Histology and histopathology Vol.31, nº2 (2016)
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- PublicationOpen AccessCo-localization of the zinc transporter ZnT8 (slc30A8) with ghrelin and motilin in the gastrointestinal tract of pigs(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Schweiger, Markus; Steffl, Martin; Amselgruber, Werner M.Zinc is an important co-factor for insulin storage in pancreatic β-cells of different species and the uptake of this ion into insulin containing secretory vesicles is managed by the zinc transporter, ZnT8, a member of the slc30A gene family. Recent studies indicate that this protein is a major autoimmune target in human type 1A diabetes and has also been implicated by genome-wide association studies in type 2 diabetes. Since individuals suffering from type 1 diabetes often develop gastrointestinal motility disorders, we investigated the expression of ZnT8 in the porcine gastrointestinal tract. For this purpose, we studied the cell-type specific expression of ZnT8 in the gut and its co-expression with endocrine hormones that are closely linked to intestinal motility regulation. Nested RT-PCR and immunostaining of sequential serial sections, as well as double-immunostaining using antibodies directed against ZnT8, ghrelin, motilin, neurotensin, serotonin and glucagon-like peptide 1, indicated that ZnT8 is colocalized with ghrelin and motilin. Our findings provide important information about the cell-type specific expression of ZnT8 in the porcine gastrointestinal system. The selective and exclusive expression of ZnT8 in two endocrine cell-types that are engaged in motility functions may be of particular interest for further investigations into type I diabetes-associated gastrointestinal dysfunctions.
- PublicationOpen AccessEmergent roles for intercellular adhesion molecule-1 in the restructuring of the blood-testis barrier during spermatogenesis in the mammal(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Mruk, Dolores D.Mammalian spermatogenesis is comprised of a series of molecular, cellular, and morphological events that underscore the movement of developing germ cells across the blood-testis barrier. These events involve the restructuring of tight junctions, basal ectoplasmic specializations, gap junctions, and desmosomes, which constitute blood-testis barrier function. Previous studies show that preleptotene/leptotene spermatocytes traverse the blood-testis barrier while transiently trapped within an intermediate compartment, which sequesters primary spermatocytes away from basal and adluminal compartments of the seminiferous epithelium. Preleptotene/leptotene spermatocytes enter the adluminal compartment when stable junctions ahead of spermatocytes disassemble, while new junctions assemble behind them. While there is enormous restructuring of the seminiferous epithelium, the mechanism of germ cell movement is incompletely understood. In this perspective, the significance of intercellular adhesion molecule-1 in the restructuring of the blood-testis barrier during spermatogenesis in the mammal is discussed.
- PublicationOpen AccessThe roles and clinical significance of microRNAs in cervical cancer(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Wang, Fenfen; Li, Baohua; Xie, XingCervical carcinogenesis induced by persistent human papillomavirus (HPV) infection represents a stepwise progression from precursors to invasive cervical cancer. Accumulated evidence has shown aberrant expression of microRNAs (miRNAs) in cervical cancer tissues and cells. Further studies reveal that miRNAs play key roles in the initiation and progression of cervical cancer, via specific signaling pathways, including E6-p53, E7-pRb, phosphoinositide3 kinase (PI3K)-Akt, Notch, Wnt/β-catenin, and Hedgehog pathways. Some studies demonstrate that miRNAs might serve as biomarkers or therapeutic targets, presenting a potential prospect in clinical practice. All results provide new insights into the function of miRNAs and the pathogenesis of cervical cancer induced by viral oncoproteins. New approaches for miRNA-based prevention and management for cervical cancer will be developed in the future.
