Histology and histopathology Vol.25, nº7 (2010)

Ir a Estadísticas

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http://hdl.handle.net/10201/177693

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Open Access
Comparison of testis structure, function and thyroid hormone levels in control C57BL/6 mice and anti-mullerian hormone over expressing mice
(Murcia: F. Hernández, 2010) Chamindrani Mendis-Handagama, S.M.L.; Siril Ariyaratne, H.B.; Fecteau, Kellie A.; Grizzle, Judith M.; Jayasundera, Nilanthi K.
Anti-Mullerian hormone (AMH) is considered as a negative regulator of postnatal Leydig cell (LC) differentiation, because AMH over expressing mice (Mt-hAMH mice) testes are deficient in LC. Therefore, in the present study Mt-hAMH mice was used as a model to examine the process of postnatal LC differentiation. Testis structure-function studies were performed in age-matching Mt-hAMH and C57BL/6 (controls) mice; testicular components were quantified and circulating testosterone and thyroid hormone levels (thyroxine/T4 and triiodothyronine/T3; necessary for postnatal LC differentiation) were determined. Results revealed that Mt-hAMH mice were heavier and their testis weights were smaller compared to controls. Mast cells were present in Mt-AMH testis interstitium, but absent in controls. The absolute volumes of seminiferous tubules (ST), testis interstitium, LC and blood vessels per testis were lower and lymphatic space was higher in Mt-hAMH mice than in controls (p<0.05). The average cell LC volume and their number per testis, ST length, plasma testosterone, luteinizing hormone-stimulated testosterone secretion per testis and per LC in vitro, plasma T4 and T3 were significantly lower in Mt-hAMH mice compared to controls (p<0.05). Increased body weight in Mt-hAMH mice could be attributed to the reduced T4 and T3. Reduced testis weight in Mt-AMH mice is explained by the reduced ST volume in them. Reduced plasma testosterone, testicular and LC testosterone secretion in vitro in Mt-hAMH mice can be explained by the reduced number, size and steroidogenic potential of LC in Mt-hAMH mice. Study revealed several structure-function deficiencies in Mt-AMH mouse compared to controls, which were not documented in previous investigations. As hypothyroidism causes arrest in postnatal LC differentiation, it is suggested that the reduced LC number in Mt-hAMH testes could be at least in part due to their reduced thyroid hormone levels. However, latter concept needs to be further tested in future investigations.
Open Access
The effects of nitric oxide inhibition prior to kainic acid treatment on neuro- and gliogenesis in the rat dentate gyrus in vivo and in vitro
(Murcia: F. Hernández, 2010) Cosgrave, A. Siobhan; McKay, Jennifer S.; Morris, Richard; Quinn, John P.; Thippeswamy, Thimmasettappa
Treatment with the nitric oxide synthase (NOS) inhibitor, L-NAME prior to the induction of seizures with kainic acid (KA) [L-NAME+KA] increases the expression of activity-dependent neuroprotective protein (ADNP) in cells in the subgranular zone (SGZ) of the rat dentate gyrus 3-days after seizure induction (Cosgrave et al., 2009). Using the incorporation of BrdU we found that this protocol [LNAME+KA] stimulates neuro- and gliogenesis. By comparison, L-NAME or KA alone produced smaller effects. Doublecortin+ (BrdU negative) neuroblasts in the SGZ also significantly increased with L-NAME+KA treatment, suggesting that L-NAME+KA cause more cells to differentiate into neurons. L-NAME alone increased BrdU+ astrocytes in the hilus implying that NO inhibits stem cell differentiation into astrocytes and may also influence their migration. Although NOS inhibition increased cell proliferation in vivo and in vitro it disrupted cell clustering as revealed by ADNP immunoreactivity. In vitro KA treatment resulted in eccentric nuclei, reduced neurite extension and branching in neurons and retracted processes of glia cells, these changes were inhibited with prior treatment of L-NAME suggesting that KA-induced NO production affects cell morphology. Consequently, this data suggests an important role for NO in regulating stem cell proliferation and their fate in the SGZ.
Open Access
Claudin-7 protein differentiates canine cholangiocarcinoma from hepatocellular carcinoma
(Murcia : F. Hernández, 2010) Jakab, Cs.; Kiss, A.; Schaff, Z.; Szabó, Z.; Rusvai, M.; Gálfi, P.; Szabára, Á.; Sterczer, A.; Kulka, J.
