Lymph and Blood Enzymes and Pathologic Alterations in Canine Experimental Pancreatitis after Administration of Benzo-Pyrones

Bartoš,; Kolc, J; Vanĕcek, R; Málek, P.

doi:10.3109/00365527909179894

Cited by 6 publications

(3 citation statements)

References 10 publications

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“…Immuno‐nanogold electron microscopy showed that T1α/podoplanin is predominantly localized to the apical, luminal plasma membrane of intestinal lymphatic endothelial cells. This localization is similar to that reported for other cell types (Dobbs et al ., 1988; Rishi et al ., 1995; Williams et al ., 1996; Breiteneder‐Geleff et al ., 1997; Zimmer et al ., 1997) and is compatible with a protective function towards the proteinase‐containing lymph (Bartos et al ., 1979). It is of interest that T1α/podoplanin is also expressed by alveolar epithelial cells, cells of the choroid plexus, ependymal epithelia and mesothelia that are also exposed to an external or internal fluid compartment.…”

Section: Discussionmentioning

confidence: 99%

“…In vivo expression of T1a/ podoplanin in lymphatic endothelium was ®rst reported by Wetterwald et al (1996), who named it `E11 antigen'. It was characterized further under the name `podoplanin', because of its low level expression in kidney podocytes (Breiteneder-Geleff et al, 1997). Podoplanin is homologous to T1a, which was originally found to encode an antigen that is selectively expressed at the apical surface of alveolar type I cells in rat lung (Dobbs et al, 1988;Rishi et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

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T1 /podoplanin deficiency disrupts normal lymphatic vasculature formation and causes lymphedema

et al. 2003

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V.Schacht and M.I.Ramirez contributed equally to this workWithin the vascular system, the mucin-type transmembrane glycoprotein T1a/podoplanin is predominantly expressed by lymphatic endothelium, and recent studies have shown that it is regulated by the lymphatic-speci®c homeobox gene Prox1. In this study, we examined the role of T1a/podoplanin in vascular development and the effects of gene disruption in mice. T1a/podoplanin is ®rst expressed at around E11.0 in Prox1-positive lymphatic progenitor cells, with predominant localization in the luminal plasma membrane of lymphatic endothelial cells during later development. T1a/podoplanin ±/± mice die at birth due to respiratory failure and have defects in lymphatic, but not blood vessel pattern formation. These defects are associated with diminished lymphatic transport, congenital lymphedema and dilation of lymphatic vessels. T1a/podoplanin is also expressed in the basal epidermis of newborn wild-type mice, but gene disruption did not alter epidermal differentiation. Studies in cultured endothelial cells indicate that T1a/podoplanin promotes cell adhesion, migration and tube formation, whereas small interfering RNA-mediated inhibition of T1a/podoplanin expression decreased lymphatic endothelial cell adhesion. These data identify T1a/podoplanin as a novel critical player that regulates different key aspects of lymphatic vasculature formation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

T1 /podoplanin deficiency disrupts normal lymphatic vasculature formation and causes lymphedema

et al. 2003

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“…Like the experimental data of Schiller et al [24], Konstantinov and Jantschulev [11] and Bartos et al [2], clinical reports on tho racic duct drainage have been conflicting in contrast to the results of Brzek and Bartos [3] and Pikovsky and Alexeev [19]. Harlan Stone et al [7] had to terminate a clinical trial of thoracic duct drainage because of an unacceptable high rate of mortality.…”

Section: Discussionmentioning

confidence: 48%

Pathways of Enzyme Transfer in Sodium Taurocholate-Induced Acute Hemorrhagic Pancreatitis

et al. 1986

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The pathways of enzyme transfer from the pancreas into the systemic circulation were analyzed in sodium taurocholate-induced acute hemorrhagic pancreatitis in the rat by estimating lipase concentrations in blood, lymph and ascites. During the first few hours of pancreatitis high enzyme levels were observed in thoracic duct lymph. However, cannulation of the thoracic duct did not prevent a significant increase in the lipase concentration in peripheral blood. The portal vein lipase concentration was found to exceed the peripheral values by approximately 10%. Extremely high concentrations of lipase were measured in the ascites collected during pancreatitis. When the ascites was transferred to the peritoneal space of healthy rats, a significant increase in the lipase concentration in peripheral blood was measured. This increase could not be prevented by transection of the parasternal lymphatics. It was concluded that the hematogenous rather than the lymphatic transport of lipase from the pancreas and the peritoneal surface is the most important pathway. In this respect, this study does not support thoracic duct drainage but advocates peritoneal lavage as a logical therapeutic measure to reduce the concentration of circulating toxic substances from the pancreas in acute pancreatitis.

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M

Blaschek¹,

Hänsel²,

Keller³

et al. 1998

Hagers Handbuch Der Pharmazeutischen Praxis

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Lymph and Blood Enzymes and Pathologic Alterations in Canine Experimental Pancreatitis after Administration of Benzo-Pyrones

Cited by 6 publications

References 10 publications

T1 /podoplanin deficiency disrupts normal lymphatic vasculature formation and causes lymphedema

T1 /podoplanin deficiency disrupts normal lymphatic vasculature formation and causes lymphedema

Pathways of Enzyme Transfer in Sodium Taurocholate-Induced Acute Hemorrhagic Pancreatitis

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