- PublicationOpen AccessInducible factors for cancer-associated fibroblasts in liver cancer versus myofibroblasts in inflammatory liver disease(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Okabe, Hirohisa; Hayashi, Hiromitsu; Nakagawa, Shigeki; Imai, Katsunori; Nitta, Hidetoshi; Arima, Kota; Hashimoto, Daisuke; Chikamoto, Akira; Ishiko, Takatoshi; Beppu, Toru; Baba, HideoThe importance of cancer-associated fibroblasts (CAFs) in liver cancer, cholangiocarcinoma (CC) and hepatocellular carcinoma (HCC), has been appreciated in the past 5 years. We focused on how they get activated in the tumor microenvironment in this review. Not only hepatic stellate cells (HSCs) but also portal fibroblasts (PFs) have been appreciated to be key players in liver fibrogenesis, and their different roles have just started to be recognized. Since the role of cholangiocyte in biliary fibrogenic disease might have some similarities to that of CC, we focused on the role of cholangiocytes activating stromal fibroblasts, which would presumably be helpful for better understanding the mechanism of tumor-CAFs interaction. In addition, the activation of CAFs should be different from that of CAFs in HCC, which we consider to be potentially similar to MFs in hepatocyte injury-dependent liver fibrogesis. Herein, we describe the activation of CAFs in CC in comparison to MFs seen in other liver diseases such as 1) MFs in liver fibrosis caused by hepatocyte injury such as alcoholic hepatitis, viral hepatitis, and nonalcoholic steatosis, 2) MFs in liver fibrosis caused by cholestatic disease, and 3) CAFs in hepatocellular carcinoma (HCC). This review on the activation of fibroblasts either in liver cancer or in chronic liver disease would contribute to CAF-targeted therapy in liver cancer.
- PublicationOpen AccessThe role of high cholesterol-high fructose diet on coronary arteriosclerosis(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Swier, Vicki J.; Tang, Lin; Radwan, Mohamed M.; Hunter III, William J.; Agrawa, Devendra K.The effect of fructose in conjunction with high cholesterol diet in the development of atherosclerotic lesions in coronary arteries is not well established. Microswine were fed high cholesterol (HC) or a high cholesterol-high fructose (HCHF) diet containing 18-20% calories from fructose. All swine had high levels of serum cholesterol and non-HDL, thickened intima and accumulation of collagen in the coronaries. Swine fed with HC diet had less stenosis in coronary arteries, lower serum levels of non-HDL, triglycerides, cholesterol, and blood glucose than HCHF group. Coronary lesions in the HC swine were not as progressed as in HCHF and showed low LDL-expressed lipid-laden foam cells. The M1/M2 macrophage phenotype in the HCHF swine differed with the progression of atherosclerosis, with higher density of M1-phenotype in HCHF swine. There was high expression of CCR7 (M1-phenotype) in more advanced lesions in the fibrous cap-like areas, whereas M2- macrophages were abundant in the foam-cell cores. These findings suggest that the addition of a fructose to high cholesterol diet accelerates atherosclerotic lesions in coronary arteries with an increase in M1-macrophages and the propensity to develop features of metabolic syndrome.
- PublicationOpen AccessMRL/MpJ mice show unique pathological features after experimental kidney injury(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Shiozuru, Daichi; Ichii, Osamu; Kimura, Junpei; Nakamura, Teppei; Ali Elewa, Yaser Hosny; Otsuka-Kanazawa, Saori; Kon, YasuhiroClarification of the renal repair process is crucial for developing novel therapeutic strategies for kidney injury. MRL/MpJ mice have a unique repair process characterized by low scar formation. The pathological features of experimentally injured MRL/MpJ and C57BL/6 mouse kidneys were compared to examine the renal repair process. The dilation and atrophy of renal tubules were observed in folic acid (FA)-induced acute kidney injury (AKI) in both strains, and the histopathological injury scores and number of interleukin (IL)-1F6-positive damaged distal tubules and kidney injury molecule 1 (KIM-1)-positive damaged proximal tubules drastically increased 1 day after AKI induction. However, KIM-1- positive tubules and the elevation of serum renal function markers were significantly fewer and lower, respectively, in MRL/MpJ mice at days 2 and 7 after AKI. After traumatic kidney injury (TKI) via needle puncture, severe tubular necrotic lesions in the punctured area and fibrosis progressed in both strains. Indices for fibrosis such as aniline blue-positive area, number of alpha smooth muscle actin-positive myofibroblasts, and messenger RNA expression levels of Tgfb1 and Mmp2 indicated lower fibrotic activity in MRL/MpJ kidneys. Characteristically, only MRL/MpJ kidneys manifested remarkable calcification around the punctured area beginning 7 days after TKI. The pathological features of injured MRL/MpJ and C57BL/6 kidneys differed, especially those of kidneys with mild proximal tubular injuries after FA-induced AKI. Lower fibrotic activity and increased calcification after TKI were observed in MRL/MpJ kidneys. These findings clarified the unique pathological characteristics of MRL/MpJ mouse kidneys and contribute to understanding of the renal repair process after kidney injury
