Long non‐coding <scp>RNA MALAT</scp>1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Liu, Hengwei; Zhang, Zhibing; Xiong, Wenqian; Zhang, Ling; Du, Yu; Liu, Yi; Xiong, Xingao

doi:10.1111/jcmm.13947

Cited by 65 publications

(59 citation statements)

References 43 publications

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“…Previously, autophagy, a cellular mechanism to remove or recycle unnecessary or dysfunctional components to produce energy, has been thought to play crucial roles in protecting cells from oxidative stressinduced cell apoptosis [99,104]. Indeed, autophagy is reported to be upregulated in the ovarian endometriosis [6,89] and blocking hypoxia-induced autophagy enhances apoptosis of endometrial stromal cells [88]. Recently, it is further demonstrated that hypoxia-induced long non-coding RNA MALAT1 (lncRNA-MALAT1) is involved in autophagy to protect cells from apoptosis [88].…”

Section: Hypoxia and Cell Adhesion Endometriosis Is Initiated By Retrmentioning

confidence: 99%

“…Indeed, autophagy is reported to be upregulated in the ovarian endometriosis [6,89] and blocking hypoxia-induced autophagy enhances apoptosis of endometrial stromal cells [88]. Recently, it is further demonstrated that hypoxia-induced long non-coding RNA MALAT1 (lncRNA-MALAT1) is involved in autophagy to protect cells from apoptosis [88]. However, the underlying mechanism that how lncRNA-MALAT1 regulates hypoxia-induced autophagy is still unclear.…”

Section: Hypoxia and Cell Adhesion Endometriosis Is Initiated By Retrmentioning

confidence: 99%

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Pathophysiological implications of hypoxia in human diseases

et al. 2020

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Oxygen is essentially required by most eukaryotic organisms as a scavenger to remove harmful electron and hydrogen ions or as a critical substrate to ensure the proper execution of enzymatic reactions. All nucleated cells can sense oxygen concentration and respond to reduced oxygen availability (hypoxia). When oxygen delivery is disrupted or reduced, the organisms will develop numerous adaptive mechanisms to facilitate cells survived in the hypoxic condition. Normally, such hypoxic response will cease when oxygen level is restored. However, the situation becomes complicated if hypoxic stress persists (chronic hypoxia) or cyclic normoxia-hypoxia phenomenon occurs (intermittent hypoxia). A series of chain reaction-like gene expression cascade, termed hypoxia-mediated gene regulatory network, will be initiated under such prolonged or intermittent hypoxic conditions and subsequently leads to alteration of cellular function and/or behaviors. As a result, irreversible processes occur that may cause physiological disorder or even pathological consequences. A growing body of evidence implicates that hypoxia plays critical roles in the pathogenesis of major causes of mortality including cancer, myocardial ischemia, metabolic diseases, and chronic heart and kidney diseases, and in reproductive diseases such as preeclampsia and endometriosis. This review article will summarize current understandings regarding the molecular mechanism of hypoxia in these common and important diseases.

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Section: Hypoxia and Cell Adhesion Endometriosis Is Initiated By Retrmentioning

confidence: 99%

Section: Hypoxia and Cell Adhesion Endometriosis Is Initiated By Retrmentioning

confidence: 99%

Pathophysiological implications of hypoxia in human diseases

et al. 2020

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“…They are the most common noncoding RNAs and are involved in cell proliferation, differentiation, and apoptosis; all processes central in the pathobiology of endometriosis [21]. Some lnc-RNAs proposed as diagnostic markers of endometriosis include: H19 [22], CHL1-AS2 microRNA and Overcoming the Challenges of Their Use in the Diagnosis of Endometriosis DOI: http://dx.doi.org/10.5772/intechopen.91324 [23,24], AC002454.1 [25], lncRNA SRA (steroid receptor RNA activator) [26], MALAT-1 [27], and LINC01279 [28]. Results of a recent study revealed the lnc-RNA are carried in circulating extracellular vesicles in women with endometriosis [29].…”

Section: Candidate Clinical Markers Of Endometriosismentioning

confidence: 99%

microRNA and Overcoming the Challenges of Their Use in the Diagnosis of Endometriosis

