Pub Date : 2020-01-09eCollection Date: 2020-01-01DOI: 10.1155/2020/6198628
Laurits J Holm, Mia Øgaard Mønsted, Martin Haupt-Jorgensen, Karsten Buschard
Peroxisome proliferator-activated receptors (PPARs) are a family of transcription factors with a key role in glucose and lipid metabolism. PPARs are expressed in many cell types including pancreatic beta cells and immune cells, where they regulate insulin secretion and T cell differentiation, respectively. Moreover, various PPAR agonists prevent diabetes in the non-obese diabetic (NOD) mouse model of type 1 diabetes. PPARs are thus of interest in type 1 diabetes (T1D) as they represent a novel approach targeting both the pancreas and the immune system. In this review, we examine the role of PPARs in immune responses and beta cell biology and their potential as targets for treatment of T1D.
{"title":"PPARs and the Development of Type 1 Diabetes.","authors":"Laurits J Holm, Mia Øgaard Mønsted, Martin Haupt-Jorgensen, Karsten Buschard","doi":"10.1155/2020/6198628","DOIUrl":"https://doi.org/10.1155/2020/6198628","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptors (PPARs) are a family of transcription factors with a key role in glucose and lipid metabolism. PPARs are expressed in many cell types including pancreatic beta cells and immune cells, where they regulate insulin secretion and T cell differentiation, respectively. Moreover, various PPAR agonists prevent diabetes in the non-obese diabetic (NOD) mouse model of type 1 diabetes. PPARs are thus of interest in type 1 diabetes (T1D) as they represent a novel approach targeting both the pancreas and the immune system. In this review, we examine the role of PPARs in immune responses and beta cell biology and their potential as targets for treatment of T1D.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2020 ","pages":"6198628"},"PeriodicalIF":2.9,"publicationDate":"2020-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/6198628","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37923567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice.
Methods: To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection.
Results: Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ), and the protective effects of piperine were abolished by the treatment of the PPAR-γ antagonist in vivo and in vitro.
Conclusions: Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice.
{"title":"Piperine Alleviates Doxorubicin-Induced Cardiotoxicity via Activating PPAR-<i>γ</i> in Mice.","authors":"Jie Yan, Si-Chi Xu, Chun-Yan Kong, Xiao-Yang Zhou, Zhou-Yan Bian, Ling Yan, Qi-Zhu Tang","doi":"10.1155/2019/2601408","DOIUrl":"https://doi.org/10.1155/2019/2601408","url":null,"abstract":"<p><strong>Background: </strong>Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice.</p><p><strong>Methods: </strong>To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection.</p><p><strong>Results: </strong>Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-<i>γ</i> (PPAR-<i>γ</i>), and the protective effects of piperine were abolished by the treatment of the PPAR-<i>γ</i> antagonist in vivo and in vitro.</p><p><strong>Conclusions: </strong>Piperine could suppress DOX-related cardiac injury via activation of PPAR-<i>γ</i> in mice.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 ","pages":"2601408"},"PeriodicalIF":2.9,"publicationDate":"2019-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/2601408","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37539008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Purpose Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear hormone receptor with a key role in lipid metabolism. Previous studies have identified various roles of PPAR-γ in cell cycle progression, cellular proliferation, and tumor progression. However, no report has described a role for PPAR-γ in human nasopharyngeal carcinoma (NPC). Notably, some studies have reported a relationship between PPAR-γ and E2F transcription factor 2 (E2F2), which has been identified as a regulator of cell cycle, apoptosis, and the DNA damage response. Notably, E2F2 has also been reported to correlate with a poor prognosis in patients with various malignancies. Methods We used immunohistochemical (IHC) and western blot methods to evaluate PPAR-γ and E2F2 expression and function in nonkeratinizing NPC and nasopharyngitis (NPG) tissue samples, as well as western blotting and CCK8 analyses in the NPC cell lines, CNE1 and CNE2. Results We observed lower levels of PPAR-γ expression in nonkeratinizing NPC tissues compared with NPG tissues and determined an association between a low level of PPAR-γ expression with a more advanced tumor stage. Furthermore, strong E2F2 expression was detected in nonkeratinizing NPC tissues. We further demonstrated that rosiglitazone, a PPAR-γ agonist, reduced E2F2 expression and proliferation in NPC cell lines. Conclusions Our study results revealed a novel role for the PPAR-γ–E2F2 pathway in controlling NPC cell proliferation and metastasis.