- PublicationOpen AccessEffect of rehabilitation protocols on muscle function and morphology following hindlimb disuse in weanling rats(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Leite Nogut, Keite i; Bianchi, Eduardo; Chesca Simões, Deise Lúcia; Mattiello-Sverzut, Ana Claudia; de Moura-Jucá, Renata Viana BrígidoBackground: Primary or secondary disorders in developing skeletal muscles are prevalent in physical therapy practice. Assessment of gait functional changes and morphological aspects of hindlimb muscles of weanling rats have not been reported simultaneously in the literature. Rehabilitation by active (eccentric training) and passive (stretching) exercises after hypomobility needs to be investigated. Methods: After ten days of immobilisation in a plantar flexion-shortened position, animals underwent eccentric training on treadmills, intermittent (a single series of ten exercises of 30 seconds each, with a 30-s interval) or continuous stretching protocols for 40 minutes, or had free cage activity for three days. Analysis of gait variables and muscle morphology (immunohistochemical staining of soleus and plantar muscles for fibronectin and types I and III collagen and immunofluorescence staining for dystrophin, laminin, Pax-7, and CD68) were performed. Results: On the third day, the rehabilitated animals touched the ground surface with their toes, except for the group undergoing continuous stretching. The total amount of extracellular macrophages was higher in the rehabilitated animals. The number of satellite cells was not significantly different between groups. Conclusion: Three days of active training (eccentric exercise) showed greater effectiveness compared to the other rehabilitation programs. Weanling rats seem to respond differently to external stimuli such as disuse and remobilisation.
- PublicationOpen AccessNotch signaling in prostate cancer: refining a therapeutic opportunity(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Su, Qingtai; Xin, Liy. Notch is an evolutionarily conserved signaling pathway that plays a critical role in specifying cell fate and regulating tissue homeostasis and carcinogenesis. Studies using organ cultures and genetically engineered mouse models have demonstrated that Notch signaling regulates prostate development and homeostasis. However, the role of the Notch signaling pathway in prostate cancer remains inconclusive. Many published studies have documented consistent deregulation of major Notch signaling components in human prostate cancer cell lines, mouse models for prostate cancers, and human prostate cancer specimens at both the mRNA and the protein levels. However, functional studies in human cancer cells by modulation of Notch pathway elements suggest both tumor suppressive and oncogenic roles of Notch. These controversies may originate from our inadequate understanding of the regulation of Notch signaling under versatile genetic contexts, and reflect the multifaceted and pleiotropic roles of Notch in regulating different aspects of prostate cancer cell biology, such as proliferation, metastasis, and chemo-resistance. Future comprehensive studies using various mouse models for prostate cancer may help clarify the role of Notch signaling in prostate cancer and provide a solid basis for determining whether and how Notch should be employed as a therapeutic target for prostate cancer.
- PublicationOpen AccessA subset of solitary fibrous tumors express nuclear PAX8 and PAX2: a potential diagnostic pitfall(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) McDaniel, Andrew S.; Palanisamy, Nallasivam; Smith, Steven C.; Robinson, Dan R.; Wu, Yi-Mi; Chinnaiyan, Arul M.; McHugh, Jonathan B.; Greenson, Joel K.; Kunju, Lakshmi P.Solitary fibrous tumor (SFT), a mesenchymal neoplasm with widespread anatomic distribution, can be diagnostically challenging in limited samples. We recently encountered an aspirate of a pancreatic mass, incorrectly interpreted as metastatic renal cell carcinoma based on strong PAX8 expression by immunohistochemistry (IHC). After resection, morphologic features with additional IHC (CD34 positivity) correctly identified this lesion as a SFT. PAX8 and PAX2 are commonly used as renal tumor markers; however, no series has investigated PAX8 or PAX2 expression in SFT. IHC for PAX8 and PAX2 was performed on 41 SFTs (biopsy and resections) from varying sites. Eight were histologically malignant and eight were recurrences of previous resections. PAX8 staining was observed at least focally in 26.8% (11 of 41) SFT cases; additionally, PAX2 was positive in 12.2% (5 of 41 cases) of SFTs. For PAX8 and PAX2 positive cases 45.6% and 40%, respectively, showed diffuse expression. No correlation was found between PAX8/PAX2 positivity and age, tumor size, site, malignancy, or recurrence. In conclusion, a substantial minority of SFTs express PAX8 and PAX2 via IHC. This presents a diagnostic pitfall when evaluating possible metastases from the kidney, particularly when primary tumors show sarcomatoid or spindle cell morphologies.
