA) is a degenerative joint disorder characterized by the destruction of articular cartilage, subchondral bone and other joint tissues. Although multiple growth factors and cytokines have been shown to be involved in articular cartilage degeneration and subchondral bone destruction, which eventually leads to OA, the molecular mechanisms underlying the pathogenesis of OA are largely unknown. The canonical transforming growth factor beta 1 (TGFβ1) signaling functions as one of the key factors in cartilage and bone formation, remodeling, and maintenance. However, the effects of TGF-β1 signaling on the development of OA are unclear. Numerous studies provide evidence that TGF-β1 is required for the formation of articular cartilage at early stages of joint development. In contrast, other investigations indicate that TGF-β1 may, in fact, be a factor in joint destruction. Therefore, we, in this review article, discuss the “conflicting” roles of TGF-β1 signaling in the development of OA.
- PublicationOpen AccessDifferentiation of human mesenchymal stromal cells cultured on collagen sponges for cartilage repair(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Sanjurjo Rodríguez, Clara; Martínez Sánchez, Adela Helvia; Hermida Gómez, Tamara; Fuentes Boquete, Isaac; Díaz Prado, Silvia; Blanco, Francisco J.y. Aim: The aim of this study was to evaluate proliferation and chondrogenic differentiation of human bone-marrow mesenchymal stromal cells (hBMSCs) cultured on collagen biomaterials. Materials and Methods: hBMSCs were seeded on five different collagen (Col) sponges: C1C2 (types I and II Col), C1C2HS (types I and II Col plus heparan sulphate (HS)), C1C2CHS (types I and II Col plus chondroitin sulphate (CHS)), C1-OLH3 (type I Col plus low molecular weight heparin) and C1CHS (type I Col plus CHS). The resulting constructs were analyzed by histological and immunohistochemical staining, molecular biology and electron microscopy. Col released into culture media was measured by a dye-binding method. Results: hBMSCs on biomaterials C1C2, C1C2HS and C1C2CHS had more capacity to attach, proliferate and synthesize Col II and proteoglycans in the extracellular matrix (ECM) than on C1-OLH3 and C1CHS. The presence of aggrecan was detected only at the gene level. Total Col liberated by the cells in the supernatants in all scaffold cultures was detected. The level of Col I in the ECM was lower in C1-OLH3 and that of Col II was highest in C1C2 and C1C2HS. Electron microscopy showed differently shaped cells, from rounded to flattened, in all constructs. Col fibers in bundles were observed in C1C2CHS by transmission electron microscopy. Conclusions: The results show that Col I and Col II (C1C2, C1C2HS and C1C2CHS) biomaterials allowed cell proliferation and chondrogenic-like differentiation of hBMSCs at an early stage. Constructs cultured on C1C2HS and C1C2CHS showed better cartilage-like phenotype than the other ones.
- PublicationOpen AccessIntravascular papillary endothelial hyperplasia (IPEH). Evidence supporting a piecemeal mode of angiogenesis from vein endothelium, with vein wall neovascularization and papillary formation(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Díaz-Flores, L.; Gutiérrez, R.; García Suárez, M.P.; González Alvarez, M.P.; Díaz Flores Jr, L.; Sáez, F.J.; Madrid Cuevas, Juan FranciscoIntravascular papillary endothelial hyperplasia (IPEH) is a reactive process of questioned pathogenesis (primary proliferation of endothelial cells/ECs versus organizing thrombi). The aim of this study is to assess the organization of morphologic patterns, with precise location of neovascularization and papillary distribution in IPEH to clarify the role of the vein wall (mainly vein intimal ECs) in lesion development and papillary formation. We studied 12 cases of IPEH in skin and subcutaneous veins by serial histological sections and immunohistochemical procedures. In four well-structured cases (the remaining cases showed overlapping events), we found four principal histological patterns organized by zone: 1) invaginated vein wall zone with microvascular networks. The intraparietal microvessels presented CD34+ and CD31+ ECs arising from ECs of the vein intima, and αSMA+ pericyte-like cells originating from modified SMCs of the media layer. 2) Papillary zone, generally with myriad papillae, formed by ECs of intraparietal microvessel networks encircling vein wall components (parietal papillae). 3) Organizing thrombotic zone from microvascular networks of invaginated vein wall zone. 4) Unorganized thrombotic zone partially covered by ECs, also originating from vein intimal endothelium and arranged in a monolayer or encircling thrombotic fibrin (thrombotic papillae). In conclusion, the capacity of vein intimal ECs and those originating from them (in newlyformed microvessels in the vein itself and covering the unorganized thrombi) to encircle vein wall components or fibrin, and to form papillae (ECs form the cover and encircled components the core) supports a piecemeal mode of angiogenesis as a pathogenic basis of IPEH. This mechanism encompasses the two histogenetic hypotheses outlined above.
