Histology and histopathology Vol.30, nº8 (2015)
Permanent URI for this collection
Browse
Browsing Histology and histopathology Vol.30, nº8 (2015) by Issue Date
Now showing 1 - 11 of 11
Results Per Page
Sort Options
- PublicationOpen AccessA novel proteotoxic stress associated mechanism for macular corneal dystrophy(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Kaarniranta, Kai; Szalai, Eszter; Smedowski, Adrian; Hegy, Zoltán; Kivinen, Niko; Viiri, Johanna; Wowra, Bogumil; Dobrowolski, Dariusz; Módis Jr, László; Berta, András; Wylegala, Edgar; Felszeghy, SzabolcsMacular corneal dystrophy is a rare autosomal recessive eye disease affecting primarily the corneal stroma. Abnormal accumulation of proteoglycan aggregates has been observed intra- and extracellularly in the stromal layer. In addition to the stromal keratocytes and corneal lamellae, deposits are also present in the basal epithelial cells, endothelial cells and Descemet's membrane. Misfolding of proteins has a tendency to gather into aggregating deposits. We studied interaction of molecular chaperones and proteasomal clearance in macular dystrophy human samples and in human corneal HCE-2 epithelial cells. Seven cases of macular corneal dystrophy and four normal corneal buttons collected during corneal transplantation were examined for their expression patterns of heat shock protein 70, ubiquitin protein conjugates and SQSTM1/p62. In response to proteasome inhibition the same proteins were analyzed by western blotting. Slitlamp examination, in vivo confocal cornea microscopy and transmission electron microscopy were used for morphological analyses. Heat shock protein 70, ubiquitin protein conjugates and SQSTM1/p62 were upregulated in both the basal corneal epithelial cells and the stromal keratocytes in macular corneal dystrophy samples that coincided with an increased expression of the same molecules under proteasome inhibition in the HCE-2 cells in vitro. We propose a novel regulatory mechanism that connects the molecular chaperone and proteasomal clearance system in the pathogenesis of macular corneal dystrophy.
- PublicationOpen AccessThe role of oxidative stress in corneal diseases and injuries(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Čejková, J.; Čejka, ČIn various corneal injuries (such as chemical burns or irradiation of corneas with UVB radiation) and ocular diseases (e.g. dry eye disease, keratokonus, bullous keratopathy, Fuchs’ endothelial dystrophy), the expressions of malondialdehyde (a marker of lipid peroxidation) and nitrotyrosine (a marker of oxidative stress) appeared in cells of individual corneal layers and conjunctival cells (dry eye disease). This is in contrast to healthy corneas in which negligible levels of malondialdehyde and no expressions of nitrotyrosine are present. The injured or diseased corneas reveal decreased capacity of antioxidants (enzymatic as well as non-enzymatic), whereas the levels of pro-oxidants (e.g. oxidases that generate reactive oxygen species) remain at physiological levels or even increase, leading to the antioxidant/prooxidant imbalance and oxidative stress. Oxidative stress in the cornea stimulates generation of pro-inflammatory cytokines, proteolytic enzymes and enzymes that generate nitric oxide (nitric oxide synthases). An abundant amout of reactive oxygen species and nitric oxide lead to the formation of toxic reactive products contributing to tissue damage. This review aims to summarize immunohistochemical changes in severe corneal injuries and diseases in which oxidative stress has been proved.
