Histology and histopathology Vol.29, nº 6 (2014)
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- PublicationOpen AccessMesenchymal stem cell - based tissue engineering strategies for repair of articular cartilage(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Ahmed, Tamer A.E.; Hincke, Maxwell T.Restoration of articular cartilage function and structure following pathological or traumatic damage is still considered a challenging problem in the orthopaedic field. Currently, tissue engineering-based reconstruction of articular cartilage is a feasible and continuously developing strategy to restore structure and function. Successful articular cartilage tissue engineering strategy relies largely on several essential components including cellular component, supporting 3D carrier scaffolding matrix, bioactive agents, proper physical stimulants, and safe gene delivery. Designing the right formulations from these components remain the main concern of the orthopaedic community. Utilization of mesenchymal stem cells (MSCs) for articular cartilage tissue engineering is continuously increasing compared to use of chondrocytes. Various sources of MSCs have been investigated including adipose tissue, amniotic fluid, blood, bone marrow, dermis, embryonic stem cells, infrapatellar fat pad, muscle, periosteum, placenta, synovium, trabecular bone, and umbilical cord. MSCs derived from bone marrow and umbilical cord are currently in different phases of clinical trials. A wide range of matrices have been investigated to develop tissue engineering - based strategies including carbohydrate-based scaffolds (agarose, alginate, chitosan/chitin, and hyaluronate), protein-based scaffolds (collagen, fibrin, and gelatin), and artificial polymers (polyglycolic acid, polylactic acid, poly(lacticco-glycolic acid), polyethylene glycol, and polycaprolactone). Collagen - based scaffolds and photopolymerizable PEG - based scaffolds are currently in different phases of clinical trials. TGF-ß1, TGF-ß3, BMP-2, and hypoxic environment are the recommended bioactive agents to induce optimum chondrogenesis of MSCs, while TGF-ß1, TGF-ß3, SOX-9, BMP-2, and BMP-7 genes are the best candidate for gene delivery to MSCs. Electromagnetic field and the combination of shear forces/dynamic compression are the best maturation-promoting physical stimulants.
- PublicationOpen AccessGASC1 expression in lung carcinoma is associated with smoking and prognosis of squamous cell carcinoma(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Uimonen, Katri; Merikallio, Heta; Pääkkö, Paavo; Harju, Terttu; Mannermaa, Arto; Palvimo, Jorma; Kosma, Veli-Matti; Soini, YlermiGASC1 (gene amplified in squamous cell carcinoma 1) encodes a nuclear protein that epigenetically catalyses the lysine demethylation of histones. We investigated the expression of GASC1 in different histological subtypes of lung cancer (n=289). Percentage value of GASC1 immunohistochemical expression was evaluated separately in the nuclei and cytoplasms of epithelial cancer cells. The results were compared with clinicopathologic factors and the smoking history of the patients. In lung tumor cells, 38% of nuclei and 54% of the cytoplasms stained positive for GASC1. Adenocarcinomas expressed more GASC1 nuclear (p=0.00011) and cytoplasmic (p=0.00074) positivity than squamous cell carcinoma. Smokers displayed less nuclear and cytoplasmic GASC1 expression than non-smokers (p=0.028 and p=0.036, respectively). Similarly, patients with more cytoplasmic positive staining had fewer pack years (p=0.043). Nuclear GASC1 expression had an impairing effect on survival when all histological lung cancer types were analysed together (p=0.039) and separately in squamous cell lung carcinoma (p=0.016). The results reveal that GASC1 expression is higher in adenocarcinoma than squamous cell carcinoma. Smoking decreases GASC1 expression in tumor cells, indicating that tobacco smoke may influence the methylation of histone 3 lysine residues in lung cancer. Nonetheless, nuclear GASC1 predicts a poor prognosis, especially in squamous cell carcinoma.
