Cited by 28

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Apoptosis and mammary gland involution: reviewing the process

Furth, P. A., Bar-Peled, U., Li, M.·1997·Apoptosis

Abstract

Apoptosis is a process of programmed cell death. Mammary gland involution is a tissue remodelling process. Mammary epithelial cell apoptosis is an integral component of tissue remodelling but it is only one element. Equally important are the factors which degrade basement membrane and extracellular matrix. Both operations are required for completion of mammary gland involution. The primary apoptotic process occurs first and is temporally distinct from the second stage of involution typified by lobular-alveolar collapse. Local factors related to milk accumulation trigger the first stage, but loss of systemic hormonal stimulation governs the second stage. Changes in the expression patterns of cell cycle control genes and bcl-2 family member genes are found in the first stage. Proteinase gene activation dominates the second stage. These findings support a two stage model of mammary gland involution. Both mammary epithelial cell apoptosis and mammary gland remodelling advance through a process which includes both loss of survival factors and gain of death factors. This review focuses on signalling pathways and genetic controls which are activated and repressed during mammary gland involution.

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Crossref · 10.1023/a:1026454207398

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  • Rapid cell death and tissue regression during mammary involution is a tightly controlled process, and TGF-beta signaling is known to play a crucial role.

    “The rapid cell death and tissue regression during mammary involution is a tightly controlled process (Furth et al., 1997; Furth, 1999), and TGF-beta signaling is known to play a crucial role (Bierie et al., 2009).”

    From Endocytosis and Physiology: Insights from Disabled-2 Deficient Mice (2016) · cites this paper as Furth et al., 1997

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Research works printed but not linked: 31

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Metadata

Authors
Furth, P. A., Bar-Peled, U., & Li, M.
Venue
Apoptosis
Published
1997-01
Volume
2
Issue
1
Pages
19-24
ISSN
  • 1360-8185
  • 1573-675X
Cited by
28
References
0
Language
en

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