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Turning Blood into Liver
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Bryon E. Petersen, Neil D. Theise
In humans, the canal of Hering data, as mentioned above, was one of the routes of investigation which led to demonstration that some hepatic progenitors arrived from extra-hepatic sources, certainly in part or entirely, from the bone marrow.18-20 Confirmation of this process in humans has been made.34 In fact, in the study in which quantification of this process was attempted,18 in cases in which there was a marked ductular reaction in response to post-transplant strictures from biliary anastamosis or recurrence of primary disease (primary sclerosing cholangitis, hepatitis C), it was shown that up to 40% of hepatocytes and cholangiocytes were deriving from the circulation. Thus, the contribution of extra-hepatic progenitors to organ reconstitution in humans was not only nontrivial, but obviously of clinical significance.
The accessory organs: Pancreas, liver and gallbladder
Published in Paul Ong, Rachel Skittrall, Gastrointestinal Nursing, 2017
One of the functions of hepatocytes is to produce bile. Bile consists of water, electrolytes, bile acids, cholesterol, phospholipids and bilirubin. Bile plays a key role in the digestion of fats within the small intestine. Bile is secreted by hepatocytes into canaliculi which transport bile out of the lobule where it drains into bile ductules, interlobular bile ducts and then collects in the right and left hepatic ducts outside the liver. These then join up to form the common hepatic duct (Figure 6.11). As bile flows through the bile ducts the ductal epithelial cells (cholangiocytes) that line its surface modify the bile by secreting a watery, bicarbonate-rich secretion. This secretion plays an important role in neutralising the acid environment in the duodenum so that pancreatic and small intestine enzymes can function. The bile then either flows via the common bile duct emptying into the duodenum or it enters the cystic duct and is stored in the gallbladder. The gallbladder stores and concentrates bile between meals and overnight. Bile will remain within the gallbladder until its release is triggered by the contraction of the walls of the gallbladder. During the time that bile remains in the gallbladder, water and some electrolytes are absorbed causing the bile to become more concentrated.
Hepatotoxins
Published in John F. Pohl, Christopher Jolley, Daniel Gelfond, Pediatric Gastroenterology, 2014
Clinically, all three patterns overlap in the symptoms they produce. When Step 1 metabolites damage hepatocytes, children present with a hepatitis picture of nausea, vomiting, anorexia, and elevated transaminases. When Step 1 metabolites injure cholangiocytes, cholestatic symptoms of pruritis and jaundice occur. Step 1 metabolites can also injure any of the other liver cells, including endothelial cells creating a vaso-occlusive disorder picture. Often, DILI affects multiple cells in the liver and creates a mixed hepatic–cholestatic clinical picture that can occur acutely, subacutely, or chronically. If not addressed, DILI can lead to liver fibrosis, cirrhosis, and ultimately liver failure.
Open hepatic artery flow with portal vein clamping protects against bile duct injury compared to pringles maneuver
Published in Scandinavian Journal of Gastroenterology, 2023
Siliang Zhang, Pingli Cao, Pinduan Bi, Fu Yang, Ming Wu, Ding Luo, Bin Yang
TUNEL staining was used to investigate the apoptosis and necrosis of the liver and cholangiocytes (Figure 3(A)). In all the groups, only a small amount of hepatocyte apoptosis was observed in the CPM groups, and no obvious hepatocyte necrosis was found in the other groups. However, in the bile duct tissue, each group had a different number of TUNEL-positive cholangiocytes. Cholangiocyte apoptosis in the PM groups was significantly more than that in the HAFO group. There was no significant difference between the CHAFO and IHAFO groups (Figure 3(D)). Similarly, the number of active caspase-3- positive bile duct cells in the HAFO group was much lower than that in the PM groups at 24 h after the operation (p < .05) (Figure 3(B,E)). Compared to the Sham group, PM and HAFO increased the proliferation of cholangiocytes as evidenced by increased Ki67 expression in bile duct sections. There was a significant increase in the number of proliferating cholangiocytes in the bile duct of PM rats compared with that of HAFO rats. (Figure 3(C,F)).
Targeted therapies for extrahepatic cholangiocarcinoma: preclinical and clinical development and prospects for the clinic
Published in Expert Opinion on Investigational Drugs, 2021
Massimiliano Cadamuro, Alberto Lasagni, Angela Lamarca, Laura Fouassier, Maria Guido, Samantha Sarcognato, Enrico Gringeri, Umberto Cillo, Mario Strazzabosco, Jose JG Marin, Jesus M Banales, Luca Fabris
Cholangiocarcinomas (CCA) encompass a heterogeneous group of epithelial cancers with features of diverse degree of cholangiocyte differentiation that can arise from any segment of the biliary tree, except from the gallbladder, which represents a distinct type of cancer [1]. Currently, CCAs are classified as intrahepatic (iCCA), perihilar (pCCA), and distal (dCCA), based on the different anatomical location, each characterized by specific epidemiological and clinical features [1–3]. As shown in Figure 1, the point of demarcation between iCCA and pCCA is the confluence of the second-order bile ducts, whereas the insertion of the cystic duct represents the border between pCCA and dCCA, which extends to the Vater’s ampulla. Generally, pCCA and dCCA are grouped in a single extrahepatic CCA (eCCA) entity, although they represent subtypes with distinct clinicopathological features, prognosis, and therapeutic options. Unfortunately, most clinical trials have been conducted considering all CCAs as a single disease, sometimes including even gallbladder cancer, thereby hindering the development of tailored therapies aimed at the specific type of biliary tract cancer [4].
Preclinical insights into cholangiopathies: disease modeling and emerging therapeutic targets
Published in Expert Opinion on Therapeutic Targets, 2019
Keisaku Sato, Shannon Glaser, Lindsey Kennedy, Suthat Liangpunsakul, Fanyin Meng, Heather Francis, Gianfranco Alpini
Cholangiocytes are heterogeneous with small and large cholangiocytes displaying different cell sizes and functions [133]. Small cholangiocytes have a larger nucleus to cytosol ratio compared to large cholangiocytes, and previous studies have demonstrated that during CCl4-induced large cholangiocyte damage, small cholangiocytes de novo proliferate and differentiate into large to compensate the damaged population of large cholangiocytes indicating the possible stem cell-like features of small cholangiocytes [134,135]. A previous study has demonstrated that transplantation of small cholangiocytes decreases ductular reaction and liver fibrosis in BDL mice, but large cholangiocyte transplantation exhibits no effects [136]. Although further studies are needed to elucidate whether small cholangiocytes are liver stem cells or have stem cell-like abilities to differentiate into large cholangiocytes or other liver cells, these previous studies suggest that stem cell transplantation could be a therapeutic tool for cholangiopathies.