- PublicationOpen AccessAdvantages of exercise in rehabilitation, treatment and prevention of altered morphological features in knee osteoarthritis. A narrative review(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Musumeci, Giuseppe; Loreto, Carla; Imbesi, Rosa; Trovato, Francesca Maria; Di Giunta, Angelo; Lombardo, Claudia; Castorina, Sergio; Castrogiovann, PaolaKnee osteoarthritis (OA) represents one of the most common causes of disability in the world. It leads to social, psychological and economic costs with financial consequences, also because a further increase is expected. Different knee OA treatments are usually considered in relation to the stage of the disease, such as surgical management and pharmacologic and nonpharmacologic treatments. Treatment should begin with the safest and least invasive one, before proceeding to more invasive, expensive ones. Non-pharmacologic, behavioral treatments of knee OA are recommended not only in rehabilitation but also in prevention because many risk factors, such as excess weight, obesity and joint tissue inflammation, can be monitored and thus prevented. In the present review, we analyze data from the most recent literature in relation to the effects of physical exercise on prevention, therapy and rehabilitation in knee OA. All data suggest that physical exercise is an effective, economical and accessible tool to everyone, in the treatment and prevention of knee OA. The literature search was conducted on PubMed, Scopus and Google Scholar using appropriate keywords in relation to knee osteoarthritis.
- PublicationOpen AccessDental stem cells - characteristics and potential(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Bojic, Sanja; Volarevic, Vladislav; Ljujic, Biljana; Stojkovic, MiodragSoft dental tissues have been identified as easily accessible sources of multipotent postnatal stem cells. Dental stem cells are mesenchymal stem cells (MSC) capable of differentiating into at least three distinct cell lineages: osteo/odontogenic, adipogenic and neurogenic. They express various markers including those specific for MSC, embryonic stem cells and neural cells. Five different types of dental stem cells have been isolated from mature and immature teeth: dental pulp stem cells, stem cells from exfoliated deciduous teeth, periodontal ligament stem cells, stem cells from apical papilla and dental follicle progenitor cells. Dental stem cells may be used in dental tissue engineering including dental, enamel and periodontal tissue regeneration. They could also be used as a promising tool in potential treatment of neurodegenerative, ischemic and immune diseases.
- PublicationOpen AccessThe PI3K/Akt and MAPK-ERK1/2 pathways are altered in STZ induced diabetic rat placentas(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Ozmen, Aslı; Unek, Gozde; Kipmen-Korgun, Dijle; Turkay Korgun, EminDiabetic pregnancy is associated with complications such as early and late embryonic death, fetal growth disorders, placental abnormalities, and embryonal-placental metabolic disorders. Excessive apoptosis and/or changes of proliferation mechanisms are seen as a major event in the pathogenesis of diabetesinduced embryonic death, placental weight and structural anomalies. Akt and ERK1/2 proteins are important for placental and fetal development associated with cellular proliferation and differentiation mechanisms. The mechanism underlying the placental growth regulatory effects of hyperglycemia have not been elucidated. Moreover, it is still not determined how Akt and ERK1/2 proteins related proliferation and apoptosis mechanisms are influenced by Streptozotocin (STZ) induced diabetic rat placental development. The aim of this study was to investigate the expression levels and spatio-temporal immunolocalizations of Akt, p-Akt, ERK1/2 and p-ERK1/2 proteins in normal and STZ-treated diabetic rat placental development. In order to compose the diabetic group, pregnant females were injected with a single dose of 40mg/kg STZ intraperitonally seven days before their sacrifice at 12th, 14th, 16th, 18th and 20th day of their gestation. We found that maternal diabetic environment led to a decrease in ERK1/2 and Akt phosphorylation during rat placental development. It could be said that MAPK ERK1/2 and PI3K/Akt cell signaling pathways are affected from hyperglycemic conditions in rat placentas. In conclusion, hyperglycemia-induced placental and embryonal developmental abnormalities could be associated with reduction of Akt and ERK1/2 phosphorylation.
