Histology and histopathology Vol.31,nº 11 (2016)
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- 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 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 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 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 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.