PPARγ Activation Inhibits Growth and Survival of Human Endometriotic Cells by Suppressing Estrogen Biosynthesis and PGE2 Signaling.

Lebovic, Dan I.; Kavoussi, Shahryar K.; Lee, Jehoon; Banu, Sakhila K.; Arosh, Joe A.

doi:10.1210/en.2013-1168

Cited by 34 publications

(32 citation statements)

References 53 publications

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“…115,116 Moreover, PPARγ is expressed in normal endometrium 117 but is downregulated in ectopic endometrium. 118,119 This appears to mirror what has been reported in liver fibrogenesis: PPARγ is highly expressed in quiescent hepatic stellate cells (HSCs, ie, fibroblasts) but downregulated in activated HSCs. 120,121 PPARγ promotes cellular senescence in fibroblasts, 122 and PPARγ agonists induce apoptosis and cell-cycle arrest in cancer cells.…”

Section: Tp53supporting

confidence: 67%

“…Remarkably, miR‐125b upregulation has been reported in endometriosis . Moreover, PPARγ is expressed in normal endometrium but is downregulated in ectopic endometrium . This appears to mirror what has been reported in liver fibrogenesis: PPARγ is highly expressed in quiescent hepatic stellate cells (HSCs, ie, fibroblasts) but downregulated in activated HSCs .…”

Section: Mutations Of Cancer Driver Genes In Endometriosis and Their supporting

confidence: 54%

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Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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BackgroundOne recent study reports cancer driver mutations in deep endometriosis, but its biological/clinical significance remains unclear. Since the natural history of endometriosis is essentially gradual progression toward fibrosis, it is thus hypothesized that the six driver genes reported to be mutated in endometriosis (the RP set) may play important roles in fibrogenesis but not necessarily malignant transformation.MethodsExtensive PubMed search to see whether RP and another set of driver genes not yet reported (NR) to be mutated in endometriosis have any roles in fibrogenesis. All studies reporting on the role of fibrogenesis of the genes in both RP and NR sets were retrieved and evaluated in this review.ResultsAll six RP genes were involved in various aspects of fibrogenesis as compared with only three NR genes. These nine genes can be anchored in networks linking with their upstream and downstream genes that are known to be aberrantly expressed in endometriosis, piecing together seemingly unrelated findings.ConclusionsGiven that somatic driver mutations can and do occur frequently in physiologically normal tissues, it is argued that these mutations in endometriosis are not necessarily synonymous with malignancy or premalignancy, but the result of enormous pressure for fibrogenesis.

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Section: Tp53supporting

confidence: 67%

Section: Mutations Of Cancer Driver Genes In Endometriosis and Their supporting

confidence: 54%

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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“…Ovarian endometriomas express higher levels of aromatase and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PPARGC1A) than associated ectopic lesions and eutopic endometrium (Suganuma et al 2014). Activation of peroxisome proliferator-activated receptor gamma (PPARG) inhibits the growth and survival of human endometriotic cells by suppressing E2 biosynthesis and prostaglandin E2 (PGE2) signaling (Lebovic et al 2013). The use of AIs for the treatment of endometriosis is becoming more common and is discussed below.…”

Section: Pathogenesis and Progression Of Endometriosismentioning

confidence: 99%

Endometriosis: where are we and where are we going?

Greene¹,

Lang²,

Kendziorski³

et al. 2016

Reproduction

142

106

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Endometriosis currently affects ∼5.5 million reproductive-aged women in the U.S. with symptoms such as painful periods (dysmenorrhea), chronic pelvic pain, pain with intercourse (dyspareunia), and infertility. It is defined as the presence of endometrial tissue outside the uterine cavity and is found predominately attached to sites within the peritoneal cavity. Diagnosis for endometriosis is solely made through surgery as no consistent biomarkers for disease diagnosis exist. There is no cure for endometriosis and treatments only target symptoms and not the underlying mechanism(s) of disease. The nature of individual predisposing factors or inherent defects in the endometrium, immune system, and/or peritoneal cavity of women with endometriosis remains unclear. The literature over the last 5 years (2010-2015) has advanced our critical knowledge related to hormones, hormone receptors, immune dysregulation, hormonal treatments, and the transformation of endometriosis to ovarian cancer. In this review, we cover the aforementioned topics with the goal of providing the reader an overview and related references for further study to highlight the progress made in endometriosis research, while concluding with critical areas of endometriosis research that are urgently needed.

