Current Concepts of Implantation and Decidualization
Gabor Huszar in The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Sananes et al.,132 using uterine cells from hormonally sensitized castrate rats, observed net growth of short-lived (6 days) binucleate cells (this is atypical of stromal cells cultured in this laboratory). On the other hand, Vladimirsky et al.131 found that endometrial cells from pseudopregnant rats developed into populations of dispersed stellate cells which did not increase in number, but doubled their cytoplasmic and nuclear volume. They also noted proliferating colonies of closely packed polygonal cells which became bi- and multinucleate. These differences could be due to dissimilarities in the physiological status of stem cells at the time of separation or, alternatively, to the particular population of stromal cells selected by each separation method. Bell and Searle125 attribute these discrepancies to seeding densities. The morphologically distinct cell seen at low seeding densities (<100 cells per square millimeter) was a large mon-onucleated stellate cell which increased in area (cytoplasmic, nuclear), but not in number.125,131 At higher seeding densities (up to 1000 cells per square millimeter) both Sananes et al.132,134 and Bell and Searle125 obtained two cell types: a mononuclear stellate cell and a significant number of binucleate cells with a prolonged survival time.
Pancreatic disease
Nizar Zein, Bret Lashner in The Year in Gastroenterology and Hepatology, 2005
The structural evaluation of the pancreas has always been difficult, given its retroperitoneal location. A new synthetic porcine secretin has been developed that facilitates cannulation of the dorsal pancreatic duct during ERCP. In addition, staining of the minor papilla with methylene blue has been reported to help the therapeutic endoscopist at cannulation of the minor papilla. An endoscopically inserted endoluminal receiver for high-resolution magnetic resonance imaging (MRI) has been able to help with imaging of the pancreas and has been shown to be effective in animal models. The measurement of pancreatic excretory function has been difficult and limited to a few centres. An endoscopic pancreatic function test has been reported that shows promise. Methods for the evaluation and treatment of familial pancreatic cancer kindreds have not been completely established and the leading institution in the diagnosis and treatment of familial pancreatic cancer has reported a decision analysis that leads to cost-effective screening. Finally, the pathophysiology of alcohol-induced pancreatic injury is beginning to be worked out. It appears that the stellate cell is integrally involved in the pathogenesis of pancreatic fibrosis.
Advances in Nanonutraceuticals: Indian Scenario
Harishkumar Madhyastha, Durgesh Nandini Chauhan in Nanopharmaceuticals in Regenerative Medicine, 2022
Persistent inflammation, following liver damage, often results in the formation of fibrous tissue. Therefore, often, any medication which is given to reduce the inflammation ideally has an anti-fibrotic effect. The sequence of steps, which lead to fibrosis are outlined as oxidative stress caused by the generation of ROS followed by scar formation, leading to a reduced inflammatory response. This inflammation causes the crippling of hepatic stellate cell (HSC) activation causing fibrogenesis as seen in cirrhosis of the liver. In this context, it can be said, that certain natural compounds or Unani preparations which are identified as antioxidants, can be given as a therapy to reduce the ROS and in a way to prevent fibrosis of hepatic tissue. The effectiveness of this treatment depends upon the agility of the antioxidant reaching the target site i.e., liver (Kawada et al. 1998).
Relevance of vitamin D on NAFLD and liver fibrosis detected by vibration controlled transient elastography in US adults: a cross-sectional analysis of NHANES 2017–2018
Published in Annals of Medicine, 2023
Yuan Ji, Chang-Bao Wei, Wei Gu, Lin-Lin Hou
Currently, why vitamin D could effectively suppress the LF in NAFLD patients remains unclear. During the development of LF, hepatic stellate cell activation plays important effect. Activated hepatic stellate cells can effectively induce cell growth and transformation from a quiescent vitamin A-storing cell into an activated myofibroblast-like cell, increasing the production of extracellular matrix and tissue inhibitors of metalloproteinases [33]. Through inhibiting the activation of TGF-β/Smad signalling pathway in hepatic stellate cells, vitamin D can effectively impair the fibrosis of liver [34]. A recent study further indicated that vitamin D reduced hepatic stellate cells and TGF-β/Smad signalling activation through negative regulation of histidine-rich calcium binding protein [35].
DNA released from neutrophil extracellular traps (NETs) activates pancreatic stellate cells and enhances pancreatic tumor growth
Published in OncoImmunology, 2019
Jennifer L. Miller-Ocuin, Xiaoyan Liang, Brian A. Boone, W. Reed Doerfler, Aatur D. Singhi, Daolin Tang, Rui Kang, Michael T. Lotze, Herbert J. Zeh
Extracellular DNA has been implicated in pancreatic cancer invasion and metastasis, but its origin has not been definitively determined.11 Given that extracellular DNA is the principal component released from NETs, we hypothesized the neutrophil-derived DNA released during NETs may have effects on pancreatic tumor growth and in the tumor microenvironment. Inhibition of NETs mediated by direct small molecule PADI4 inhibition or depletion of extracellular DNA with DNase treatment diminishes liver metastasis12 and has demonstrable antitumor effects.13 Furthermore, pancreatic cancer is characterized by a dense, fibrotic stroma as a result of pancreatic stellate cell (PSC) activation.14,15 DNA in the form of bacterial CpG motifs activates pancreatic stellate cells (PSCs) to become fibrogenic and promote epithelial proliferation.16 Based on these findings, we hypothesized that extracellular DNA derived from NETs promotes activation of PSC within the tumor microenvironment.
Increased heat shock protein 70 expression attenuates pancreatic fibrosis induced by dibutyltin dichloride
Published in Scandinavian Journal of Gastroenterology, 2018
Jae Min Lee, Kwang Gyun Lee, Hyuk Soon Choi, Eun Sun Kim, Bora Keum, Yeon Seok Seo, Yoon Tae Jeen, Hoon Jai Chun, Hong Sik Lee, Soon Ho Um, Chang Duck Kim
According to a previous study, HSP overexpression through warm water immersion is effective against pancreatic damage due to cerulein-induced acute pancreatitis [25]. HSP seems to suppress cellular damage and promote pancreatic recovery [26]. Thus, this fibrosis suppression effect would be expectedly effective in preventing pancreatic fibrosis in chronic pancreatitis. The severity of pancreatic fibrosis can be measured by collagen expression. Moreover, pancreatic fibrosis is closely related not only to recurrent inflammation but also to pancreatic stellate cell activation [27]. Stellate cell activation and pathway can be induced using α-SMA. Whether pancreatic fibrosis progression was related to stellate cell activation as the mechanism of HSP70 in the pancreas could be suggested by α-SMA.
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