Effects of Calcium Depletion on the Junctional Complex Between Oxyntic Cells of Gastric Glands

Sedar, Albert W.; Forte, John G.

doi:10.1083/jcb.22.1.173

Cited by 222 publications

(82 citation statements)

References 25 publications

(25 reference statements)

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“…These results suggest that involucrin-positive cells growing as a monolayer already have the properties that will determine their suprabasal position . Calcium ions are required for the formation of desmosomes (28) and tight junctions (20) and it seems likely that the only effect of increasing the concentration of calcium ions in the medium is to allow these intimate cell contacts to form. The ability to stratify is an intrinsic property of a mixed population of keratinocytes at different stages of terminal differentiation .…”

Section: Discussionmentioning

confidence: 99%

Selective migration of terminally differentiating cells from the basal layer of cultured human epidermis.

Watt¹

1984

The Journal of Cell Biology

180

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How terminally differentiating cells are selectively expelled from the basal layer of epidermis has been a source of interest and speculation for many years . The problem can now be studied in culture, using involucrin synthesis as an early marker of terminal differentiation in human keratinocytes . When keratinocytes are forced to grow as a monolayer by reducing the calcium ion concentration of the culture medium, they still begin to synthesize involucrin . Raising the level of calcium ions induces stratification, and cells that are synthesizing involucrin are selectively expelled from the basal layer. I have found that during calciuminduced stratification no new proteins or glycoproteins are synthesized, and the rate of cell division does not change . Movement of involucrin-positive cells out of the basal layer was found to be unaffected by cycloheximide, tunicamycin, or cytosine arabinoside . These results suggest that keratinocytes growing as a monolayer already have the necessary properties to determine their position when stratification is induced . Addition of calcium simply allows formation of desmosomes and other intimate cell contacts required for stratification . The properties of involucrin-positive cells that determine their suprabasal position include a reduced affinity for the culture substrate and preferential adhesion to other cells at the same stage of terminal differentiation . The molecular basis of these adhesive changes is discussed .

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Section: Discussionmentioning

confidence: 99%

Selective migration of terminally differentiating cells from the basal layer of cultured human epidermis.

Watt¹

1984

The Journal of Cell Biology

180

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“…We therefore asked (i) whether MDP induces NOD2 signaling in a polarized manner, and (ii) whether FRMPD2 is involved in compartmentalized NOD2 signaling. To this aim, we used small intestinal organ cultures from WT and Nod2 KO mice and disrupted epithelial junctions by calcium depletion to facilitate substance diffusion to the basolateral compartment (26,27) or left tissue in normal media. MDP-mediated KC release was only induced in calcium-free cultured intestinal segments from WT mice, not in Nod2-deficient mice (Fig.…”

Section: Frmpd2 Controls Nod2 Signaling From the Basolateral Membrane Inmentioning

confidence: 99%

RNAi screening identifies mediators of NOD2 signaling: Implications for spatial specificity of MDP recognition

Lipinski

Grabe

Jacobs

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The intracellular nucleotide-binding oligomerization domain-2 (NOD2) receptor detects bacteria-derived muramyl dipeptide (MDP) and activates the transcription factor NF-κB. Here we describe the regulatome of NOD2 signaling using a systematic RNAi screen. Using three consecutive screens, we identified a set of 20 positive NF-κB regulators including the known pathway members RIPK2, RELA, and BIRC4 (XIAP) as well as FRMPD2 (FERM and PDZ domain-containing 2). FRMPD2 interacts with NOD2 via leucinerich repeats and forms a complex with the membrane-associated protein ERBB2IP. We demonstrate that FRMPD2 spatially assembles the NOD2-signaling complex, hereby restricting NOD2-mediated immune responses to the basolateral compartment of polarized intestinal epithelial cells. We show that genetic truncation of the NOD2 leucine-rich repeat domain, which is associated with Crohn disease, impairs the interaction with FRMPD2, and that intestinal inflammation leads to down-regulation of FRMPD2. These results suggest a structural mechanism for how polarity of epithelial cells acts on intestinal NOD-like receptor signaling to mediate spatial specificity of bacterial recognition and control of immune responses.intestinal epithelium | nuclear factor kappaB | innate immune responses

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“…It has long been recognized that calcium is a key element for maintaining cellular adhesiveness, as shown from live tissues and cultured cells dissociating whenever exposed to a calcium-depleted environment [1,2]. Cadherins are Ca 2+ -dependent cell adhesion molecules that play a crucial role in homophilic cell-cell association [3].…”

Section: Introductionmentioning

confidence: 99%

Lateral self‐assembly of E‐cadherin directed by cooperative calcium binding

Alattia¹,

Ames²,

Porumb³

et al. 1997

FEBS Letters

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Effects of Calcium Depletion on the Junctional Complex Between Oxyntic Cells of Gastric Glands

Cited by 222 publications

References 25 publications

Selective migration of terminally differentiating cells from the basal layer of cultured human epidermis.

Selective migration of terminally differentiating cells from the basal layer of cultured human epidermis.

RNAi screening identifies mediators of NOD2 signaling: Implications for spatial specificity of MDP recognition

Lateral self‐assembly of E‐cadherin directed by cooperative calcium binding

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