2015
DOI: 10.1097/mpg.0000000000000875
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P‐Selectin (CD62P) Expression in Liver Tissue of Biliary Atresia

Abstract: The significant expression of P-selectin in endothelium, platelets, and bile duct epithelium in patients with BA suggests a potential role for this adhesion molecule in the pathogenesis of this devastating neonatal hepatic disorder. It further suggests that platelets in BA are activated and may have a role in the inflammatory process in BA.

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Cited by 12 publications
(8 citation statements)
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“…The present study’s strength is analyzing a large cohort of NC cases with a long period of follow-up. Moreover, the designed simple algorithmic approach for the etiological diagnosis based on long-term experience [ 8 , 9 , 17 , 18 , 20 - 28 ] is another crucial point.…”
Section: Discussionmentioning
confidence: 99%
“…The present study’s strength is analyzing a large cohort of NC cases with a long period of follow-up. Moreover, the designed simple algorithmic approach for the etiological diagnosis based on long-term experience [ 8 , 9 , 17 , 18 , 20 - 28 ] is another crucial point.…”
Section: Discussionmentioning
confidence: 99%
“…The reason for this separation is not to point out the discriminative laboratory or clinical parameters between both groups. We have already covered this issue extensively in our previous studies [10,11,21,22], so it will not be discussed here. But as BA is the main etiologic cause of neonatal cholestasis [23] and as CMV has been proposed as a possible etiologic agent for BA [18], this separation seemed logical.…”
Section: Discussionmentioning
confidence: 99%
“…The initial event may be a viral infection, which targets the biliary epithelium [8]. This is followed by activation of immune cells and release of proinfl ammatory cytokines [9] and adhesion molecules [10,11] that perpetuates the injury and causes biliary destruction, leading to the atresia phenotype [12].…”
Section: Introductionmentioning
confidence: 99%
“…The role of immune-mediate mechanism in the pathogenesis of BA has been based by the assumption that the initial damage of biliary epithelium is followed by the activation of immune cells and the release of proinflammatory cytokines that perpetuate the injury up to biliary destruction, which is followed by collagen deposition to produce biliary fibrosis (Besso and Bezerra 2011;Srivastava 2011;Sira et al 2015).…”
Section: Etiology and Pathogenesismentioning
confidence: 99%