The aim of the present study was to characterise the expression pattern of claudin-7 tight junction protein in canine normal liver, hyperplastic and primary neoplastic lesions of the canine liver and whether this tight junction protein can help differentiate canine cholangiocarcinomas from canine hepatocellular carcinomas. Methods and results: Necropsy samples included 15 canine normal liver tissue samples, 10 hepatocellular nodular hyperplasias, 6 hepatocellular adenomas, 15 well-differentiated and 6 poorly differentiated hepatocellular carcinomas, 6 cholangiocellular hyperplasias, 10 cholangiocellular adenomas, 15 well-differentiated and 6 poorly differentiated cholangiocarcinomas, 6 normal extrahepatic bile ducts, 8 normal gall bladder tissue samples, and 5 cystic mucinous hyperplasias of the gall bladder. In all canine normal liver tissue samples the hepatocytes were negative for claudin-7 and the normal biliary epithelial cells showed intense basolateral membrane claudin-7 positivity. In all cholangiocellular hyperplasia samples and in all cholangiocellular adenoma samples the benign cholangiocytes showed intense basolateral membrane positivity for claudin-7. In all samples of the well-differentiated and poorly differentiated cholangiocarcinomas, the malignant neoplastic biliary epithelial cells showed intense basolateral membrane positivity for claudin-7. Neither the hyperplastic nodules of the liver cells nor the hepatocellular adenomas reacted with claudin-7. The well-differentiated and poorly differentiated hepatocellular cancers were negative for claudin-7. The epithelial cells of canine normal extrahepatic bile ducts, gall bladder and cystic mucinous hyperplasias of the gall bladder showed intense basolateral membrane positivity for claudin-7. Differences in the intensity of claudin-7 reaction were not apparent among different types of proliferative lesions of cholangiocytes or degrees of cellular differentiation of neoplastic biliary epithelial cells. Conclusion: Consequently, we hypothesize that claudin-7 is an excellent immunohistochemical marker of the cholangiocellular differentiation in canines and can be used to detect benign and malignant proliferative lesions of the canine biliary tract. It can also help to differentiate canine cholangiocarcinomas from hepatocellular carcinomas.
Open Access
Primary cilia in fibroblast-like type B synoviocytes lie within a cilium pit, a site of endocytosis
(Murcia : F. Hernández, 2010) Rattner, Jerome B.; Sciore, Paul; Ou, Young; van der Hoorn, Frans A.; Lo, I.K.Y.
The synovium is a thin connective tissue that lines the joint space of free moving articulations. In this report, the expression, structure, and composition of non-motile (primary) cilia in fibroblast-like synoviocytes (FLS) that populate the synovium have been studied. Primary cilia are non-motile, microtubule-based organelles that have been found in a variety of vertebrate cell types. We document that primary cilia are expressed in normal human synovium FLS, cultured human FLS, and FLS cells present in human synovial fluid, and that the cellular region occupied by the primary cilium shows a similar and highly defined architecture within these FLS. This architecture includes the presence of a unique structure that surrounds the lower portion of the cilium shaft. This structure, given the term cilium-pit, includes a space, the pit reservoir. Actin filament bundles surround the cilium-pit, and when these bundles are removed experimentally the volume of the cilium-pit and its continuity with the extracellular environment changes. Finally, this study documents that the cilium-pit is a site of endocytosis and is also the site for the localization of receptors (TNF receptors TNFR1 and TNFR2) associated with synoviocyte function. Taken together, the results of the present study suggest that the FLS cilium-pit functions to regulate the exposure of the primary cilium, both spatially and temporally to extracellular molecules and to couple primary cilium based signaling pathways with those linked to endocytosis.
Open Access
Animal models for retinitis pigmentosa induced by MNU; disease progression, mechanisms and therapeutic trials
(Murcia : F. Hernández, 2010) Tsubura, A.; Yoshizawa, K.; Kuwata, M.; Uehara, N.
Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases in humans characterized by loss of photoreceptor cells leading to visual disturbance and eventually to blindness. A single systemic administration of N-methyl-N-nitrosourea (MNU) causes retinal degeneration in various animal species. The retinal degeneration is highly reproducible, and the photoreceptor cell loss occurs within seven days after MNU administration via apoptosis resembling human RP. Here, we describe the disease progression, disease mechanisms, and therapeutic trials of MNUinduced retinal degeneration.

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