- PublicationOpen AccessIncreased aquaporin 1 expression in the tunica albuginea of Peyronie's disease patients: an in vivo pilot study(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Castorina, A.; Loreto, C.; Vespasiani, G.; Giunta, S.; Musumeci, G.; Castorina, S.; Basic, D.; Sansalone, S.Peyronie's disease (PD) is a localized disorder of the connective tissue of the tunica albuginea (TA) whose etiology has not been elucidated. Although several studies have implicated genetic susceptibility and/or mechanical trauma as triggering events for PD, the underlying molecular mechanisms remain largely unknown. Aquaporin 1 (AQP1) is a water channel protein potentially implicated in connective tissue resistance to mechanical stress, acting primarily by increasing tension within the collagen network. Although it represents a potentially attractive molecular target in PD, to date no studies had ever addressed whether AQP1 is detectable and/or differentially expressed in the TA of these patients. Herein the present study, through immunohistochemical and biochemical approaches, we were able to detect AQP1 expression in the TA of control and PD affected patients. We demonstrated that AQP1-like immunoreactivity and expression are significantly increased in plaques of PD patients Vs controls, implying that AQP1 overexpression might be the consequence of a localized maladaptive response of the connective tissue to repeated mechanical trauma. In summary, these data support the idea that AQP1 might represent a potentially useful biomarker of mechanical injury in the TA and a promising target for the treatment of PD.
- PublicationOpen AccessEstablishment and characterization of a transplantable tumor line (RMM) and cell line (RMM-C) from a malignant amelanotic melanoma in the F344 rat, with particular reference to galectin-3 expression in vivo and in vitro(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Bondoc, Alexandra; Katou Ichikawa, Chisa; Golbar, Hossain M.; Tanaka, Miyuu; Izawa, Takeshi; Kuwamura, Mitsuru; Yamate, JyojiTo investigate characteristics of malignant melanomas with various pathobiological features, a homotransplantable tumor line (RMM) was established from a spontaneous amelanotic melanoma found in the pinna of an aged F344 rat. RMM tumors were transplanted in syngeneic rats by serial subcutaneous implantation with 100% intake. The original and RMM tumors consisted of spindle-shaped cells arranged mainly in interlacing bundles. Immunohistochemically, the neoplastic cells were positive to PNL-2 (melanocytes), nestin (neuroectodermal stem cells), S-100 (neurogenic cells) and vimentin (mesenchymal cells). Electron microscopically, tumor cells possessed single membrane-bound pre-melanosomes. Further, a cell line (RMM-C) was induced from an RMM tumor. RMM-C cells and the induced tumors in syngeneic rats showed immunohistochemical reactions similar to the original and RMM tumors. Interestingly, serum level of galectin3 expression was increased with growing RMM tumors, and the expression was influenced by TNF-α (increase) or TGF-β1 (decrease), indicating a possible biomarker of amelanotic melanomas. The RMM tumors and RMM-C cell line could become useful tools for studies on the pathobiology, including tumor immunity, and development of therapeutic strategies against this malignancy. These tools are the first tumor lines of amelanotic melanomas in the rat.