Turpin¹,

Леонова²,

Agarwal³

et al. 2021

Endometriosis

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Endometriosis is a common estrogen dependent and inflammatory disease affecting approximately 176 million women worldwide. Currently, the time between onset of symptoms and a definitive diagnosis has been reported by several international studies to range from 6 to 12 years. Presently, laparoscopic surgery followed by histopathological confirmation of lesions remains the gold standard for diagnosis. In part because of cost and invasiveness, current trends favor reduced laparoscopic surgeries in preference of the non-surgical diagnosis of endometriosis. However, the search for a clinical marker or markers of endometriosis that provide equal or similar sensitivity and specificity to laparoscopy has remained elusive. Thus, the search for a diagnostic test for the diagnosis of endometriosis continues to be a high priority research and clinical issue. Recent studies have reported favorable results with microRNA; however, lack of replication and absence of validation suggest that circulating miRNA may not be reliable for clinical use. Use of different screening platforms together with divergent methods may account for some of the lack or reproducibility in the literature. Herein we critically assess the recent literature and explore sources for discrepant findings. We suggest that prospective studies using validated reference miRNA to normalize results together with improved study design may yet reveal a suitable diagnostic marker or panel of markers for the diagnosis of endometriosis.

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“…All cultured EESCs undergo all following experimental procedures after the third passage. Immunofluorescence assay was carried out to detect EESCs marker vimentin (Liu et al, 2019). The vimentin antibody (ab92547, Abcam, Cambridge, MA, USA) was used as primary antibodies, and the second antibody was labeled green (A11037, Invitrogen, USA).…”

Section: Isolation and Culture Of Human Escs/eescsmentioning

confidence: 99%

“…Autophagy refers to a lysosome-dependent pathway by which cytoplasmic components are delivered to lysosome for degradation (Leidal et al, 2018). Over the years, accumulating evidence showed that autophagy was critically implicated in the progression of endometriosis (Mei et al, 2015;Zhan et al, 2018a;Liu et al, 2019). It was further indicated that autophagy was implicated in NLR-mediated inflammation.…”

Section: Introductionmentioning

confidence: 99%

NLRC5 Inhibits Inflammation of Secretory Phase Ectopic Endometrial Stromal Cells by Up-Regulating Autophagy in Ovarian Endometriosis

Liu

Zhang

et al. 2020

Front. Pharmacol.

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Nod-like receptor (NLR) family caspase activation and recruitment domain containing 5 (NLRC5) is a newly identified sub-class of the NLR family. It regulates inflammation and has a key function in innate and adaptive immunologic reactions. Autophagy has been reported to be crucially linked to the pathogenesis of endometriosis. Our recent study identify there is a negative correlation between NLRC5 and autophagy in endometriosis, indicating that NLRC5 and autophagy together act as promising predictors in endometriosis patients. However, the mechanism associating NLRC5 and autophagy in endometriosis is still not completely understood. We hypothesize that autophagy could be involved in NLRC5-mediated inflammation in endometriosis. In order to validate the assumption, we evaluate the effects of NLRC5 and autophagy in the inflammation of ectopic endometrial stromal cells (EESCs) of ovarian endometriosis patients, to specifically determine whether autophagy is involved in NLRC5-mediated inflammation in EESCs. Our results show that over-expression of NLRC5 results in the up-regulation of autophagy in EESCs and inhibition of NLRC5 restricts the level of autophagy in EESCs. Furthermore, over-expression of NLRC5 and promotion of autophagy inhibit interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) expressions, whereas inhibition of NLRC5 and autophagy up-regulate IL-6 and TNF-a expressions in EESCs. Additionally, promotion of autophagy contributes to the NLRC5-mediated inhibition of IL-6 and TNF-a expressions in EESCs; inhibition of autophagy restricts NLRC5-mediated inhibition of IL-6 and TNF-a expressions in EESCs. Our results suggest that over-expression of NLRC5 promotes autophagy, thereby inhibiting inflammation in ovarian endometriosis.

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Long non‐coding RNA MALAT1 mediates hypoxia‐induced pro‐survival autophagy of endometrial stromal cells in endometriosis

Cited by 65 publications

References 43 publications

Pathophysiological implications of hypoxia in human diseases

Pathophysiological implications of hypoxia in human diseases

microRNA and Overcoming the Challenges of Their Use in the Diagnosis of Endometriosis

NLRC5 Inhibits Inflammation of Secretory Phase Ectopic Endometrial Stromal Cells by Up-Regulating Autophagy in Ovarian Endometriosis

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