Histology and histopathology Vol.21, nº 5 (2006)

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https://hdl.handle.net/10201/21274

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Lewis y antigen (CD174) and apoptosis in gastric and colorectal carcinomas, Correlations with clinical and prognostic parameters
(Murcia : F. Hernández, 2006) Baldus, S.E.; Mönig, S.P.; Zirbes, T.K.; Thakran, J.; Köthe, D.; Köppel, M.; Hanisch, F.G.; Thiele, J.; Schneider, P.M.; Hölscher, A.H.; Dienes, H.P.
Lewisy (Ley), also designated CD174, represents a carbohydrate blood group antigen which is strongly expressed in neoplastic gastrointestinal tissues. Previous reports indicated an association between Ley expression and apoptosis. Therefore, we tried to elucidate its clinicopathological relevance in a series of 160 gastric and 215 colorectal carcinomas by immunohistochemical detection of Ley and visualization of apoptotic cells applying the in-situ-end labelling (ISEL) method, followed by semiquantitative scoring of the specimens. In both gastric as well as colorectal carcinomas, between 40 and 50% of the cases were Ley reactive. Signet-ring cell carcinomas of the stomach exhibited a significantly stronger Ley expression compared to other tumor types. In colorectal cancers, Ley was associated with increased tumor staging, showing the strongest positivity in stage IV. Further correlations with clinicopathological variables or prognosis were not observed. On the other hand, the amount of apoptotic cells was significantly reduced in mucinous adenocarcinomas of the colorectum compared to non-mucinous carcinomas. Scoring of apoptotic cells did not result in any other clinicopathologically relevant correlations. In addition, a significant association between Ley antigen expression and apoptosis score could not be established. Therefore, the hypothesis of a functional relationship between these two aspects of gastrointestinal tumor biology is not confirmed by our data.
Open Access
Naris occlusion alters transductory protein immunoreactivity in olfactory epithelium
(Murcia : F. Hernández, 2006) Coppola, D.M.; Waguespack, A.M.; Reems, M.R.; Butman, M.L.; Cherry, J.A.
We have recently shown that unilateral naris occlusion (UNO) causes an increase in olfactory marker protein (OMP) immunoreactivity (IR) in mouse olfactory sensory neurons (OSN) from the occluded side of the nasal cavity and a decrease in OMP-IR on the non-occluded side, relative to controls. Given OMP's demonstrated role in olfactory modulation, these OMPIR changes have been interpreted as a compensatory response by OSNs to odor deprivation on the occluded side and to supernormal exposure to odor on the nonoccluded side of the nasal cavity. In the current study, we examined the developmental timing and the regional distribution of this process throughout the nasal cavity using immunocytochemistry. Results demonstrate that OMP-IR diverges in OSNs from the occluded side relative to the non-occluded side of the nasal cavity within eleven days after UNO, with statistically significant differences measurable after 17 days (n=16). We also measured relative levels of the Type 4 phosphodiesterase (PDE4A), another potential olfactory modulator, in nasal cavity tissue from UNO (n=8) and untreated mice (n=9) using western blots and immunocytochemistry. Like OMP, PDE4A-IR increased on the occluded side of the nasal cavity after UNO. Finally, we used immunocytochemistry to assess relative levels of olfactory-specific adenylyl cyclase (ACIII, n=4) and G-protein (Golf, n=2) in OSNs from the occluded and non-occluded sides of the nasal cavity of UNO mice. Following UNO, ACIII but not Golf -IR levels diverged comparing the occluded to the non-occluded sides of the nasal cavity. Taken together, our findings provide support for the previously unknown phenomenon of compensatory responses by OSNs to odor environment.
Open Access
Genetics of pigment cells, lessons from the tyrosinase gene family
(Murcia : F. Hernández, 2006) Murisier, F.; Beermann, Friedrich
