IGF-I, EGF, and sex steroids regulate autophagy in bovine mammary epithelial cells via the mTOR pathway

Sobolewska, Agnieszka; Gajewska, Małgorzata; Zarzyńska, Joanna; Gajkowska, B; Motyl, T.

doi:10.1016/j.ejcb.2008.09.004

Cited by 113 publications

(99 citation statements)

References 48 publications

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“…823 Earlier studies show that intensified autophagy is observed in bovine MECs at the end of lactation and during the dry period, when there is a decrease in the levels of lactogenic hormones, increased expression of auto/paracrine apoptogenic peptides, increased influence of sex steroids and enhanced competition between the intensively developing fetus and the mother organism for nutritional and bioactive compounds. 824,825 These studies were based on some of the methods described elsewhere in these guidelines, including GFP-Atg8/LC3 fluorescence microscopy, TEM, and western blotting of LC3 and BECN1. Creation of a specific GFP-LC3 construct by insertion of cDNA encoding bovine LC3 into the pEGFP-C1 vector makes it possible to observe induction of autophagy in bovine MECs in a more specific manner than can be achieved by immunofluoresce techniques, in which the antibodies do not show specific reactivity to bovine cells and tissues.…”

Section: 818mentioning

confidence: 99%

“…Creation of a specific GFP-LC3 construct by insertion of cDNA encoding bovine LC3 into the pEGFP-C1 vector makes it possible to observe induction of autophagy in bovine MECs in a more specific manner than can be achieved by immunofluoresce techniques, in which the antibodies do not show specific reactivity to bovine cells and tissues. 823,825 However, it is important to remember that definitive confirmation of cause-and-effect is challenging for studies on large animals, given the lack or poor availability of specific antibodies and other molecular tools, the frequent inability to utilize genetic approaches, and the often prohibitive costs of administering pharmacological inhibitors in these translational preparations.…”

Section: 818mentioning

confidence: 99%

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Guidelines for the use and interpretation of assays for monitoring autophagy

Klionsky¹,

Abdalla²,

Abeliovich³

et al. 2012

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In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

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Section: 818mentioning

confidence: 99%

Section: 818mentioning

confidence: 99%

Guidelines for the use and interpretation of assays for monitoring autophagy

Klionsky¹,

Abdalla²,

Abeliovich³

et al. 2012

Self Cite

View full text Add to dashboard Cite

show abstract

“…In mammary epithelial cells, estrogen and P 4 exhibit a stimulatory effect on autophagy, which accompanies suppression of the mTOR pathway (Sobolewska et al 2009). In osteoblasts, it has been shown that estradiol enhances autophagy via promoting the dephosphorylation of mTOR (Yang et al 2013).…”

Section: Autophagic Response In Isolated Mouse Uterine Cellsmentioning

confidence: 99%

Suppression of autophagic activation in the mouse uterus by estrogen and progesterone

Choi¹,

Shin²,

Song

et al. 2014

Journal of Endocrinology

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Autophagy is a major cellular catabolic pathway tightly associated with cell survival. The involvement of autophagy in the prolonged survival of blastocysts in the uterus is well established, and it was assumed that ovarian steroid hormones -progesterone (P 4 ) and estrogens -have important roles in the regulation of autophagy. However, information is scarce regarding whether these hormones regulate autophagy in certain hormoneresponsive cellular systems. In this study, we investigated the effects of estrogen and P 4 on autophagic response in the uteri of pregnant mice and in ovariectomized (OVX) mice treated with hormones. During pregnancy, autophagic response is high on days 1 and 2 when the uterus shows an inflammatory response to mating, but it subsides around the time of implantation. Dexamethasone treatment to day 1 pregnant mice reduced autophagy in the uterus. In OVX mouse uteri, estrogen or P 4 reduces autophagic response within 6 h. Glycogen content in OVX uteri was increased by 3-methyladenine treatment, suggesting that autophagy is involved in glycogen breakdown in the hormone-deprived uterus. The classical nuclear receptor antagonists, ICI 182 780 or mifepristone, lead to the recovery of the autophagic response in OVX uteri. The suppression of autophagy by 17b-estradiol is inversely correlated with the accumulation of phospho-mouse target of rapamycin, and rapamycin treatment is moderately effective in the upregulation of autophagic response in OVX mouse uteri. Collectively, this study establishes that the uterine autophagy is induced in hormone-derived environment and is suppressed by hormone treatment. Uterine autophagy may have multiple functions as a responsive mechanism to acute inflammation and as an energy provider by breaking down glycogen under hormone deprivation.

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“…Autophagy is also tightly controlled by mTOR (mammalian target of rapamycin) kinase which is a known nutrient sensor in cells and becomes inactivated during starvation period (Gajewska et al 2007, Niedźwiedzka-Rystwej and Deptuła 2009, Sobolewska et al 2010. Recent studies on bovine mammary gland development (Sobolewska et al 2009) revealed that growth factors: IGF-I and EGF regulate the process of autophagy in epithelial cells through the mTOR signaling pathway. Another important protein engaged in this process is BNIP3 (BCL2/adenovirus E1B 19 kDa-interacting protein3), which determines the fusion of lysosomes by its specific transmembrane (TM) domain (Swoboda and Strządała 2009).…”

Section: Autophagymentioning

confidence: 99%

Autophagy in physiological and pathological processes – selected aspects

Niedźwiedzka-Rystwej¹,

Tokarz–Deptuła²,

Deptuła³

2013

Polish Journal of Veterinary Sciences

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This paper describes a model of cell death, called autophagy, one among other typical and atypical processes of cell death. This phenomenon is present in the organism, from conception until death, and is conditioned by many genes of ATG family, or mTOR kinase and specific proteins, like BNIP3. This process plays a very important role not only in physiological functions of the organism but also in pathological, such as Alzheimer or Huntington disease, as well as diseases caused by viruses.

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IGF-I, EGF, and sex steroids regulate autophagy in bovine mammary epithelial cells via the mTOR pathway

Cited by 113 publications

References 48 publications

Guidelines for the use and interpretation of assays for monitoring autophagy

Guidelines for the use and interpretation of assays for monitoring autophagy

Suppression of autophagic activation in the mouse uterus by estrogen and progesterone

Autophagy in physiological and pathological processes – selected aspects

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