Dissociation and reassembly of adherens junctions during experimental acute pancreatitis

Lerch, Markus M.; Lutz, Manfred P.; Weidenbach, H; Müller-Pillasch, F.; Gress, Thomas M.; Leser, Jürgen; Adler, Guido

doi:10.1053/gast.1997.v113.pm9322531

Cited by 83 publications

(75 citation statements)

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“…The progression of Munc18c displacement from the plasma membrane correlated very well with the progression of actin disassembly (Figure 8, e, h, and k), which is well known to occur in this pancreatitis model (30,31). Also, parallel histologic sections obtained from these pancreata demonstrate progressive changes of edematous pancreatitis.…”

Section: Figuresupporting

confidence: 69%

“…This cellular location of Munc18c overlaps with the location of syntaxin-4 (Figure 1e) and SNAP-23 ( Figure 1g). F-actin staining with phalloidin ( Figure 1, d, f, and h) is used to define the apical membrane where the actin signal is strongest (30)(31)(32). Taken together, the basolateral plasma membrane of the acinar cell contains a set of t-SNARE proteins capable of forming a fusion complex with the ZG VAMP-2, and Munc18c may be responsible for preventing this complex from forming (15).…”

Section: Resultsmentioning

confidence: 99%

“…This was performed as we have previously described (30,31). Male Wistar rats (200-250 g) were equipped with an intravenous cannula, followed by the indicated infusion protocols.…”

Section: Methodsmentioning

confidence: 99%

“…We believe that the Munc18c displacement from the plasma membrane would render the membrane extremely receptive to pathologic exocytosis to occur. The parallel changes of actin disassembly (30,31) would further allow free access of the ZGs to the acinar cell surface (56). Indeed, actin and associated cytoskeletal proteins have been postulated to be involved in physiologic (56) and pathologic exocytoses of the pancreatic acinar cell (30,31).…”

Section: Figurementioning

confidence: 99%

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Supramaximal cholecystokinin displaces Munc18c from the pancreatic acinar basal surface, redirecting apical exocytosis to the basal membrane

Gaisano¹,

Lutz²,

Leser³

et al. 2001

J. Clin. Invest.

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Section: Figuresupporting

confidence: 69%

Section: Resultsmentioning

confidence: 99%

“…This was performed as we have previously described (30,31). Male Wistar rats (200-250 g) were equipped with an intravenous cannula, followed by the indicated infusion protocols.…”

Section: Methodsmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

See 2 more Smart Citations

Supramaximal cholecystokinin displaces Munc18c from the pancreatic acinar basal surface, redirecting apical exocytosis to the basal membrane

Gaisano¹,

Lutz²,

Leser³

et al. 2001

J. Clin. Invest.

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“…The epithelial cell membrane marker E-cadherin is also transiently diminished in these ADMs. 40 During recovery from caerulein pancreatitis, ADMs are prominent at day 3 but diminish by day 7, coincident with reconstitution of the pancreatic parenchyma to a near-normal histologic appearance ( Figure 1B). At day 3 in H&E-stained sections from vehicle-and VPD-treated animals, there were similar numbers of ADMs in both groups (12 AE 1 ADMs per HPF; Figure 6A).…”

Section: Hdacs Are Crucial For Proper Recovery and Redifferentiation mentioning

confidence: 94%

Valproic Acid Limits Pancreatic Recovery after Pancreatitis by Inhibiting Histone Deacetylases and Preventing Acinar Redifferentiation Programs

Eisses

Criscimanna

Dionise

et al. 2015

The American Journal of Pathology

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The mechanisms by which drugs induce pancreatitis are unknown. A definite cause of pancreatitis is due to the antiepileptic drug valproic acid (VPA). On the basis of three crucial observationsdthat VPA inhibits histone deacetylases (HDACs), HDACs mediate pancreas development, and aspects of pancreas development are recapitulated during recovery of the pancreas after injurydwe hypothesized that VPA does not cause injury on its own, but it predisposes patients to pancreatitis by inhibiting HDACs and provoking an imbalance in pancreatic recovery. In an experimental model of pancreatic injury, we found that VPA delayed recovery of the pancreas and reduced acinar cell proliferation. In addition, pancreatic expression of class I HDACs (which are the primary VPA targets) increased in the midphase of pancreatic recovery. VPA administration inhibited pancreatic HDAC activity and led to the persistence of acinar-to-ductal metaplastic complexes, with prolonged Sox9 expression and sustained b-catenin nuclear activation, findings that characterize a delay in regenerative reprogramming. These effects were not observed with valpromide, an analog of VPA that lacks HDAC inhibition. This is the first report, to our knowledge, that VPA shifts the balance toward pancreatic injury and pancreatitis through HDAC inhibition. The work also identifies a new paradigm for therapies that could exploit epigenetic reprogramming to enhance pancreatic recovery and disorders of pancreatic injury. We have recently gained a greater appreciation that the pancreas has a tremendous ability to recover and regenerate after injury.

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Endocytosis of the apical junctional complex: mechanisms and possible roles in regulation of epithelial barriers

2005

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Tight junctions (TJ) and adherens junctions (AJ) regulate cell-cell adhesion and barrier function of simple polarized epithelia. These junctions are positioned in the apical end of the lateral plasma membrane and form the so-called apical junctional complex (AJC). Although initially seen as purely structural features, the AJC is now known to play important roles in cell differentiation and proliferation. The AJC is a highly dynamic entity, undergoing rapid remodeling during normal epithelial morphogenesis and under pathologic conditions. There is growing evidence that remodeling of the AJC is mediated by internalization of junctional proteins. This review summarizes what is known about endocytic pathways, intracellular destinations and signaling cascades involved in internalization of AJC proteins. Potential biological roles for AJC endocytosis in maintaining functional apical junctions, reversible opening of epithelial barrier and disruption of intercellular adhesion are also discussed.

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Dissociation and reassembly of adherens junctions during experimental acute pancreatitis

Cited by 83 publications

References 0 publications

Supramaximal cholecystokinin displaces Munc18c from the pancreatic acinar basal surface, redirecting apical exocytosis to the basal membrane

Supramaximal cholecystokinin displaces Munc18c from the pancreatic acinar basal surface, redirecting apical exocytosis to the basal membrane

Valproic Acid Limits Pancreatic Recovery after Pancreatitis by Inhibiting Histone Deacetylases and Preventing Acinar Redifferentiation Programs

Endocytosis of the apical junctional complex: mechanisms and possible roles in regulation of epithelial barriers

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