PublicationMetadata onlyAltered distribution of extracellular matrix proteins in the periodontal ligament of periostin-deficient mice(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Tabata, Chihiro; Hongo, Hiromi; Sasaki, Muneteru; Hasegawa, Tomoka; Luiz de Freitas, Paulo Henrique; Yamada, Tamaki; Yamamoto, Tomomaya; Suzuki, Reiko; Yamamoto, Tsuneyuki; Oda, Kimimitsu; Li, Minqi; Kudo, Akira; Iida, Junichiro; Amizuka, NorioVerifying whether periostin affects the distribution of type I collagen, fibronectin and tenascin C in the periodontal ligament (PDL) is important to contribute to a more thorough understanding of that protein’s functions. In this study, we have histologically examined incisor PDL of mandibles in 20 week-old male wild-type and periostin-deficient (periostin-/-) mice, by means of type I collagen, fibronectin, tenascin C, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)-1 and F4/80-positive monocyte/ macrophage immunostaining, transmission electron microscopy and quantitative analysis of cell proliferation. Wild-type PDL featured well-arranged layers of collagen bundles intertwined with PDL cells, whose longitudinal axis ran parallel to the collagen fibers. However, cells in the periostin-/- PDL were irregularly distributed among collagen fibrils, which were also haphazardly arranged. Type I collagen and fibronectin reactivity was seen throughout the wild-type PDL, while in the periostin-/- PDL, only focal, uneven staining for these proteins could be seen. Similarly, tenascin C staining was evenly distributed in the wildtype PDL, but hardly seen in the periostin-/- PDL. MMP1 immunoreactivity was uniformly distributed in the wild-type PDL, but only dotted staining could be discerned in the periostin-/- PDL. F4/80-positive monocyte/macrophages were found midway between tooth- and bone-related regions in the wild-type PDL, a pattern that could not be observed in the periostin-/- PDL. In summary, periostin deficiency may not only cause PDL collagen fibril disorganization, but could also affect the distribution of other major extracellular matrix proteins such as fibronectin and tenascin C.- PublicationOpen AccessImmunohistochemistry of connexin43 and zonula occludens-1 in the myocardium as markers of early ischemia in autopsy material(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Kawamoto, Osamu; Michiue, Tomomi; Ishikawa, Takaki; Maeda, HitoshiImmunohistochemistry of the terminal complement complex (C5b-9) and fibronectin (FN) is useful to detect myocardial ischemia preceding necrosis in the postmortem diagnosis of sudden cardiac death. The present immunohistochemical study examined connexin43 (Cx43) and zonula occludens-1 (ZO-1) as markers of early myocardial ischemia in addition to the above-mentioned markers, using forensic autopsy cases of acute deaths due to myocardial infarction (MI, n=15) and acute ischemic heart disease (AIHD) without apparent myocardial necrosis (n=8), compared with those of acute mechanical asphyxiation (As, n=24) and drowning (D, n=10) as controls. Immunopositivities of each marker in the myocardium were semi-quantitatively graded by scoring. ZO-1, C5b-9 and FN were detected in the myocardial cytoplasm, whereas Cx43 and nonphosphorylated (np) Cx43 showed varied localizations at the intercalated disc, in the cytoplasm and along the lateral cell border. ZO-1 and FN showed a tendency to be detected more intensely in MI and IHD than in As and D. C5b-9 showed specific staining at the site of ischemia in MI (n=10/15) and AIHD (n=6/8), while the distribution of npCx43 was different in most cases of MI (n=14/15) and AIHD (n=5/8), compared with As and D; npCx43 positivity score was higher in the cytoplasm than at the intercalated disc, indicating redistribution due to myocardial ischemia. Such findings were detected in a few cases of As (n=3/24). These findings suggest that the combination of npCx43 and C5b-9 immunohistochemistry is useful for detecting early lesions of myocardial ischemia in sudden cardiac death.