- PublicationOpen AccessHigh glucose concentration-induced expression of pentraxin-3 in a rat model of continuous peritoneal dialysis(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Ishimatsu, Nana; Miyamoto, Tetsu; Ueno, Hiromichi; Hasegawa, Emi; Kuma, Akihiro; Fujimoto, Yoko; Bando, Kenichiro; Nakamata, Junichi; Furuno, Yumi; Serino, Ryota; Baba, Ryoko; Morimoto, Hiroyuki; Doi, Yoshiaki; Tamura, Masahito; Otsuji, YutakaBackground: Continuous exposure to peritoneal dialysis fluids (PDFs) is associated with pathological responses such as persistent microinflammation, which leads to ultrafiltration failure. Pentraxin-3 (PTX3), a multifunctional soluble pattern recognition receptor, is produced at sites of inflammation by a wide range of cell types. This study investigates the in vivo expression of PTX3 in the peritoneal membrane of a rat continuous peritoneal dialysis (PD) model, as well as the effect of high glucose on the in vitro expression of PTX3. Methods: The expression of PTX3 was analyzed using RT-PCR, real-time PCR, immunohistochemistry and western blotting in a PD rat model receiving saline or conventional PDF containing 3.86% glucose for 8 weeks. The effects of high glucose on the expression of PTX3 were examined in cultured rat peritoneal mesothelial cells (RPMCs), mouse macrophage-like cells, and mouse fibroblasts. Results: In a rat model of PD, eight-week instillation of the conventional PDF produced increased submesothelial thickening, followed by substantially enhanced PTX3 protein levels in the submesothelial layer of peritoneal membrane. PTX3 was detected in peritoneal mesothelial cells, macrophages and fibroblasts in the thickened submesothelial area. Glucose was found to induce PTX3 protein expression in RPMCs as well as macrophage-like cells and fibroblasts. Conclusion: Continuous exposure to conventional PDF induces PTX3 expression in the peritoneal membrane of rats. High glucose may be involved in the mechanism of PDF-induced local micro-inflammation in the peritoneum.
- PublicationOpen AccessThe importance of physical activity in osteoporosis. From the molecular pathways to the clinical evidence(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Castrogiovanni, Paola; Trovato, Francesca Maria; Szychlinska, Marta Anna; Nsir, Houda; Imbesi, Rosa; Musumeci, GiuseppeOsteoporosis is a very common bone disorder characterized by low bone mass and signs of deterioration, responsible for bone fragility typical in this pathology. The risk factors for the onset of osteoporosis are many and different from each other. Some of them cannot be modified, such as age, hereditary diseases and endocrine diseases. Others are modifiable, so that prevention is an advisable tool to reduce the incidence of osteoporosis. Among preventive tools, physical activity is certainly a valid instrument of prevention, in fact physical activity contributes to a healthy energy balance and increases muscle mass and bone mass. In the present narrative review, we wanted to pay attention to the possible influence of physical activity on the pathophysiological molecular pathways of osteoporosis and to the use of different exercise training in treatment of osteoporosis. From the literature analyzed, in relation to the effects of physical activity on bone metabolism, it is shown that exercise acts on molecular pathways of bone remodeling involving all cellular types of bone tissue. In relation to clinical trials adopted in patients with osteoporosis, it is evident that a multi-component training, including aerobic activity and other types of training (resistance and/or strength exercises), is the best kind of exercise in improving bone mass and bone metabolism in older adults and especially osteopoenic and osteoporotic women. With regard to whole-body-vibration training, it seems to be a valid alternative to current methods due to its greater adaptability to patients. In conclusion, physical activity, whatever the adopted training, always has beneficial effects on patients suffering from osteoporosis, and not only on bone homeostasis but on the whole skeletal muscle system.