- PublicationOpen AccessNovel features of neurodegeneration in the inner retina of early diabetic rats(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Énzsöly, Anna; Szabó, Arnold; Szabó, Klaudia; Szél, Ágoston; Németh, János; Lukáts, ÁkosThe literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where diabetic degeneration preceded apoptotic loss of cells (Enzsöly et al., 2014). Here, we investigated the histopathology of the inner retina in early diabetes using the same specimens. We examined rat retinas with immunohistochemistry and Western blotting, 12 weeks after streptozotocin induction of diabetes. Glial reactivity was observed in all diabetic retinal specimens; however, it was not detectable all over the retina, but appeared in randomly arranged patches, with little or no glia activation in between. Similarly, immunoreactivity of parvalbumin (staining mostly AII amacrine cells) was also decreased only in some regions. We propose that these focal changes appear prior to affecting the whole retina and overt loss of cells. In contrast to these, most other markers used (calretinin, recoverin, tyrosin hydroxylase anti-Brn-3a and also calbindin in the optic part of the retina) did not show any major alterations in the intensity of immunoreactivity or in the number of stained elements. Interestingly, under diabetic conditions, the labeling pattern of PKC-α and calbindin in the ciliary retina showed a clear resemblance to the pattern described during development. This observation is in line with our previous study, reporting an increase in the number of dual cones, coexpressing two photopigments, which is another common feature with developing retinas. These data may indicate a previously uninvestigated regenerative capacity in diabetic retina
- PublicationOpen AccessMight the Masson trichrome stain be considered a useful method for categorizing experimental tendon lesions?(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Martinello, Tiziana; Pascoli, Francesco; Caporale, Giovanni; Perazzi, Anna; Iacopetti, Ilaria; Patruno, MarcoStrain injuries of tendons are the most common orthopedic injuries in athletic subjects, be they equine or human. When the tendon is suddenly damaged, an acute inflammatory phase occurs whereas its repetitive overloading may cause chronic injuries. Currently the criteria used for grading injuries are general and subjective, and therefore a reliable grading method would be an improvement. The main purpose of this study was to assess qualitatively the histological pattern of Masson trichrome stain in healthy and injured tendons; indeed, the known “paradox” of Masson staining was used to create an evaluation for the matrix of tendons, following experimental lesions and natural repair processes. A statistically significant difference of aniline-staining between healthy and lesioned tendons was observed. Overall, we think that the Masson staining might be regarded as an informative tool in discerning the collagen spatial arrangement and therefore the histological characteristics of tendons.
- PublicationOpen AccessThymic alterations induced by partial hepatectomy: upregulation of glycoprotein 96, CD91 and TLR2 and generation of regulatory T cells(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Jakovac, Hrvoje; Ćuk, Mira; Trobonjača, Zlatko; Mrakovčić-Šutić, Ines; Radošević-Stašić, BiserkaGlycoprotein 96 (gp96) is an endoplasmic reticulum (ER)-resident heat shock protein. It controls the folding of nascent membrane-spanning and secretory proteins, participates in stress-induced unfolded protein response (UPR) and in pathways leading to proteolysis of damaged proteins through ER-associated degradation pathways and chaperone-mediated autophagy. In addition, gp96 controls the steroid biosynthesis and Ca2+ homeostasis and participates in insulin-IGF/signaling pathways. Besides, owing to its peptide chaperone capacity and ability to interact with antigen-presenting cells, gp96 has been implicated in priming of innate and adaptive immunity. In an attempt to visualize the intensity of ER-stress in thymus and possible participation of gp96 in generation of auto-reactive T cell clones that were detected in regenerating liver, in this study we investigated the dynamics of gp96 expression in partially hepatectomized (pHx) and sham Hx mice. Simultaneously, we detected the thymic expression of receptors responsible for endocytosis of gp96- chaperoned peptides (CD91) and intracellular activation of ER-stress pathways (TLR2), as well as the expression of TGF-β and the distribution of CD4+CD25+FoxP3+ cells. The data have shown that both pHx and sham Hx induced an accelerated apoptosis and hypoplasia in thymus. Partial Hx induced, however, a higher expression of gp96, the translocation of the CD91, TLR2 and TGF-β immunostaining from medulla to cortex and an appearance of Treg cells. The data show that pHx triggers in thymus the ERstress and UPR response and suggest that gp96 participates in the generation of natural Treg cells, which might be involved in the control of liver regeneration in the periphery.
