The variable expression of lectin-like oxidized low-density lipoprotein receptor (LOX-1) and signs of autophagy and apoptosis in freshly harvested human granulosa cells depend on gonadotropin dose, age, and body weight

Vilser, Constanze; Hueller, H; Nowicki, Marcin; Hmeidan, Fayez Abu; Blumenauer, Verona; Spanel‐Borowski, Katharina

doi:10.1016/j.fertnstert.2009.02.038

Cited by 58 publications

(25 citation statements)

References 41 publications

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“…18 We postulated a lower rate of autophagy in ob/ob mice than in the other groups because of granulosa cells from obese women undergoing in vitro fertilisation therapy display a low LC3-II/LC3-I ratio. 23 Our assumption was confirmed with a weak ratio in the ob/ob group (Figures 4c and d). The highest ratio was detected in WT and ob/ þ mice.…”

Section: Resultssupporting

confidence: 62%

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Leptin-deficient (ob/ob) mouse ovaries show fatty degeneration, enhanced apoptosis and decreased expression of steroidogenic acute regulatory enzyme

et al. 2011

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OBJECTIVE: Leptin-deficient (ob/ob) mice are obese and infertile. Dysfunctions of the ovaries are preferentially related to leptin-deficiency. DESIGN: Morphological and molecular biological obesity-dependent changes in ob/ob ovaries. SUBJECTS: Ovaries were obtained from three-month-old mice either homozygote (ob/ob) and heterozygote (ob/ þ ) or wild-type (C57BL6, WT) for the investigation by light and electron microscopy, as well as for western blot analysis of lectin-like oxidised low density lipoprotein receptor (LOX-1), Toll-like receptor 4 (TLR4), CD36, cleaved caspase-3, microtubule-associated protein light chain 3 (LC3), and the steroidogenic acute regulatory protein (StAR). RESULTS: Compared with control ovaries with corpora lutea, ob/ob ovaries lacked corpora lutea, follicular atresia was at a higher rate; lipid droplets accumulated in follicle cells and in the oocyte with damaged mitochondria; the basement membrane of follicles was thickened. LOX-1 and CD36 expressions were comparable for all three groups. Ob/ob ovaries showed significantly higher levels of TLR4 and cleaved caspase-3 than the ones from the control groups. The high LC3-II/I ratio in the WT and ob/ þ ovaries was related to the presence of corpora lutea. The StAR protein was lower in the ob/ob ovaries signifying reduced steroidogenesis. CONCLUSIONS: Excessive lipid storage causes disorders of ovarian function in ob/ob mice. The local lipid overload leads to advanced follicular atresia with apoptosis and defect steroidogenesis. We suggest that the changes in lipid metabolism lead to increased oxidative stress and thereby, they are an important reason of anovulation and infertility.

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Section: Resultssupporting

confidence: 62%

“…This suggestion is supported by findings of autophagosomes in freshly harvested human granulosa cells. 23 Additionally, evidence is given that altered apoptotic cell death occurs in granulosa cells. 36 It is noteworthy that annular junctions in regressing antral follicles of ob/ob mice might be mistaken for autophagosomes.…”

Section: Discussionmentioning

confidence: 99%

Leptin-deficient (ob/ob) mouse ovaries show fatty degeneration, enhanced apoptosis and decreased expression of steroidogenic acute regulatory enzyme

et al. 2011

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“…LOX1 stimulation by oxLDL has also been associated with an increased level of reactive oxygen species (ROS) leading to oxidative stress and apoptotic cell death. In younger, normal weight women, reparative autophagy is induced in response to low levels of ROS in order to avoid apoptosis and promote cell survival (Vilser et al 2010). An increase in ROS levels, as well as a decline in autophagic markers (LC3-II) in human granulosa cells of older women suggests that there is a decline in reparative autophagy with age leading to granulosa cell apoptosis (Tatone et al 2006, Vilser et al 2010).…”

Section: Ovaries and Testesmentioning

confidence: 99%

“…In younger, normal weight women, reparative autophagy is induced in response to low levels of ROS in order to avoid apoptosis and promote cell survival (Vilser et al 2010). An increase in ROS levels, as well as a decline in autophagic markers (LC3-II) in human granulosa cells of older women suggests that there is a decline in reparative autophagy with age leading to granulosa cell apoptosis (Tatone et al 2006, Vilser et al 2010). This result is in concordance with the well-documented, age-related decline in female fertility (Carbone et al 2003, Tatone et al 2006.…”

Section: Ovaries and Testesmentioning

confidence: 99%

Autophagy in the endocrine glands

Weckman¹,

Ieva²,

Rotondo³

et al. 2014

Journal of Molecular Endocrinology

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Autophagy is an important cellular process involving the degradation of intracellular components. Its regulation is complex and while there are many methods available, there is currently no single effective way of detecting and monitoring autophagy. It has several cellular functions that are conserved throughout the body, as well as a variety of different physiological roles depending on the context of its occurrence in the body. Autophagy is also involved in the pathology of a wide range of diseases. Within the endocrine system, autophagy has both its traditional conserved functions and specific functions. In the endocrine glands, autophagy plays a critical role in controlling intracellular hormone levels. In peptide-secreting cells of glands such as the pituitary gland, crinophagy, a specific form of autophagy, targets the secretory granules to control the levels of stored hormone. In steroid-secreting cells of glands such as the testes and adrenal gland, autophagy targets the steroid-producing organelles. The dysregulation of autophagy in the endocrine glands leads to several different endocrine diseases such as diabetes and infertility. This review aims to clarify the known roles of autophagy in the physiology of the endocrine system, as well as in various endocrine diseases.

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“…The high range of dead cells is explained by different degrees of oxidative stress, thus not only attributed to the gonadotropin releasing hormone treatment, which induces classical apoptosis at the level of the ovary (Tsai et al, 2005;Giampietro et al, 2006). Different degrees of oxidative stress could modify different forms of cell death, which appear to occur simulteously in mature follicles (van Wezel et al, 1999;Stocco et al, 2007;Serke et al, 2009;Vilser et al, 2010).…”

Section: Danger In Preovulatory Follicles For Onset Of Inim Functionmentioning

confidence: 99%

Ovulation as danger signaling event of innate immunity

Spanel‐Borowski

2011

Molecular and Cellular Endocrinology

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The variable expression of lectin-like oxidized low-density lipoprotein receptor (LOX-1) and signs of autophagy and apoptosis in freshly harvested human granulosa cells depend on gonadotropin dose, age, and body weight

Cited by 58 publications

References 41 publications

Leptin-deficient (ob/ob) mouse ovaries show fatty degeneration, enhanced apoptosis and decreased expression of steroidogenic acute regulatory enzyme

Leptin-deficient (ob/ob) mouse ovaries show fatty degeneration, enhanced apoptosis and decreased expression of steroidogenic acute regulatory enzyme

Autophagy in the endocrine glands

Ovulation as danger signaling event of innate immunity

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