Histology and histopathology Vol.29, nº 5 (2014)
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- PublicationOpen AccessMorphological and immunohistochemical evaluation of ganglion cysts. Cross-sectional study of 354 cases(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) O’Valle, Francisco; Hernández-Cortés, Pedro; Aneiros Fernández, José; Caba Molina, Mercedes; Gómez-Morales, Mercedes; Cámara, Miguel; Payá, Jorge A.; Aguilar, David; Del Moral, Raimundo G.; Aneiros, JoseThe aim of this study was to characterize the morphology and immunophenotype of ganglion cysts (GCs) and explore their histogenetic origin. Material and Methods: A cross-sectional morphological and immunohistochemical study of 354 GCs used the following antibody panel: vimentin, specific actin, ß- actin, smooth-muscle actin, smoothelin, h-caldesmon, ß- catenin, desmin, calponin, podoplanin, keratins 5/6, Ecadherin, cyclooxygenase 2 (COX-2), lysozyme, CD10, CD31, CD33, CD34, CD68, Ki-67, and PCNA. Doubleblind semi-quantitative analyses were conducted to evaluate the immunopositivity on a 4-point scale. Samples from 10 synovial membranes and 10 scapholunate ligaments were compared. GCs showed a hyalinized wall with mesenchymal spindle cells and were intensely positive for vimentin, actins, h-caldesmon, calponin in all cases and for podoplanin in 53% of cases, suggesting features of early muscle differentiation, without ruling out a myofibroblastic origin. Focal cavity lining of nonsynovial flat or raised cells (CD34/CD31/CD10/Ecadherin-negative and podoplanin-positive in 34% of cases) was detected in 93% of cases, showing differential expression with synovial membrane and scapholunate ligament cells. Nuclear positivity for proliferative markers was observed in GC wall cells (258.1±255; 1019.3±316 positive cells/mm2, Ki-67 and PCNA, respectively) but positivity for these markers was significantly lower (p<0.001 Mann Whitney U-test) in scapholunate ligament samples. Conclusion: In this first immunohistochemical study of GCs, focal cellular lining of the cavity was observed in almost all cases, and the immunophenotype was identical to that of GC wall cells. These cells are immunohistochemically different from synoviocytes and scapholunate ligament cells and show characteristics of myofibroblasts or mesenchymal cells undergoing early muscle differentiation.
- PublicationOpen AccessTubulointerstitial nephritis in systemic lupus erythematosus: innocent bystander or ominous presage(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Dhingra, Sadhna; Qureshi, Raza; Abdellatif, Abdul; Gaber, Lillian W.; Truong, Luan D.SLE-associated tubulointerstitial injury (SLE TIN) is increasingly recognized in two forms, i.e., secondary and primary. The secondary form coexists with lupus glomerulonephritis, whereas the primary form develops against the background of no or mild glomerular or vascular involvement. Secondary SLE TIN is frequent, but its frequency and severity correlate with the class of the associated lupus glomerulonephritis (GN), being almost universal in Class IV lupus GN and less frequent in GN of other classes. Although the presence of underlying GN may mask its clinical manifestation, secondary SLE TIN has a major prognostic implication for the renal outcome. Yet, SLE TIN is not factored in the current therapyfocused International Society of Nephrology/Renal Pathology Society schema of renal lupus classification, and its management remains to be elucidated. The pathogenesis of secondary SLE TIN is either immunologic, i.e., the tubulointerstitial injury being mediated by SLE-related immunologic mechanisms akin to those responsible for lupus GN; or non-immunologic, i.e., a nonspecific tubulointerstitial injury secondary to any type of advanced glomerular lesion, regardless of etiology. Primary SLE TIN is rare with about 15 reported cases. It has a rather uniform and distinctive clinical manifestation including acute kidney injury with no or mild proteinuria. It responds well to steroid and usually carries a good prognosis. Its pathogenesis is almost certain immunologic, with immunoglobulin/complement deposits along the tubular basement membrane in each reported case. In spite of these profound clinical implications, the current review underlies a limited knowledge on the pathobiology of SLE TIN.
- PublicationOpen AccessRedox dependence of endoplasmic reticulum (ER) Ca2+ signaling(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Raturi, Arun; Ortiz-Sandoval, Carolina; Simmen, ThomasThe endoplasmic reticulum (ER) is a multifunctional organelle that accommodates a large array of functions. Recent publications have shown that many of these functions are influenced by the ongoing oxidative folding of secretory and membrane proteins. Conversely, successful ER protein folding critically depends on the cellular redox state, but also the availability of Ca2+. These findings suggest the existence of regulatory mechanisms that steer ER Ca2+ homeostasis according to the cellular redox state. Indeed, accumulating evidence demonstrates that ER Ca2+ uptake and release by sarco-endoplasmic reticulum Ca2+ transport ATPases (SERCAs), stromal interaction molecule 1 (STIM1), Orai1, inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) and ryanodine receptors (RyR) depends on redox modifications of these channels and pumps. In addition, ER chaperones and oxidoreductases moonlight as regulators of ER Ca2+ channels and pumps. Discrete redox conditions of channels, pumps and oxidoreductases exist that allow for opening and closing. Through these functions, redox regulation of ER Ca2+ influences signaling mechanisms governing cell growth and migration, apoptosis and mitochondrial energy production. Therefore, pharmacological intervention based on ER redox or on ER redox-sensitive chaperones and oxidoreductases is a promising strategy to influence all metabolic syndromes including cancer and neurodegeneration.
- PublicationOpen AccessInfection through structured polymicrobial Gardnerella biofilms (StPM-GB)(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Swidsinsk, Alexander; Loening-Baucke, Vera; Mendling, Werner; Dörffel, Yvonne; Schilling, Johannes Schilling; Halwani, Zaher; Jiang, Xue-feng; Verstraelen, Hans; Swidsinski, SonjaBACKGROUND: We analysed data on bacterial vaginosis (BV) contradicting the paradigm of mono-infection. METHODOLOGY: Tissues and epithelial cells of vagina, uterus, fallopian tubes and perianal region were investigated using fluorescence in situ hybridization (FISH) in women with BV and controls. RESULTS: Healthy vagina was free of biofilms. Prolific structured polymicrobial (StPM) Gardnerella-dominated biofilm characterised BV. The intact StPM-Gardnerellabiofilm enveloped desquamated vaginal/prepuce epithelial cells and was secreted with urine and sperma. The disease involved both genders and occurred in pairs. Children born to women with BV were negative. Monotherapy with metronidazole, moxifloxacin or local antiseptics suppressed but often did not eradicate StPMGardnerella-biofilms. There was no BV without Gardnerella, but Gardnerella was not BV. Outside of StPM-biofilm, Gardnerella was also found in a subset of children and healthy adults, but was dispersed, temporal and did not transform into StPM-Gardnerella-biofilm. CONCLUSIONS: StPM-Gardnerella-biofilm is an infectious subject. The assembly of single players to StPM-Gardnerella-biofilm is a not trivial every day process, but probably an evolutionary event with a long history of growth, propagation and selection for viability and ability to reshape the environment. The evolutionary memory is cemented in the structural differentiation of StPM-Gardnerella-biofilms and imparts them to resist previous and emerging challenge