Dataset Information

Crosstalk Between Activated Myofibroblasts and ? Cells in Injured Mouse Pancreas.

ABSTRACT: In injury conditions, myofibroblasts are induced to lay down matrix proteins and support the repair process. In this study, we investigated the role of myofibroblasts, particularly stellate cells, in the growth and regeneration of pancreatic ? cells.We used both in vitro and in vivo approaches to address whether stellate cells may promote the growth of ? cells.Our experiments demonstrated that activated stellate cells support the proliferation of ? cells in vitro. In vivo, mesenchymals surrounding the pancreatic islets are activated (induced to proliferate) in the islet regeneration model of Pten null mice. These mesenchymals display markers of pancreatic stellate cells, such as desmin and to a lesser extent, smooth muscle actin ?. We have shown previously that targeted ?-cell deletion of Pten lead to a significant increase in total islet mass. This phenotype was accompanied by an increase in peri-islet mitotic activity, particularly in islets injured by streptozotocin, a ? cell-specific toxin.Together with the in vitro observations, our data, here, suggest that that these mesenchymal cells may support the regeneration of the islets. Identifying how the communication occurs may provide clinically relevant mechanism for inducing ?-cell regeneration.

SUBMITTER: Bayan JA

PROVIDER: S-EPMC4780408 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature

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Publications

Crosstalk Between Activated Myofibroblasts and β Cells in Injured Mouse Pancreas.

Bayan Jennifer-Ann JA Peng Zhechu Z Zeng Ni N He Lina L Chen Jingyu J Stiles Bangyan L BL

Pancreas 20151001 7

<h4>Objectives</h4>In injury conditions, myofibroblasts are induced to lay down matrix proteins and support the repair process. In this study, we investigated the role of myofibroblasts, particularly stellate cells, in the growth and regeneration of pancreatic β cells.<h4>Methods</h4>We used both in vitro and in vivo approaches to address whether stellate cells may promote the growth of β cells.<h4>Results</h4>Our experiments demonstrated that activated stellate cells support the proliferation o ...[more]

PMID: 26333110

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Project description:AimsRecent studies have demonstrated electrotonic coupling between scar tissue and the surrounding myocardium in cryoinjured hearts. However, the electrical dynamics occurring at the myocyte-nonmyocyte interface in the fibrotic heart remain undefined. Here, we sought to develop an assay to interrogate the nonmyocyte cell type contributing to heterocellular coupling and to characterize, on a cellular scale, its voltage response in the infarct border zone of living hearts.Methods and resultsWe used two-photon laser scanning microscopy in conjunction with a voltage-sensitive dye to record transmembrane voltage changes simultaneously from cardiomyocytes and adjoined nonmyocytes in Langendorff-perfused mouse hearts with healing myocardial infarction. Transgenic mice with cardiomyocyte-restricted expression of a green fluorescent reporter protein underwent permanent coronary artery ligation and their hearts were subjected to voltage imaging 7-10 days later. Reporter-negative cells, i.e. nonmyocytes, in the infarct border zone exhibited depolarizing transients at a 1:1 coupling ratio with action potentials recorded simultaneously from adjacent, reporter-positive ventricular myocytes. The electrotonic responses in the nonmyocytes exhibited slower rates of de- and repolarization compared to the action potential waveform of juxtaposed myocytes. Voltage imaging in infarcted hearts expressing a fluorescent reporter specifically in myofibroblasts revealed that the latter were electrically coupled to border zone myocytes. Their voltage transient properties were indistinguishable from those of nonmyocytes in hearts with cardiomyocyte-restricted reporter expression. The density of connexin43 expression at myofibroblast-cardiomyocyte junctions was ∼5% of that in the intercalated disc regions of paired ventricular myocytes in the remote, uninjured myocardium, whereas the ratio of connexin45 to connexin43 expression levels at heterocellular contacts was ∼1%.ConclusionMyofibroblasts contribute to the population of electrically coupled nonmyocytes in the infarct border zone. The slower kinetics of myofibroblast voltage responses may reflect low electrical conductivity across heterocellular junctions, in accordance with the paucity of connexin expression at myofibroblast-cardiomyocyte contacts.

Dataset Information

Crosstalk Between Activated Myofibroblasts and ? Cells in Injured Mouse Pancreas.

Publications

Crosstalk Between Activated Myofibroblasts and β Cells in Injured Mouse Pancreas.

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