Histology and histopathology Vol.23, nº2 (2008)

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http://hdl.handle.net/10201/177374

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Open Access
Human galectin-2: nuclear presence in vitro and its modulation by quiescence/stress factors
(2008) Dvoránková, B.; Smetana, K. Jr.; Lacina, L.; Lensch, M.; Manning, J.C.; André, S.; Gabius, H.J.
Open Access
The urokinase-system - role of cell proliferation and apoptosis
(Murcia : F. Hernández, 2008) Hildenbrand, Ralf; Gandhari, Mukesh; Stroebel, Philipp; Marx, Alexander; Allgayer, Heike; Arens, Norbert
The serine protease urokinase-type plasminogen activator (uPA) and its receptor (uPAR) are involved in the control of extracellular matrix turnover, cell migration, invasion and cell signalling leading to a variety of different responses, under both physiological and pathological conditions. The urokinase receptor, binding to the growth factor-like domain of uPA, directs membrane-associated extracellular proteolysis and signals through transmembrane proteins, thus regulating tissue regeneration, angiogenesis, cancer growth and metastasis. Since these physiological and pathophysiological processes of the uPA-system are known, less informations concerning uPA-induced cell proliferation and anti-apoptotic effects of the uPAsystem are available. Recent studies show a close relationship of the uPA-system and cell proliferation/ apoptosis. uPA is responsible for the activation and release of different growth factors and modulates the cell proliferation/apoptosis ratio through the dynamic control of cell-matrix interactions. This article focuses on the important role of the uPA/uPAR-system for cell proliferation and apoptosis.
Open Access
Immunohistochemical and in situ hybridization observations favor a local catecholamine production in the human Achilles tendon
(Murcia : F. Hernández, 2008) Bjur, Dennis; Danielson, Patrik; Alfredson, Hàkan; Forsgren, Sture
Results of recent studies using immunohistochemistry show evidence of an occurrence of catecholamine production in the cells (tenocytes) of patellar tendons exhibiting tendinopathy (tendinosis). In the present study, antibodies against the catecholaminesynthesizing enzyme tyrosine hydroxylase (TH) and a1- adrenoreceptors were applied to sections of specimens of normal and tendinosis Achilles tendons. In situ hybridization using a probe detecting human TH mRNA was also utilized. It was found that sympathetic innervation was very scarce. On the other hand, there were distinct a1-adrenoreceptor immunoreactions in blood vessel walls. Interestingly, tenocytes, particularly from tendinosis samples in which the tenocytes showed an abnormal shape (not the typical slender appearance), displayed TH immunoreactions and reactions for TH mRNA. Of further interest was the finding of a1- adrenoreceptor immunoreactions in tenocytes. The observations show not only evidence of local catecholamine production at the protein level, which was the case in recent studies for the patellar tendon, but also at the mRNA level. The observations suggest that the tenocytes, especially those with disfigured appearances in tendinosis, can produce catecholamines and also that they can respond to sympathetic transmitters. This is of interest as adrenergic stimulation in other parts of the body is known to induce degenerative/apoptotic and proliferative events, features which are seen in Achilles tendinosis. These observations are completely new findings concerning the human Achilles tendon. It is likely that locally produced catecholamines and the occurrence of autocrine/paracrine effects of these substances are of great relevance during the process of tendinosis.
Open Access
Therapeutic perspectives for the treatment of Huntington s disease, Treating the whole body
(Murcia : F. Hernández, 2008) Martin, Bronwen; Golden, Erin; Keselman, Alex; Stone, Matthew; Mattson, Mark P.; Egan, Josephine M.; Maudsley, Stuart
Huntington’s disease (HD) is a tremendously debilitating disorder that strikes relatively young individuals and progresses rapidly over the next ten to fifteen years inducing a loss of cognitive and motor skills and eventually death occurs. The primary locus of the disorder is a polyglutamine expansion of the protein product of the huntingtin (htt) gene. The htt protein appears to be a scaffolding protein that orchestrates the complex assembly of multiple intracellular proteins involved in multiple processes, including vesicular movement and cell metabolism. The htt protein is ubiquitously expressed in human tissues but the predominance of the interest in the pathology lies in its effects on the central nervous system (CNS). Most of the current therapeutics for HD thus have been targeted at preventing neuronal damage in the CNS, however, a considerable body of evidence has been accumulating to suggest that the maintenance of a healthy nervous system is tightly linked with peripheral physiological health. Therefore treatment of both the peripheral and central pathophysiologies of HD could form the basis of a more effective HD therapeutic strategy.
Open Access
Pathomechanism of entrapment neuropathy in diabetic and nondiabetic rats reared in wire cages
(Murcia : F. Hernández, 2008) Nishimura, Toshico; Hirata, Hitoshi; Tsujil, Masaya; Iida, Ryu; Hoki, Yoko; Iino, Takahiro; Ogawa, Satoru; Uchida, Atsumasa
To examine the pathomechanism of entrapment neuropathy associated with diabetes with special emphasis on the roles of mast cells and Tenascin- C using a rat model of Streptozotocin-induced diabetes. The roles of mast cells and Tenascin-C in development of tarsal tunnel syndrome were analyzed electrophysiologically and histologically in 20 male Ws/Ws-/-rats (mast cell deficient) and 20 of their male wild type counterparts (12-16 weeks old; 250-300g). Rats were assigned randomly to one of the following three groups; diabetic group and nondiabetic group reared in cages with a wire grid flooring; non-diabetic group in cages with sawdust covered plastic flooring. No significant role for mast cells in entrapment neuropathy was found in the rats with streptozotocin-induced diabetes. Distal latency was prolonged in diabetic rats compared with nondiabetic rats, and positively correlated with increases in blood glucose levels. Tenascin-C expression levels in the endoneurium at the tarsal tunnel in diabetic rats were found to be correlated with distal latency. The anti-alpha-smooth muscle actin (a-SMA) positive myofibroblast was scattered in nerve fascicles overexpressing Tenascin-C. It seems likely that Tenascin-C expressing myofibroblasts constrict axons by inducing collagen contraction of the endoneurium. Our data indicate that metabolic and phenotypic abnormalities of endoneurium and perineurum lie behind the vulnerability of diabetic patients to entrapment neuropathy.

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