- PublicationOpen AccessExpression of Drebrin, an actin binding protein, in basal cell carcinoma, trichoblastoma and trichoepithelioma(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Mizutani, Yoko; Iwamoto, Ikuko; Kanoh, Hiroyuki; Seishima, Mariko; Nagata, Koh-ichiDrebrin, an F-actin binding protein, is known to play important roles in cell migration, synaptogenesis and neural plasticity. Although drebrin was long thought to be specific for neuronal cells, its expression has recently been reported in non-neuronal cells. As for skin-derived cells, drebrin was shown to be enriched at adhering junctions (AJs) in cultured primary keratinocytes and also be highly expressed in basal cell carcinoma (BCC) cells. Since BCC and two types of benign neoplasm, trichoblastoma and trichoepithelioma, are considered to derive from the same origin, follicular germinative cells, it is sometimes difficult to morphologically distinguish BCC from trichoblastoma and trichoepithelioma. In this study, we performed immunohistochemical staining of drebrin in BCC, trichoblastoma and trichoepithelioma, to examine whether drebrin could serve as a biomarker for BCC diagnosis. In western blotting, drebrin was detected highly and moderately in the lysates from a squamous cell carcinoma cell line, DJM-1, and normal human epidermis, respectively. In immunofluorescence analyses, drebrin was colocalized with markers of AJs and tight junctions in DJM-1 cells and detected at cellcell junction areas of human normal epidermis tissue. We then examined the distribution patterns of drebrin in BCC, trichoblastoma and trichoepithelioma. In BCC tissues, intense and homogeneous drebrin expression was observed mainly at tumor cell-cell boundaries. In contrast, drebrin was stained only weakly and nonhomogeneously in trichoblastoma and trichoepthelioma tissue samples. For differential diagnosis of BCC, drebrin may be a novel and useful marker.
- PublicationOpen AccessCurrent trends in stem cell therapy for improvement of bone quality(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Yamada, Yoichi; Nakamura, Sayaka; Klein, Ophir D.As the average lifespan of humans continues to increase, improvement in the quality of life for elderly people is important. Among the most severe problems during aging are bone loss-associated diseases such as poor fracture healing and osteoporosis. Therapy-induced bone loss such as bisphosphonate-associated osteonecrosis of the jaw also increases in incidence with age. Most of the current treatment strategies are focused on antiresorptive and bone formation pharmacological agents, but it is hard to obtain appropriate bone augmentation and there are concerns regarding their long-term safety without side effects. Therefore, a novel method for improvement of bone quality is required, and stem cells are of great interest as potential therapeutic tools for diseases that remain without clinically effective therapies. In this review, we describe the concept of stem cell-based therapy and evaluate the current progress of cell therapy for the improvement of bone quality. In addition, we report and discuss a new clinical strategy in which improved bone quality was obtained by applying bone-marrow derived MSCs with platelet rich plasma in clinical therapy.
- PublicationOpen AccessChronic administration of thiamine pyrophosphate decreases age-related histological atrophic testicular changes and improves sexual behavior in male Wistar rats(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Hernández-Montiel, H. L.; Vásquez López, C. M.; González-Loyola, J. G.; Vega-Anaya, G. C.; Villagrán-Herrera, M. E.; Gallegos-Corona, M. A.; Saldaña, C.; Ramos Gómez, M.; García Horshman, P.; García Solís, P.; Solís-S, J. C.; Robles-Osorio, M. L.; Ávila-Morales, J.; Varela-Echavarría, A.; Paredes Guerrero, R.Aging is a multifactorial universal process and constitutes the most important risk factor for chronic-degenerative diseases. Although it is a natural process, pathological aging arises when these changes occur quickly and the body is not able to adapt. This is often associated with the generation of reactive oxygen species (ROS), inflammation, and a decrease in the endogenous antioxidant systems, constituting a physiopathological state commonly found in chronicdegenerative diseases. At the testicular level, aging is associated with tissue atrophy, decreased steroidogenesis and spermatogenesis, and sexual behavior disorders. This situation, in addition to the elevated generation of ROS in the testicular steroidogenesis, provides a critical cellular environment causing oxidative damage at diverse cellular levels. To assess the effects of a reduction in the levels of ROS, thiamine pyrophosphate (TPP) was chronically administered in senile Wistar rats. TPP causes an activation of intermediate metabolism routes, enhancing cellular respiration and decreasing the generation of ROS. Our results show an overall decrease of atrophic histological changes linked to aging, with higher levels of serum testosterone, sexual activity, and an increase in the levels of endogenous antioxidant enzymes in TPP-treated animals. These results suggest that TPP chronic administration decreases the progression of age-related atrophic changes by improving the intermediate metabolism, and by increasing the levels of antioxidant enzymes.