Evaluation of the Fas/FasL signaling pathway in diabetic rat testis

Bayram, Şinasi; Kizilay, Gulnur; Topcu-Tarladacalisir, Yeter

doi:10.3109/10520295.2015.1129556

Cited by 15 publications

(8 citation statements)

References 26 publications

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“…Notably, the Fas/FasL interaction induces Fas to bind with Fasassociated death domain (FADD), which activates Caspase-8. As a result, the effector caspases, such as Caspase-3, can be activated and cause cell apoptosis (Bayram et al 2016). Uniquely, we showed that, PA induced the expression of both Fas and FasL at the with the control cells; ## p < 0.01, compared with the cells treated with PA alone.…”

Section: Discussionmentioning

confidence: 72%

“…The majority of the studies have illustrated an involvement of oxidative stress in the cytotoxic effects of saturated FFAs. For example, in the L02 cell line, PA treatment led to over-accumulation of ROS that impaired the oxidative capacity of the mitochondria (Bayram et al 2016). By contrast, ω-3 PUFAs exerted a protective role in normal cells due to their antioxidant activity (Nakagawa et al 2014).…”

Section: Discussionmentioning

confidence: 99%

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Effects of saturated palmitic acid and omega-3 polyunsaturated fatty acids on Sertoli cell apoptosis

Liang

et al. 2018

Systems Biology in Reproductive Medicine

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FFA: free fatty acid; HFD: high-fat diet; SD: standard diet; PA: palmitic acid; PUFA: polyunsaturated fatty acid; AI: apoptotic index; MTT: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide; ROS: reactive oxygen species; HE: Hematoxylin and eosin; WT1: Wilm Tumor 1; NAFLD: non- alcoholic fatty liver disease; DCFH-DA: 2', 7' dichloroﬂuorescin diacetate; 36B4: acidic ribosomal phosphoprotein P0; SD: standard deviation; EPA: eicosapentaenoic acid; PI: propidium iodide; DHA: docosahexenoic acid.

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Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Effects of saturated palmitic acid and omega-3 polyunsaturated fatty acids on Sertoli cell apoptosis

Liang

et al. 2018

Systems Biology in Reproductive Medicine

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“…Nonetheless, further studies are needed to confirm this, namely using proliferation and apoptotic markers, such as Ki67 (Jørgensen et al 2015) and TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) (Bayram et al 2016). In fact, it is already known that to become fully competent Sertoli cells must undergo a radical change, around puberty, in their morphology and function, shifting from an immature, high proliferative state to a mature, non-proliferative one.…”

Section: Discussionmentioning

confidence: 97%

High glucose levels affect spermatogenesis: an in vitro approach

Tavares

Portela

Sousa

et al. 2017

Reprod. Fertil. Dev.

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Besides known factors that may cause male infertility, systemic diseases such as diabetes mellitus may further exacerbate a decline in male fertility. This metabolic disease, clinically characterised by a hyperglycaemic phenotype, has devastating consequences in terms of human health, with reproductive dysfunction being one of the associated clinical complications. Nonetheless, the mechanisms responsible for such alterations are still poorly understood due to the multiplicity of factors involved in the induced pathophysiological changes. With this in mind, we focused on the main mediator of diabetes-associated alterations and performed an in vitro approach to address the effects of high glucose conditions on spermatogenesis, avoiding other confounding in vivo factors. Mouse (5 days post partum) testis fragments were cultured on agar gel stands at a gas-liquid interface with either 5, 25 or 50mM D-glucose for 3 weeks. Stereological analysis revealed that high D-glucose levels increased Sertoli cell number (P<0.05) and decreased tubular luminal area (P<0.01), suggesting an impairment of this somatic cell type. Moreover, higher proliferative activity in a TM4 Sertoli cell line exposed to high D-glucose was found (P<0.05) without compromising cell viability (P>0.05), further suggesting altered Sertoli cell maturation. Overall, high D-glucose concentrations may lead to impairment of Sertoli cell function, which, given their significant role in spermatogenic control, may compromise male fertility.

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“…In the present study, treatment with emodin and FK866 significantly induced PMN apoptosis, alongside increases in the expression levels of Bax and cleaved caspase-3, and a decrease in Bcl-xL expression, in PMNs. Fas is a member of the tumor necrosis factor (TNF) family and FasL belongs to the TNF receptor family ( 41 ). It is well known that activation of Fas/FasL signaling leads to cell apoptosis ( 42 ).…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that activation of Fas/FasL signaling leads to cell apoptosis ( 42 ). Initially, the interaction of Fas with FasL activates caspase-8 via the Fas-associated death domain protein, which then activates downstream caspases-3, 6 and 7 ( 41 , 43 ). The present study demonstrated that the protein expression levels of Fas and FasL were downregulated in PMNs from the SAP group.…”

Section: Discussionmentioning

confidence: 99%

Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis

Cui

Shu

Xu³

et al. 2017

Molecular Medicine Reports

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The present study aimed to evaluate the protective effects of emodin on severe acute pancreatitis (SAP)-associated acute lung injury (ALI), and investigated the possible mechanism involved. SAP was induced in Sprague-Dawley rats by retrograde infusion of 5% sodium taurocholate (1 ml/kg), after which, rats were divided into various groups and were administered emodin, FK866 [a competitive inhibitor of pre-B-cell colony-enhancing factor (PBEF)] or dexamethasone (DEX). DEX was used as a positive control. Subsequently, PBEF expression was detected in polymorphonuclear neutrophils (PMNs) isolated from rat peripheral blood by reverse transcription-quantitative polymerase chain reaction and western blotting. In addition, histological alterations, apoptosis in lung/pancreatic tissues, apoptosis of peripheral blood PMNs and alterations in the expression of apoptosis-associated proteins were examined by hematoxylin and eosin staining, terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay, Annexin V/propidium iodide (PI) assay and western blotting, respectively. Serum amylase activity and wet/dry (W/D) weight ratios were also measured. An in vitro study was also conducted, in which PMNs were obtained from normal Sprague-Dawley rats and were incubated with emodin, FK866 or DEX in the presence of lipopolysaccharide (LPS). Apoptosis of PMNs and the expression levels of apoptosis-associated proteins were examined in cultured PMNs in vitro by Annexin V/PI assay and western blotting, respectively. The results demonstrated that emodin, FK866 and DEX significantly downregulated PBEF expression in peripheral blood PMNs. In addition, emodin, FK866 and DEX reduced serum amylase activity, decreased lung and pancreas W/D weight ratios, alleviated lung and pancreatic injuries, and promoted PMN apoptosis by regulating the expression of apoptosis-associated proteins: Fas, Fas ligand, B-cell lymphoma (Bcl)-2-associated X protein, cleaved caspase-3 and Bcl-extra-large. In addition, the in vitro study demonstrated that emodin, FK866 and DEX significantly reversed the LPS-induced decrease of apoptosis in PMNs by regulating the expression of apoptosis-associated proteins. In conclusion, the present study demonstrated that emodin may protect against SAP-associated ALI by decreasing PBEF expression, and promoting PMN apoptosis via the mitochondrial and death receptor apoptotic pathways.

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Evaluation of the Fas/FasL signaling pathway in diabetic rat testis

Cited by 15 publications

References 26 publications

Effects of saturated palmitic acid and omega-3 polyunsaturated fatty acids on Sertoli cell apoptosis

Effects of saturated palmitic acid and omega-3 polyunsaturated fatty acids on Sertoli cell apoptosis

High glucose levels affect spermatogenesis: an in vitro approach

Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis

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