Peri‐ and postnatal development of heterogeneity in the amounts of endoplasmic reticulum in mouse hepatocytes
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Abstract The surface density and area per cell of the endoplasmic reticulum (ER) in periportal and perihepatic hepatocytes from male ddY mice, “17‐, 18‐, and 19‐day‐old fetuses,” “newborn and 1‐, 5‐, 10‐, and 20‐day‐old animals,” and “adult animals” were analyzed by quantitative electron microscopy. The surface density of rough ER was not significantly different between periportal and perihepatic cells in all age groups examined, except for 19‐day‐old fetuses in which the value was greater in periportal cells than perihepatic cells. The surface density of smooth ER and total (rough and smooth) ER did not significantly differ between the periportal and perihepatic cells from 17‐day‐old fetuses to 5‐day‐old animals. In 10‐ and 20‐day‐old and adult animals, the values of smooth and total ER were greater in perihepatic cells than in periportal cells. When the data were expressed as area per cell, the patterns of subacinar distributions hardly differed, but age‐related changes differed considerably from the patterns seen in the surface density data. The differences were generally caused by the increase in hepatocyte volume between 20 days of age and adulthood, especially in perihepatic cells, and by the changes in volume during the perinatal period. The results show that differences in the surface density and area per cell of smooth and total ER between periportal and perihepatic hepatocytes evident in adult animals are not present in fetal and newborn animals but arise during postnatal development.Keywords:
Hepatic stellate cell
Hepatic stellate cell
Liver Regeneration
Desmin
Liver cytology
Immunostaining
Intravital microscopy
Perisinusoidal space
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Hepatic stellate cell
Liver Regeneration
Desmin
Liver cytology
Intravital microscopy
Immunostaining
Perisinusoidal space
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Citations (10)
Activation of stellate cells as a target for the treatment of liver fibrosisIn his thesis, Zhang introduces the crucial role of hepatic stellate cell activation in the development of liver fibrosis. Activated liver stellate cells are the main precursors of myofibroblasts. Therapy targeting hepatic stellate cells can prevent or reverse liver fibrosis.The aging ("senescence") of hepatic stellate cells is interpreted as a mechanism that protects against the progression of liver fibrosis. The biomarkers, signaling pathways and likely effects of hepatic stellate cell senescence are explained. Zhang proposes that the biomarkers P21 (cell cycle arrest), senescence-associated β-galactosidase (lysosomal galactosidase), and interleukin-6 (senescence-associated secretory phenotype) can be used to identify senescent hepatic stellate cells. Although the senescence of liver stellate cells has not yet been fully elucidated, therapy-induced senescence of hepatic stellate cells, followed by senolytics, may be an optimal strategy for combating liver fibrosis.Esculetin, a coumarin derivative, has also been shown to cause the senescence of hepatic stellate cells. It appears that in senescent hepatic stellate cells, collagen production and cell proliferation are reduced. In addition, senescent hepatic stellate cells develop resistance to a return to active proliferation.
Hepatic stellate cell
Senescence
Hepatic fibrosis
Liver cytology
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Comparison with the findings in the cells of other plants and animals showed that the endoplasmic reticulum in the root apex ofFagopyrum has the same general character and function as in other biological objects, i.e. in secretory processes and especially in this case in the transport of the substances produced. Detailed studies of the morphology and activity of the endoplasmic reticulum showed some functional differences which are characteristic for this object. The endoplasmic reticulum participates apparently in the transport of the mass of known but functionally and nomenclatorically controversial formations which here are called dense bodies. Dense bodies exist inFagopyrum in a considerable amount as compared to other objects. Frequent contact of the dense bodies with the ends of the endoplasmic reticulum, contact with the endoplasmic retieulum passing through the plasmodesm, accumulation of the dense bodies along the cell wall and in proximal distance of the plasmodesms and intensive staining of some plasmodesms was observed. The dense vacuoles in this object represent dilated spaces of the endoplasmic reticulum which apparently have the function of reservoirs of the dense mass. The endoplasmic reticulum in the calyptra cells appears to participate in the formation of the cell walls. This object differs hereby from others, where the participation of the Golgi apparatus has been observed in this function.
