Identification of markers for quiescent pancreatic stellate cells in the normal human pancreas

Nielsen, Michael Friberg Bruun; Mortensen, Michael Bau; Detlefsen, Sönke

doi:10.1007/s00418-017-1581-5

Cited by 39 publications

(36 citation statements)

References 82 publications

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“…In contrast to quiescent hepatic stellate cells, immunohistochemical markers for quiescent pancreatic stellate cells in formaldehydefixed and paraffin-embedded human tissue are lacking. Using human tissue microarrays and an extensive panel of antibodies, Nielsen et al (2017) report now that cytoglobin and adipophilin are not only markers for quiescent hepatic but also for pancreatic stellate cells. Cytoglobin in human pancreas was expressed in two types of profibrogenic cells: quiescent stellate cells and resident interlobular fibroblasts.…”

Section: Immunohistochemical Markers For Quiescent Human Pancreatic Smentioning

confidence: 99%

In focus in HCB

Taatjes

Roth

2017

Histochem Cell Biol

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immunohistochemical expression prior to CABG procedure might serve as a predictive indicator of potential early graft failure. Thymocyte-thymic epithelial cell interactions in EphB-deficient miceEpithelial free areas (EFA) are known to occur in both the cortex and medulla of the thymus in a variety of animal species. Whether the cortical and thymic EFAs represent the same or different histological and functional situations remains open for debate. Garcia-Ceca et al. (2017) have now investigated whether EFAs might represent microenvironments where thymocyte-thymic epithelial cell (TEC) interactions are disrupted, potentially resulting in altered thymic histology. As a model system, they employed EphB-deficient mice (EphB, a family of protein tyrosine kinases, and ephrins-B, their ligands are regulators of epithelial organization) previously shown by these authors to display altered thymocyte-TEC interactions (Garcia-Ceca et al. 2015). They used multilabel fluorescence microscopy, semiquantitative analysis, and transmission electron microscopy to evaluate the number and sizes of EFAs, as well as their organization and cell content in EphB-deficient mice compared to wild-type (WT) control animals. Their morphological results showed that: (1) in both WT and EphB-deficient mice, the number and size of EFAs were larger in the medulla compared to the cortex; (2) low numbers of EFAs correlate with larger areas; (3) EFA structure and cell content are similar in WT and EphB-deficient thymuses; and (4) EFAs in cortex and medulla contain different cell types and are structurally distinct with cortical areas possessing DP thymocytes and medullary regions SP thymocytes. Overall, their results suggest that EFAs in their model may be partially due to New details for predicting saphenous vein graft occlusion following CABG surgeryCoronary artery bypass grafting (CABG) is currently the method of choice for improving blood flow in the atherosclerotic vessel through surgical procedures. In younger patients (less than 65 years of age) a segment from the internal thoracic artery is classically used as the donor vessel for the graft, whereas in patients older than 65 years of age a section from the saphenous vein is typically chosen since it is less likely to undergo arterialization (Al-Sabti et al. 2013). Although much information is known concerning factors responsible for patency rates for internal thoracic artery donor vessels, very little is currently known about those responsible for saphenous vein patency in CABG procedures. However, since stem cell and progenitor cell proliferation in the graft wall have been shown to be involved in early saphenous vein graft occlusion (Timmermans et al. 2009), Malinska et al. (2017 performed a multivariate analysis of stem cell and progenitor cell markers in the donor saphenous vein wall prior to CABG procedure, followed by correlation with graft occlusion. Their results showed that strong immunohistochemical expression of CD133 (a stem cell marker) in smooth muscle cells of the tunica media ...

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Section: Immunohistochemical Markers For Quiescent Human Pancreatic Smentioning

confidence: 99%

In focus in HCB

Taatjes

Roth

2017

Histochem Cell Biol

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“…At present, there is no reliable marker to differentiate between quiescent stellate cells versus resident fibroblasts in the pancreas. 148 In this study, ultrastructurally, fibroblasts were identified in the control tissue, just few residing in inter-acinar spaces, containing no lipid droplets. Soon after insult, stellate cells were filled with RER and full and emptied lipid droplets but by day two of the experiments most of the stellate cells had no remaining lipid droplets.…”

Section: Fibrosismentioning

confidence: 58%

“…153 New special stains may aid in the identification of stellate cells in controls. 148 At the early stages of the experiments activating stellate cells were recognised by the presence of copious RER and lipid droplets in the cytoplasm and large regular shaped or elongated nuclei. The lipid droplets were seen up to three days in the CHB and duct ligation models, earlier in the caerulein model.…”

