Evolutive phases of experimental prehepatic portal hypertension

Aller, María-Ángeles; Nava, María-Paz; Cuéllar, C.; Chivato, Tomás; Arias, Jorge-Luis; Sánchez-Patán, Fernando; Vicente, Felipe de; Alvarez, Emilio; Árias, Jaime

doi:10.1111/j.1440-1746.2007.04876.x

Cited by 17 publications

(45 citation statements)

References 55 publications

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“…In different conditions related to intestinal ischemia, such as hemorrhagic shock or severe burns, mesenteric lymph node circulation has the priority over portal circulation for transporting inflammatory mediators released in the intestinal wall [41,42]. This fact suggests that in other conditions that also produce intestinal hypoxia, like portal hypertension, the mesenteric lymph is a regional pro-inflammatory mediator vehicle, that is, a splanchnic one, but with a systemic effect [9,10].…”

Section: The Immune Phenotype: the Pathological Management Of Fatmentioning

confidence: 99%

“…Thus, it has been already proposed that these phenotypes could represent the expression of trophic functional systems with increasing metabolic complexity [2,10]. Therefore, in the portal hypertensive rat it could be considered that the body adapts the support, i.e., the trophic system, to the metabolic needs characteristic of each inflammatory phenotype.…”

Section: Low-grade Inflammatory Portal Hypertension: the Vitelline Comentioning

confidence: 99%

“…It has been hypothesized that the symbiosis of inflammatory cells and bacteria for extracellular (fermentation) and intracellular (phagocytosis) could favor tissue trophism [2,10]. Improper use of oxygen persists in this immune phase and it is associated with enzymatic stress.…”

Section: The Immune Phenotype: the Pathological Management Of Fatmentioning

confidence: 99%

“…The ischemia-reperfusion phenotype secondary to the hyperdynamic syndrome could represent oxidative and nitrosative stress with edema, which favors diffusion through the inflamed tissues and organs [2,10]. Hyperdynamic circulation stands out among the splanchnic and systemic alterations related to portal hypertension [1,[11][12][13][14][15].…”

Section: The Ischemia-reperfusion Phenotype: the Hydroelectrolitic Chmentioning

confidence: 99%

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Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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Section: The Immune Phenotype: the Pathological Management Of Fatmentioning

confidence: 99%

Section: Low-grade Inflammatory Portal Hypertension: the Vitelline Comentioning

confidence: 99%

Section: The Immune Phenotype: the Pathological Management Of Fatmentioning

confidence: 99%

Section: The Ischemia-reperfusion Phenotype: the Hydroelectrolitic Chmentioning

confidence: 99%

See 2 more Smart Citations

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

Self Cite

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“…First, a midline abdominal incision with a large bilateral subcostal extension was performed and then the areas in which the collateral venous circulation developed, i.e. the splenorenal, gastroesophageal, colorectal and hepatic hilum, were carefully studied for the presence of increased collateral veins [16].…”

Section: Portosystemic Collateral Circulation Methodsmentioning

confidence: 99%

Microsurgical Extrahepatic Cholestasis in the Rat: A Histopathological Liver Study

Aller

Ortega²,

Sánchez-Patán³

et al. 2008

TOPATJ

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Fibrosis, bile duct proliferation and mast cell hyperplasia characterize extrahepatic cholestasis. We studied these liver alterations in a new microsurgical model of extrahepatic cholestasis in the rat. Male Wistar rats: Sham-operated (n=9) and Microsurgical Cholestasis (n=10). After 4 weeks, a liver morphometric study was carried out using an image analysis system to assess bile proliferation and the fibrosis. The liver expression of alpha-smooth muscle actin was assayed by an immunohistochemical technique and mast cells were also counted. Cholestatic-rats presented portal hypertension, portosystemic circulation, and increased (p=0.0001) plasma bilirubin, alkaline phosphatase, Aspartateaminotransferase, Alanine-aminotransferase, and Lactate-dehydrogenase. Plasma levels of Albumin decreased (p=0.001). Cholestatic-rats showed intense biliary duct proliferation (p=0.0001) and fibrosis (p=0.0001). Mast cells accumulate (p=0.0001) around proliferating bile ducts and fibrous septa. The microsurgical cholestasis in the rat induces fibrosis and hyperplasia of bile ducts and mast cells. Mast cell liver infiltration could be an etiopathogenic remodeling factor in experimental cholestasis.

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Upregulation of miR‐874‐3p and miR‐874‐5p inhibits epithelial ovarian cancer malignancy via SIK2

Xia

Mei

Dong

et al. 2018

J Biochem & Molecular Tox

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Based on miR-874 expression levels in the GSE47841 microarray, we hypothesized that the mature products of miR-874, miR-874-3p, or miR-874-5p, would inhibit epithelial ovarian cancer (EOC) cell proliferation, metastasis, and chemoresistance. We first examined miR-874-3p and miR-874-5p expression levels in primary EOC tumor tissue samples and found that they were significantly decreased. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) cell proliferation and transwell assays revealed that miR-874-3p and miR-874-5p significantly inhibit EOC cell proliferation, migration, and invasion. Then, using MTT and soft agar assays of paclitaxel-treated Caov3 and SKOV3 cells transfected with miR-874-3p and miR-874-5p, we found that miR-874-3p and miR-874-5p enhance EOC cell chemosensitivity. We then confirmed that serine/threonine-protein kinase 2 (SIK2) was a target gene of miR-874-3p and miR-874-5p. Overall, the results of this study indicate that SIK2 expression can serve as a prognostic biomarker for EOC and that miR-874-3p and miR-874-5p have the potential to enhance clinical treatment of EOC.

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Evolutive phases of experimental prehepatic portal hypertension

Cited by 17 publications

References 55 publications

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Microsurgical Extrahepatic Cholestasis in the Rat: A Histopathological Liver Study

Upregulation of miR‐874‐3p and miR‐874‐5p inhibits epithelial ovarian cancer malignancy via SIK2

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