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We present a case of chronic liver disease with selective and exclusive hepatocyte endoplasmic reticulum storage of δ 1 ‐antichymotrypsin in the form of granules, detected by specific immunohistochemistry at the light microscopy level and corresponding to material found in dilated endoplasmic reticulum of hepatocytes by electron microscopy. The patient had intermediate deficiency of δ 1 ‐antichymotrypsin. Thus, the hepatocyte accumulation of δ 1 ‐antichymotrypsin may indicate the presence of an export block resembling that of a closely‐related protein, namely PiZ δ 1 ‐antitrypsin. It is proposed that hepatocyte storage of δ 1 ‐antichymotrypsin may be an expression of an inborn error of metabolism bearing the characteristics of endoplasmic reticulum storage diseases such as PiZ δ 1 ‐antitrypsin deficiency and hereditary hypofibrinogenaemia.
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This study was aimed to reveal the stellate cell derived factors that regulate hepatocyte proliferation in culture. Rat hepatocytes and stellate cells were cultured in serum free Williams-E medium. We used hepatocyte monoculture and two different co-cultures of hepatocytes and stellate cells ; 1) co-culture on the same surface (Co-mix.) and 2) co-culture without contact between hepatocytes and stellate cells using a culture insert (Co-sep.) . Changes in the number and the DNA synthesis of hepatocytes was estimated. Although the number of hepatocyte decreased to 76% of the original at 48 h after starting mono-culture, it was kept at 106% in Co-mix and increased to 135% in Co-sep. The hepatocyte DNA synthesis was enhanced by carbenoxolone, gap junction blocker, in Co-mixo and reduced by NK 1 in each coculture. PD 153035, an EGF receptor specific inhibitor, had no effect. HeparitinaseI (20 mU/ml) and sodium chrolate (25 mM) reduced the hepatocyte DNA synthesis in Co-sepo to 71%. Activation of MAPK was induced in hepatocytes stimulated by conditioned mediums. These results indicated that hepatocyte proliferation was stimulated in the presence of stellate cells through HGF, extracellular heparan sulfate, and heparan sulfate proteoglycan, and might be negatively regulated by gap junction dependent mechanism.
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Liver cytology
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Hepatic stellate cells are now recognized as the major source of extracellular matrix in hepatic fibrosis. Following liver injury the hepatic stellate cell changes from a quiescent to an activated cell. The activation process includes an increased proliferation rate, a phenotypic change to a myofibroblast-like cell, loss of vitamin A stores, increased extra-cellular matrix protein synthesis and contractility. Furthermore, hepatic stellate cells have been implicated in hepatic inflammation through their ability to secrete cytokines and chemokines. Here, we review the literature on the molecular pathogenesis of hepatic stellate cells activation with emphasis on the most recent findings. The reviewed topics include transcriptional and post-transcriptional regulation of the genes encoding type I collagen in hepatic stellate cells; the role of the transcription factor nuclear factor Kappa B in the hepatic stellate cell activation; focal adhesion kinase and integrin-mediated signal transduction in hepatic stellate cell, and apoptosis in hepatic stellate cells. New insight into hepatic stellate cell activation and death may lead to the development of novel therapies for hepatic fibrosis.
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Hepatic fibrosis
Liver cytology
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Endoplasmic reticulum stress as a new concern during the pathogenesis of alcoholic liver disease(ALD)has entered the people's vision.Endoplasmic reticulum stress caused by the accumulation of misfolded and unfolded proteins in the endoplasmic reticulum.Appropriate stress was benefical to recovery of intracellular environment,however,serious and persistent stress may lead to apoptosis.Hepatocytes are one of the most sensitive cells,which contain abundant endoplasmic reticulum.Existing study has indicated that endoplasmic reticulum contributed to the development of ALD in cell and animal models.In this review,we summaried the role of endoplasmic stress in the pathogenesis of ALD.
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Hepatic stellate cell
Liver cytology
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