Restored invasion of mouse MO4 cells into chick heartin vitro through mutual conditioning at reduced temperature View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1989-05

AUTHORS

Erik A. Bruyneel, Jan G. Bolscher, Lou A. Smets, Marc De Mets, Marc M. Mareel

ABSTRACT

Invasion of malignant mouse MO4 cells into embryonic chick heart fragments in confronting organ cultures was arrested for 7 days when the temperature of incubation was lowered to 28 degrees C. Afterwards invasion resumed and progression between days 10 and 17 at 28 degrees C was comparable to that between days 0 and 7 at 37 degrees C. This pattern of progression of MO4 cell invasion at 28 degrees C was unaltered when either MO4 cells or heart fragments or both were preincubated separately at 28 degrees C for 14 days before confrontation with each other. Invasion at 28 degrees C resumed only when MO4 cells and heart tissue had been in immediate contact for at least 7 days. Metabolic labelling with [3H]fucose showed a correlation in time between transient suppression of invasion and transient inhibition of incorporation of fucosylation-precursor molecules into glycoproteins by MO4 cells. The latter activity was far less temperature-sensitive in heart cells. Our observations suggest that metabolic cooperation between invading MO4 cells and heart tissue is essential for progression of invasion in vitro. More... »

PAGES

361-371

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf01753687

DOI

http://dx.doi.org/10.1007/bf01753687

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042426764

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2924452


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51 schema:description Invasion of malignant mouse MO4 cells into embryonic chick heart fragments in confronting organ cultures was arrested for 7 days when the temperature of incubation was lowered to 28 degrees C. Afterwards invasion resumed and progression between days 10 and 17 at 28 degrees C was comparable to that between days 0 and 7 at 37 degrees C. This pattern of progression of MO4 cell invasion at 28 degrees C was unaltered when either MO4 cells or heart fragments or both were preincubated separately at 28 degrees C for 14 days before confrontation with each other. Invasion at 28 degrees C resumed only when MO4 cells and heart tissue had been in immediate contact for at least 7 days. Metabolic labelling with [3H]fucose showed a correlation in time between transient suppression of invasion and transient inhibition of incorporation of fucosylation-precursor molecules into glycoproteins by MO4 cells. The latter activity was far less temperature-sensitive in heart cells. Our observations suggest that metabolic cooperation between invading MO4 cells and heart tissue is essential for progression of invasion in vitro.
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