In mammals, the melanin pigment is produced in two cell types of distinct developmental origins. The melanocytes of the skin originate form the neural crest whereas the retinal pigment epithelium (RPE) of the eye originates from the optic cup. The genetic programs governing these two cell types are thus quite different but have evolved to allow the expression of pigment cell-specific genes such as the three members of the tyrosinase-related family. Tyrosinase, Tyrp1 and Dct promoters contain a motif termed E-box which is bound by the transcription factor Mitf. These E-boxes are also found in the promoters of the corresponding fish genes, thus highlighting the pivotal role of Mitf in pigment cell-specific gene regulation. Mitf, which displays cell type-specific isoforms, transactivates the promoters of the tyrosinase gene family in both pigment cell lineages. However, specific DNA motifs have been found in these promoters, and they correspond to binding sites for RPE-specific factors such as Otx2 or for melanocyte-specific factors such as Sox10 or Pax3. The regulation of pigment cell-specific expression is also controlled by genetic elements located outside of the promoter, such as the tyrosinase distal regulatory element located at -15 kb which acts as a melanocytespecific enhancer but also protects from spreading of condensed chromatin. Thus, by using the tyrosinase gene family as a model, it is possible to define the transcription factor networks that govern pigment production in either melanocytes or RPE.
Open Access
Development and phenotypic characterization of a high density in vitro model of auricular chondrocytes with applications in reconstructive plastic surgery
(Murcia : F. Hernández, 2006) Haisch, A.; Marzahn, U.; Mobasheri, A.; Schulze-Tanzil, G.; Shakibaei, M.
Cultivation of phenotypically stable auricular chondrocytes will have applications in autologous chondrocyte transplantation and reconstructive surgery of cartilage. Chondrocytes grown in monolayer culture rapidly dedifferentiate assuming a fibroblast-like morphology and lose their cartilage-specific pattern of gene expression. Three-dimensional high-density culture models mimic more closely the in vivo conditions of cartilage. Therefore, this study was undertaken to test whether the high-density cultures might serve as a suitable model system to acquire phenotypically and functionally differentiated auricular chondrocytes from porcine cartilage. Freshly isolated porcine auricular chondrocytes were cultured for 7 passages in monolayer culture. From each passage (passage 0 and 1-7) cells were introduced to high-density cultures and examined by transmission electron microscopy. Western blotting was used to analyse the expression of cartilage-specific markers, such as collagen type II and cartilage specific proteoglycan, fibronectin, cell adhesion and signal transduction receptor ß1-integrin, matrix metalloproteinases (MMP-9, MMP-13), cyclo-oxygenase (COX)-2 and the apoptosis commitment marker, activated caspase-3. When dedifferentiated auricular chondrocytes from monolayer passages 0-4 were cultured in high-density culture, they recovered their chondrocytic phenotype and formed cartilage nodules surrounded by fibroblast-like cells and synthesised collagen type II, proteoglycans, fibronectin and ß1-integrins. However, chondrocytes from monolayer passages 5-7 did not redifferentiate to chondrocytes even when transferred to high-density culture, and did not synthesize a chondrocyte-specific extracellular matrix. Instead, they produced increasing amounts of MMP-9, MMP-13, COX-2, activated caspase-3 and underwent apoptosis. Three-dimensional high-density cultures may therefore be used to obtain sufficient quantities of fully differentiated auricular chondrocytes for autologous chondrocyte transplantation and reconstructive plastic surgery.
Open Access
Exercise-induced apoptosis in rat kidney is mediated by both angiotensin II AT1 and AT2 receptors
(Murcia : F. Hernández, 2006) Podhorska-Okolow, M.; Dziegiel, Piotr; Gomulkiewicz, A.; Kisiela, D.; Dolinska-Krajewska, B.; Jethon, Z.; Carraro, U.; Zabel, M.
Excessive physical exercise may lead to disturbance of the entire homeostasis in the body, including damage not only in skeletal muscles but also in many distant organs. The mechanisms responsible for the exercise-induced changes could include oxidative stress or angiotensin II. We previously showed that acute exercise led to apoptosis in kidney but not as a result of oxidative stress. In this study, we examined the role of angiotensin II and its AT1 and AT2 receptors in mediation of exercise-induced apoptosis in kidney. We clearly demonstrated that acute physical exercise induced apoptosis in renal cells of distal convoluted tubuli and cortical and medullary collecting ducts. Moreover, the cells displayed an increased expression of both AT1 and AT2 angiotensin II receptors and of p53 protein. The results suggest that angiotensin II could upregulate p53 expression in renal distal convoluted tubular cells and in the cells collecting ducts via both AT1 and AT2 receptors, which might be the crucial apoptosis-mediating mechanism in kidneys after excessive exercise.

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