- PublicationOpen AccessSkin innervation: important roles during normal and pathological cutaneous repair(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Laverdet, Betty; Danigo, Aurore; Girard, Dorothée; Magy, Laurent; Demiot, Claire; Desmoulière, AlexisThe skin is a highly sensitive organ. It is densely innervated with different types of sensory nerve endings, which discriminate between pain, temperature and touch. Autonomic nerve fibres which completely derive from sympathetic (cholinergic) neurons are also present. During all the phases of skin wound healing (inflammatory, proliferative and remodelling phases), neuromediators are involved. Several clinical observations indicate that damage to the peripheral nervous system influences wound healing, resulting in chronic wounds within the affected area. Patients with cutaneous sensory defects due to lepromatous leprosy, spinal cord injury and diabetic neuropathy develop ulcers that fail to heal. In addition, numerous experimental observations suggest that neurogenic stimuli profoundly affect wound repair after injury and that delayed wound healing is observed in animal models after surgical resection of cutaneous nerves. All these observations clearly suggest that innervation and neuromediators play a major role in wound healing. Interactions between neuromediators and different skin cells are certainly crucial in the healing process and ultimately the restoration of pain, temperature, and touch perceptions is a major challenge to solve in order to improve patients’ quality of life.
- PublicationOpen AccessN-Cadherin, ADAM-10 and Aquaporin 1 expression in lung tissue exposed to fluoroedenite fibers: an immunohistochemical study(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Musumeci, Giuseppe; Loreto, Carla; Szychlinska, Marta Anna; Imbesi, Rosa; Rapisarda, Venerando; Aiello, Flavia Concetta; Castorina, Sergio; Castrogiovanni, PaolaFluoro-edenite (FE) fibers are similar to other amphibole asbestos fibers. The scientific relevance of FE is due to its ability to lead to chronic inflammation and carcinogenesis in lung tissue shown after its inhalation. These fibers stimulate aberrant host cell proliferation and induce the release of cytokines, growth factors, reactive oxygen and nitrite species, which results in DNA damage. In previous studies, we showed that FE induces functional modifications in sheep and human lung fibroblasts and alveolar epithelial cells, where the overexpression of several molecules probably involved in pathological cellular mechanisms induced by FE exposition have been detected. However, the mechanisms of cellular and molecular toxicity and the cellular response to FE fibers are still not well known. N-cadherin, ADAM-10 and AQP1 are molecules involved in carcinogenesis and in inflammatory process. In this study we analyzed, through immunohistochemistry, their expression in the lung tissue of sheep exposed to FE. Our results showed different patterns of immunolabeling for N-cadherin, ADAM-10 and AQP1. N-cadherin and ADAM-10 were more expressed in FE exposed lung tissue, when compared with the control. On the contrary, AQP1 was more expressed in non exposed lung tissue. These results suggest that NCadherin, ADAM-10 and AQP1 are probably involved in different pathological processes induced by FE fiber exposition. The aim of the study was to better understand the mechanisms of cellular and molecular toxicity and of cellular response to FE fibers in order to identify, in the future, a possible therapeutic intervention in cases of FE-associated pathogenesis.
- PublicationOpen AccessComplex and elementary histological scoring systems for articular cartilage repair(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Orth, Patrick; Madry, HenningThe repair of articular cartilage defects is increasingly moving into the focus of experimental and clinical investigations. Histological analysis is the gold standard for a valid and objective evaluation of cartilaginous repair tissue and predominantly relies on the use of established scoring systems. In the past three decades, numerous elementary and complex scoring systems have been described and modified, including those of O’Driscoll, Pineda, Wakitani, Sellers and Fortier for entire defects as well as those according to the International Cartilage Repair Society (ICRS-I/II) for osteochondral tissue biopsies. Yet, this coexistence of different grading scales inconsistently addressing diverse parameters may impede comparability between reported study outcomes. Furthermore, validation of these histological scoring systems has only seldom been performed to date. The aim of this review is (1) to give a comprehensive overview and to compare the most important established histological scoring systems for articular cartilage repair, (2) to describe their specific advantages and pitfalls, and (3) to provide valid recommendations for their use in translational and clinical studies of articular cartilage repair.
