Bile Infarcts: New Insights Into the Pathogenesis of Obstructive Cholestasis

Cai, Shi‐Ying; Boyer, James L.

doi:10.1002/hep.30291

Cited by 7 publications

(7 citation statements)

References 11 publications

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“…Here, we show a new regulatory mechanism of OATP3A1 in human cholestasis. The three main findings are: [1] increased plasma levels of TNFα significantly correlated with OATP3A1 upregulation in livers of obstructive cholestasis patients (Fig. 1D), [2] recombinant TNFα elevated OATP3A1 expression in primary mouse hepatocytes and hepatoma cells (Fig.…”

Section: Discussionmentioning

confidence: 90%

“…Cholestasis is characterized by large amounts of bile acid (BA) accumulation in hepatocytes and serum (1). During an adaptive response to cholestasis, liver injury was attenuated due to the repression of BA synthesis via downregulation of CYP7A1 and CYP8B1 genes, and the enhancement of BA efflux via upregulation of multidrug resistance-associated protein 4 (MRP4), multidrug resistance-associated protein 3 (MRP3), organic anion-transporting polypeptide 3A1 (OATP3A1) protein，bile salt export pump (BSEP) and organic solute transporter α/β (OSTα/β) (1)(2)(3)(4)(5). These BA transporters played crucial roles in maintaining bile acid homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Li¹,

Wang²,

Cheng³

et al. 2022

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Li¹,

Wang²,

Cheng³

et al. 2022

Journal of Biological Chemistry

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“…One method is by para-cellular leak 42 and other is by the formation of BCV 33 . In case of increased pressure 46 and compromised cytoskeleton, BC favors BCV-driven mechanisms 33 .…”

Section: Discussionmentioning

confidence: 99%

Bile canaliculi contract autonomously by releasing calcium into hepatocytes via mechanosensitive calcium channel

Gupta

Ng²,

Balachander³

et al. 2020

Biomaterials

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Bile canaliculi (BC) are the smallest vessels of the biliary tree. They are formed from the apical surfaces of adjoining hepatocytes, resulting in lumenal conduits for bile flow. Bile is propelled along the BC by hepatocyte contractions that arise from cyclic waves of apico-basal Ca 2+ , but the source and regulation of Ca 2+ has been unclear. We report that BC contraction correlates with cyclic transfer of Ca 2+ from BC lumen to apico-basal Ca 2+ waves in adjacent hepatocytes, and does not correlate with endoplasmic reticulum Ca 2+ . BC contractility was triggered by ionophore A23187 and unaffected by Thapsigargin. The cycles of Ca 2+ transfer could be blocked by the mechanosensitive calcium channel inhibitor GsMTx-4, resulting in cholestatic generation of BC-derived vesicles. The mechanosensitive calcium channel Piezo-1 is preferentially localized at BC membranes, and its hyper-activation by Yoda1 causes increased Ca 2+ transfer and increased BC contractility. We propose that canaliculi achieve biomechanical homeostasis through the following feedback system: the pressure of accumulated bile is sensed by mechanosensitive channel, which transmit biliary calcium into adjacent hepatocytes for contraction of the BC lumen and propulsion of the bile.

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“…Charcot-Gombault necrosis : biliary infarction, a late complication of extrahepatic cholestasis. It has been described by Charcot and Albert Gombault in 1876 [33].…”

Section: Eponymsmentioning

confidence: 99%

“Stat Rosa Pristina Nomine, Nomina Nuda Tenemus”: The Many Syndromes, Diseases, and Anatomic Structures Bearing Jean-Martin Charcot’s Name

Pedro

Souza²

2020

Eur Neurol

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The sheer magnitude of Jean-Martin Charcot's contributions to neurology, pathology, psychiatry, and internal medicine has allowed for the common usage of eponyms bearing the master's name in recognition of his work. However, these are so numerous that confusion has naturally arisen concerning the exact nature of each eponym, allowing for different specialists to refer to completely different ailments or symptoms, while using the very same expression. Previous compilations of his eponyms were often incomplete. Therefore, the authors aimed to bring some clarification into the nature and origin of each known eponym with Charcot's name.

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Bile Infarcts: New Insights Into the Pathogenesis of Obstructive Cholestasis

Cited by 7 publications

References 11 publications

Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Tumor necrosis factor α upregulates the bile acid efflux transporter OATP3A1 via multiple signaling pathways in cholestasis

Bile canaliculi contract autonomously by releasing calcium into hepatocytes via mechanosensitive calcium channel

“Stat Rosa Pristina Nomine, Nomina Nuda Tenemus”: The Many Syndromes, Diseases, and Anatomic Structures Bearing Jean-Martin Charcot’s Name

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