- PublicationOpen AccessAberrant expression of napsin A in a subset of malignant lymphomas(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Nam, Soo Jeong; Kim, Sehui; Kim, Ji Eun; Lim, Megan S.; Elenitoba-Johnson, Kojo S.J.; Kim, Chul Woo; Jeon, Yoon KyungBackground: Napsin A is commonly expressed in pulmonary adenocarcinomas and some renal cell carcinomas. However, napsin A expression in lymphoid neoplasms has never been reported. Methods: Glycoproteomic analyses of lymphoma-derived cell lines revealed napsin A expression in anaplastic large cell lymphoma (ALCL) cells. We thus investigated napsin A expression in lymphoid neoplasms. A variety of lymphomas (n=672) and histiocytic tumors (n=55) was immunostained for napsin A using patient tissues. Results: In reactive lymphoid tissues, only a few histiocytes were positive for napsin A. ALK-positive ALCLs most frequently expressed napsin A (34.4%, 11/32 cases) at a rate that was significantly higher compared with ALK-negative ALCL (8.6%, 3/35; P=0.015). Napsin A expression was also observed in 13.4% (20/149) of diffuse large B-cell lymphomas (DLBCL), 11.1% (15/134) of Hodgkin lymphomas, 4.9% (2/41) of follicular lymphomas, 6% (4/67) of peripheral T-cell lymphomas, and 3.8% (1/26) of plasma cell neoplasms. Otherwise, napsin A was not detected in any other types of lymphomas or histiocytic neoplasms. Napsin A expression in systemic ALCL was associated with a higher international prognostic index. ALCL and DLBCL patients with napsin A expression tended to have poor prognosis. Conclusion: These results demonstrated that napsin A is aberrantly expressed in a subset of lymphomas. The biological significance of napsin A in lymphomas warrants further study.
- PublicationOpen AccessPreterm birth and/or low birth weight are associated with periodontal disease and the increased placental immunohistochemical expression of inflammatory markers(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Pozo, Elena; Mesa, Francisco; Ikram, Mohamed H.; Puertas, Alberto; Torrecillas-Martínez, Laura; Ortega-Oller, Inmaculada; Magán-Fernández, Antonio; Rodríguez-Martínez, María Dolores; Padial-Molina, Miguel; Sánchez-Fernández, Elena; Galindo-Moreno, Pablo; O’Valle, FranciscoThe objective of this study was to determine whether gynecological and periodontal clinical parameters and the immunohistochemical expression in placental chorionic villi of the markers cyclooxygenase2 (COX-2), interleukin (IL)-1β, vascular endothelial growth factor receptor 1 (VEGFR1), podoplanin, and Heat Shock Protein (HSP70) are associated with preterm birth (PB) and/or low birth weight (LBW) neonates. Material and methods: An observational casecontrol study was performed in 130 puerperal women: mothers of PB/LBW neonates (cases, n=65) and mothers of full-term normal-weight neonates (controls, n=65). Data were gathered from all participants on sociodemographic, gynecological, and periodontal variables and on placental immunohistochemical COX-2, IL-1β, VEGFR1, podoplanin, and HSP70 expression. Results: Among the 42 women with mild/moderate periodontitis or gingivitis, the studied periodontal variables were significantly worse and the placental COX-2 (p=0.043), HSP70 (p=0.001), IL-1β (p=0.001), VEGFR1 (p=0.032), and podoplanin (p=0.058) expressions were significantly higher in the cases than in the controls. In comparison to the mothers without periodontitis, only COX-2 (p=0.026) and VEGFR1 (p=0.005) expressions were significantly increased in those with the disease. Increased COX-2 values were detected in the women with a history of genitourinary infection (p=0.036), premature rupture of membrane (p=0.012), or drug treatment (p=0.050). Conclusions: The etiology of preterm birth and/or low birth weight is multifactorial and involves consumption habits, social-health factors, and infectious episodes. These adverse pregnancy outcomes were associated with periodontitis and the increased placental expression of IL-1β, COX-2, VEGFR1, and HSP70.