Acute food restriction increases collagen breakdown and phagocytosis by mature decidual cells of mice

Acute food restriction increases collagen breakdown and phagocytosis by mature decidual cells of mice

Autor Spadacci-Morena, D. D. Google Scholar
Katz, S. G. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Inst Butantan
Resumo An ultrastructural study was undertaken on antimesometrial mature decidual tissue of fed and food-restricted mice, on day 9 of pregnancy. the mean ad libitum food intake was established on mice from the 8th till the 9th day of pregnancy. Fed mice were used as controls. Experimental animals were divided into two groups: one was allowed to feed 25% of normal diet and the other 50%. Extracellular collagen fibrils were scarce in fed animals and conspicuous in food restriction. Granular electron-dense deposits and filamentous aggregates of disintegrating collagen fibrils were observed in all food-deprived mice but were rarely noted in fed animals. Intracellular vacuolar structures exhibited other typical cross-banded collagen immersed in finely granular electron-translucent material (clear vacuole) or electron-dense material containing collagen fibrils with a faint periodicity (dark vacuole), the clear and dark vacuoles were scarce in fed animals and evident in food-restricted mice, mainly in those 25% food restricted. Although collagen breakdown may be part of the normal process of decidual tissue remodelling our results suggest that it is enhanced in food-restricted animals. Thus it seems that collagen breakdown is a normal mechanism that may be regulated by the food intake of the pregnant animal. (C) 2001 Harcourt Publishers Ltd.
Palavra-chave decidua
food restriction
pregnancy
electron microscopy
mice
Idioma Inglês
Data de publicação 2001-06-01
Publicado em Tissue & Cell. Edinburgh: Churchill Livingstone, v. 33, n. 3, p. 249-257, 2001.
ISSN 0040-8166 (Sherpa/Romeo, fator de impacto)
Publicador Churchill Livingstone
Extensão 249-257
Fonte http://dx.doi.org/10.1054/tice.2001.0172
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000169853500005
Endereço permanente http://repositorio.unifesp.br/handle/11600/26579

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