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“…Hence, the greater mRNA expression of CPS-I in 1WK compared with 3WK and D corroborate treatment differences in protein intake, as well as PUN concentrations 28 h after supplementation (Ryall et al, 1984;Hayden and Straus, 1995;Takagi et al, 2008). Nevertheless, the similar CPS-I mRNA expression between 3WK and D was unexpected, although others have also reported that enzyme activity can be increased without changes in its expression (Banu et al, 2009;Lebovic et al, 2013). Moreover, mRNA translation into the active enzyme requires time (Clancy and Brown, 2008); hence, one can speculate that CPS-I expression assessed 28 h after supplementation reflected the ureagenesis rate at h 36 after supplementation, when PUN concentrations were similar between 3WK and D, and reduced for both treatments compared with 1WK (Figure 1).…”

Section: Parameters Associated With Protein Intakementioning

confidence: 94%

Effects of protein supplementation frequency on physiological responses associated with reproduction in beef cows1

Cappellozza

Cooke

Marques

et al. 2015

Journal of Animal Science

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The objective of this experiment was to determine if frequency of protein supplementation impacts physiological responses associated with reproduction in beef cows. Fourteen nonpregnant, nonlactating beef cows were ranked by age and BW and allocated to 3 groups. Groups were assigned to a 3 × 3 Latin square design, containing 3 periods of 21 d and the following treatments: 1) soybean meal supplementation daily (D), 2) soybean meal supplementation 3 times/week (3WK), and 3) soybean meal supplementation once/week (1WK). Within each period, cows were assigned to an estrus synchronization protocol: 100 μg of GnRH + controlled internal drug release device (CIDR) containing 1.38 g of progesterone (P4) on d 1, 25 mg of PGF2α on d 8, and CIDR removal + 100 μg of GnRH on d 11. Grass-seed straw was offered for ad libitum consumption. Soybean meal was individually supplemented at a daily rate of 1 kg/cow (as-fed basis). Moreover, 3WK was supplemented on d 0, 2, 4, 7, 9, 11, 14, 16, and 18 whereas 1WK was supplemented on d 4, 11, and 18. Blood samples were collected from 0 (before) to 72 h after supplementation on d 11 and 18 and analyzed for plasma urea-N (PUN). Samples collected from 0 to 12 h were also analyzed for plasma glucose, insulin, and P4 (d 18 only). Uterine flushing fluid was collected concurrently with blood sampling at 28 h for pH evaluation. Liver biopsies were performed concurrently with blood sampling at 0, 4, and 28 h and analyzed for mRNA expression of carbamoyl phosphate synthetase I (CPS-I; h 28) and CYP2C19 and CYP3A4 (h 0 and 4 on d 18). Plasma urea-N concentrations were greater (P < 0.01) for 1WK vs. 3WK from 20 to 72 h and greater (P < 0.01) for 1WK vs. D from 16 to 48 h and at 72 h after supplementation (treatment × hour interaction, P < 0.01). Moreover, PUN concentrations peaked at 28 h after supplementation for 3WK and 1WK (P < 0.01) and were greater (P < 0.01) at this time for 1WK vs. 3WK and D and for 3WK vs. D. Expression of CPS-I was greater (P < 0.01) for 1WK vs. D and 3WK. Uterine flushing pH tended (P ≤ 0.10) to be greater for 1WK vs. 3WK and D. No treatment effects were detected (P ≥ 0.15) on expression of CYP2C19 and CYP3A4, plasma glucose, and P4 concentrations, whereas plasma insulin concentrations were greater (P ≤ 0.03) in D and 3WK vs. 1WK. Hence, decreasing frequency of protein supplementation did not reduce uterine flushing pH or plasma P4 concentrations, which are known to impact reproduction in beef cows.

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PPARγ Activation Inhibits Growth and Survival of Human Endometriotic Cells by Suppressing Estrogen Biosynthesis and PGE2 Signaling.

Cited by 34 publications

References 53 publications

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Endometriosis: where are we and where are we going?

Effects of protein supplementation frequency on physiological responses associated with reproduction in beef cows1

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