Section: Stellate Cells In Rat Modelsmentioning

confidence: 99%

“…129,140,[144][145][146][147] Many markers for quiescent PSCs in normal human pancreas have been evaluated recently. 148 They identified the limitations of previously proposed markers and suggested cytoglobin and adipophilin as possible but not perfect replacements.…”

Section: Pancreatic Stellate Cellsmentioning

confidence: 99%

“…In the literature there are conflicting views on the definition of fibroblasts/myofibroblasts/stellate cells. 148 Their derivation, progenitors, phenotype and function clearly differ in different tissues and they comprise heterogeneous populations. At present, there is no reliable marker to differentiate between quiescent stellate cells versus resident fibroblasts in the pancreas.…”

Section: Fibrosismentioning

confidence: 99%

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Cellular and molecular mechanisms of pancreatitis in atrophy and regeneration

Reid¹

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Pancreatitis is a debilitating disease with complex etiology, prognosis and pathology, limited treatment options and a burden on health resources. The main lesions of acute pancreatitis are injury to acinar cells and inflammation of the pancreas. Mild interstitial pancreatitis (or oedematous pancreatitis) is characterized by acute inflammation with oedema in the stroma and acinar tissue.Necrosis of acinar tissue, stroma or peri-pancreatic fat is absent and complete recovery, or regeneration of the gland is usual. Whilst there is universal agreement on many of the cellular changes that accompany acute pancreatitis, there is no clear distinction between the factors that determine whether regeneration can occur. The mechanism of regeneration and the cellular processes that influence regeneration form the primary basis of this study.Experimental models of pancreatitis have been produced in rats, mice, dogs, cats and swine by various methods. The time course and final tissue regeneration, if it occurs, vary considerably among different models, with many having the limitation that pancreatic injury is extended, so that degenerative processes are superimposed on regenerative activity. Three in vivo models of pancreatitis in rats were chosen for this project, to study pancreatitis and pancreatic regeneration that occurs in the recovery phase. These models evolve slowly, allowing detailed morphological study. In general, they have similar early events but vary considerably in regenerative outcome. (1) The infusion of caerulein is a well-established model for inducing experimental pancreatitis in rats and pancreatitis is followed by a great reparative capacity. Caerulein is a decapeptide with biological activity on gastrointestinal smooth muscle contraction and pancreatic and gastric secretion. (2) In 1-cyano-2-hydroxy-3-butene (CHB)-induced pancreatitis, acinar cell regeneration is limited to small islands of acini which fail to endure. CHB is known to induce cell death in pancreatic acini.(3) The model of partial pancreatic duct ligation leads to atrophy of the gland with little or no regeneration ensuing. Although some characteristics are known about these models of pancreatitis, there is a general lack of information on the association between pancreatic atrophy and inflammation and investigating this association was one of my overall aims. In addition, as well as investigating the three different models of pancreatitis in rats, I aimed to compare the same initiating event in other animals. Because of the selective nature of CHB pancreatotoxicity, and the ease of producing the model in rats, I sought to investigate this method in a mouse model. In addition, I sought to establish and characterise a canine CHB model.iii The pancreatic atrophy induced in the chosen models typically involved apoptosis of acinar cells and its removal by macrophages. In some situations, if acinar redifferentiation did not occur, development of fibrosis and scarring was a key to pancreatic repair. This atrophy took place in a coherent fashion...

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Generation of an Fsp1 (fibroblast‐specific protein 1)‐Flpo transgenic mouse strain

Cardot‐Ruffino

Chauvet

Caligaris

et al. 2020

Genesis

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SummaryRecombination systems represent a major breakthrough in the field of genetic model engineering. The Flp recombinases (Flp, Flpe, and Flpo) bind and cleave DNA Frt sites. We created a transgenic mouse strain ([Fsp1‐Flpo]) expressing the Flpo recombinase in fibroblasts. This strain was obtained by random insertion inside mouse zygotes after pronuclear injection. Flpo expression was placed under the control of the promoter of Fsp1 (fibroblast‐specific protein 1) gene, whose expression starts after gastrulation at Day 8.5 in cells of mesenchymal origin. We verified the correct expression and function of the Flpo enzyme by several ex vivo and in vivo approaches. The [Fsp1‐Flpo] strain represents a genuine tool to further target the recombination of transgenes with Frt sites specifically in cells of mesenchymal origin or with a fibroblastic phenotype.

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Identification of markers for quiescent pancreatic stellate cells in the normal human pancreas

Cited by 39 publications

References 82 publications

In focus in HCB

In focus in HCB

Cellular and molecular mechanisms of pancreatitis in atrophy and regeneration

Generation of an Fsp1 (fibroblast‐specific protein 1)‐Flpo transgenic mouse strain

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