- PublicationOpen AccessDifferential microscopic finding and glucose transporter 3 expression in terminal chorionic villi among birth weight-discordant twin placentas(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Lee, Mina; Choi, Song-Yi; Kang, Byung-Hun; Yoo, Heon-Jong; Song, Soo-Youn; Seong, In-Ock; Suh, Kwang-Sun; Kim, Kyung-HeeObjective: To evaluate differences in microscopic findings and glucose transporter 3 (GLUT3) expression in terminal chorionic villi (TV) among birth weight-discordant twin (BWDT) placentas compared with the birth weight-concordant twin (BWCT) placentas. Methods: We retrospectively studied a cohort of 26 BWDT, 10 BWCT, 10 pre-eclampsia singleton and 10 normal singleton pregnancies. Placentas were scored for the percentage of TV, the percentage of TV with syncytial knots, the presence of capillary branching patterns of TV, the capillary to terminal villous ratios, the membranous expression of GLUT3 and the nuclear expression of HIF-1α in trophoblasts and capillary endothelial cells of TV using immunohistochemistry. The clinical characteristics and microscopic findings were analyzed and compared. Results: BWDT placentas exhibited differential percentages of TV, percentages of TV with syncytial knots, capillary to terminal villous ratios, expression of HIF-1α in capillary endothelial cells and expression of GLUT3 in trophoblasts and capillary endothelial cells of TV among each twin pair compared with BWCT placentas (P=0.003, P=0.022, P=0.037, P=0.007, P=0.046 and P=0.002, respectively). Pre-eclampsia singleton placentas exhibited higher GLUT3 expression in trophoblasts, higher HIF-1α expression in capillary endothelial cells of TV and high capillary to terminal villous ratios compared with normal singleton placentas (P=0.001, P<0.001 and P=0.001, respectively). Conclusions: We observed a strong relationship between characteristics of adaptive change to hypoxia (GLUT3 expression, TV and syncytial knotting and higher capillary to terminal villous ratios) and BWDT pregnancy but not BWCT pregnancy.
- PublicationOpen AccessWhat understanding tendon cell differentiation can teach us about pathological tendon ossification(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Magne, D.; Bougault, C.Tendons are the structures that attach muscles to bones and transmit mechanical forces. Tendon cells are composed of mature tenocytes and a rare population of tendon stem cells. Both cell types ensure homeostasis and repair of tendon extracellular matrix to guarantee its specific mechanical properties. Moreover, tendon cells seem to present a marked potential for trans-differentiation, predominantly into the chondrocyte and osteoblast lineages. In this review article, we first present chronic tendon pathologies associated with abnormal ossification, such as spondyloarthritis and calcifying tendinopathy, and discuss how tendon cell differentiation and transdifferentiation may participate in these diseases. We moreover present the factors known to influence tendon cell differentiation and trans-differentiation, with a particular emphasis on extracellular environment, mechanical stimulation and several soluble factors that can tip the balance toward one or another lineage. A better understanding of the neglected tendon cell biology may be extremely useful to understand the pathological mechanisms of spondyloarthritis and calcifying tendinopathy.
- PublicationOpen AccessExpression of desmosomal proteins in acantholytic squamous cell carcinoma of the skin(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Jurčić, Vesna; Kukovič, Jernej; Zidar, NinaAcantholytic (adenoid) squamous cell carcinoma (ASCC) is a subtype of squamous cell carcinoma (SCC) in which neoplastic tumour cells form gland-like structures. Little is known about the pathogenetic mechanisms of ASCC. We hypothesised that they may be related to the compositon of desmosomes. We analysed the immunohistochemical expression of desmosomal proteins in 5 cases of ASCC of the skin, in comparison to 5 cases of conventional SCC of the skin. The most consistent findings were loss of desmoglein 1 (DSG 1), desmoglein 3 (DSG3), desmocollin 1 (DSC1), desmocollin 2 (DSC2), desmocollin 3 (DSC 3), and plakophilin 1 (PKP 1), and decreased expression of desmoplakin 1 (DP 1) and plakoglobin (PG). In conventional well to moderately differentiated SCC, the expression of desmosomal proteins was decreased, but membranous staining was mostly preserved with patterns similar to normal epidermis. Our results suggest that loss of desmosomal cadherins and decreased expression of desmosomal plaque proteins might be responsible for the formation of gland-like structures in ASCC. It seems that desmosomal cadherins, which correspond to the transmembrane core of desmosomes, are predominantly affected in ASCC, while DP 1 and PG, which correspond to cytoplasmic plaque of desmosomes, probably play a lesser role in maintenance of tumour cell cohesion. Our results also indicate that, in addition to previously described verrucous and spindle cell carcinoma, ASCC is another subtype of SCC with a characteristic expression pattern of desmosomal proteins.