{"title":"PPAR-γ Ligand Inhibits Nasopharyngeal Carcinoma Cell Proliferation and Metastasis by Regulating E2F2","authors":"Ping Yang, Jiashui Wang, Xiaoxia Cheng, Jingchao Chen, Hui Zhu, Xiaolin Li, Li Cao, Wei-Wei Tang","doi":"10.1155/2019/8679271","DOIUrl":"https://doi.org/10.1155/2019/8679271","url":null,"abstract":"Purpose Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear hormone receptor with a key role in lipid metabolism. Previous studies have identified various roles of PPAR-γ in cell cycle progression, cellular proliferation, and tumor progression. However, no report has described a role for PPAR-γ in human nasopharyngeal carcinoma (NPC). Notably, some studies have reported a relationship between PPAR-γ and E2F transcription factor 2 (E2F2), which has been identified as a regulator of cell cycle, apoptosis, and the DNA damage response. Notably, E2F2 has also been reported to correlate with a poor prognosis in patients with various malignancies. Methods We used immunohistochemical (IHC) and western blot methods to evaluate PPAR-γ and E2F2 expression and function in nonkeratinizing NPC and nasopharyngitis (NPG) tissue samples, as well as western blotting and CCK8 analyses in the NPC cell lines, CNE1 and CNE2. Results We observed lower levels of PPAR-γ expression in nonkeratinizing NPC tissues compared with NPG tissues and determined an association between a low level of PPAR-γ expression with a more advanced tumor stage. Furthermore, strong E2F2 expression was detected in nonkeratinizing NPC tissues. We further demonstrated that rosiglitazone, a PPAR-γ agonist, reduced E2F2 expression and proliferation in NPC cell lines. Conclusions Our study results revealed a novel role for the PPAR-γ–E2F2 pathway in controlling NPC cell proliferation and metastasis.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/8679271","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43105056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
15-Deoxy-∆-12,14-prostaglandin J2 (15d-PGJ2), a natural peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, has been explored in some detail over the last 20 years. By triggering the PPAR-γ signalling pathway, it plays many roles and exerts antitumour, anti-inflammatory, antioxidation, antifibrosis, and antiangiogenesis effects. Although many synthetic PPAR-γ receptor agonists have been developed, as an endogenous product of PPAR-γ receptors, 15d-PGJ2 has beneficial characteristics including rapid expression and the ability to contribute to a natural defence mechanism. In this review, we discuss the latest advances in our knowledge of the biological role of 15d-PGJ2 mediated through PPAR-γ. It is important to understand its structure, synthesis, and functional mechanisms to develop preventive agents and limit the progression of associated diseases.
{"title":"15-Deoxy-∆-12,14-Prostaglandin J2 (15d-PGJ2), an Endogenous Ligand of PPAR-γ: Function and Mechanism","authors":"Jingjing Li, Chuanyong Guo, Jianye Wu","doi":"10.1155/2019/7242030","DOIUrl":"https://doi.org/10.1155/2019/7242030","url":null,"abstract":"15-Deoxy-∆-12,14-prostaglandin J2 (15d-PGJ2), a natural peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, has been explored in some detail over the last 20 years. By triggering the PPAR-γ signalling pathway, it plays many roles and exerts antitumour, anti-inflammatory, antioxidation, antifibrosis, and antiangiogenesis effects. Although many synthetic PPAR-γ receptor agonists have been developed, as an endogenous product of PPAR-γ receptors, 15d-PGJ2 has beneficial characteristics including rapid expression and the ability to contribute to a natural defence mechanism. In this review, we discuss the latest advances in our knowledge of the biological role of 15d-PGJ2 mediated through PPAR-γ. It is important to understand its structure, synthesis, and functional mechanisms to develop preventive agents and limit the progression of associated diseases.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/7242030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46585936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Benedetti, R. Galzio, B. D'angelo, M. Ceru', A. Cimini
[This corrects the article DOI: 10.1155/2010/427401.].
[这更正了文章DOI:10.1155/2010/427401.]。
{"title":"Corrigendum to “PPARs in Human Neuroepithelial Tumors: PPAR Ligands as Anticancer Therapies for the Most Common Human Neuroepithelial Tumors”","authors":"E. Benedetti, R. Galzio, B. D'angelo, M. Ceru', A. Cimini","doi":"10.1155/2019/4309068","DOIUrl":"https://doi.org/10.1155/2019/4309068","url":null,"abstract":"[This corrects the article DOI: 10.1155/2010/427401.].","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/4309068","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49033670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
[This retracts the article DOI: 10.1155/2016/9282087.].
[本文撤回文章DOI: 10.1155/2016/9282087]。
{"title":"Retracted: Possible Role of Interaction between PPARα and Cyclophilin D in Cardioprotection of AMPK against In Vivo Ischemia-Reperfusion in Rats","authors":"PPAR Research","doi":"10.1155/2019/9760941","DOIUrl":"https://doi.org/10.1155/2019/9760941","url":null,"abstract":"[This retracts the article DOI: 10.1155/2016/9282087.].","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/9760941","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42403823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tatsuya Morinishi, Yasunori Tokuhara, H. Ohsaki, Emi Ibuki, K. Kadota, E. Hirakawa
Peroxisome proliferator-activated receptor alpha (PPAR-α) belongs to the PPAR family and plays a critical role in inhibiting cell proliferation and tumorigenesis in various tumors. However, the role of PPAR-α in colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-α agonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-α was expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-α increased in colorectal carcinoma tissue compared with that of normal epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-α and clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-α was significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-α may be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-α may be a therapeutic target for colorectal adenocarcinoma treatment.
{"title":"Activation and Expression of Peroxisome Proliferator-Activated Receptor Alpha Are Associated with Tumorigenesis in Colorectal Carcinoma","authors":"Tatsuya Morinishi, Yasunori Tokuhara, H. Ohsaki, Emi Ibuki, K. Kadota, E. Hirakawa","doi":"10.1155/2019/7486727","DOIUrl":"https://doi.org/10.1155/2019/7486727","url":null,"abstract":"Peroxisome proliferator-activated receptor alpha (PPAR-α) belongs to the PPAR family and plays a critical role in inhibiting cell proliferation and tumorigenesis in various tumors. However, the role of PPAR-α in colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-α agonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-α was expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-α increased in colorectal carcinoma tissue compared with that of normal epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-α and clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-α was significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-α may be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-α may be a therapeutic target for colorectal adenocarcinoma treatment.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/7486727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44527608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lei Xu, Gang Zhao, Hong Zhu, Shijun Wang, A. Sun, Y. Zou, J. Ge
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is one of the major receptors expressed on the endothelium of arterial wall with a key role in endothelial dysfunction and the development of atherosclerosis. Recent evidence suggested that LOX-1 is upregulated under the condition of insulin resistance and could be suppressed by the antidiabetic drugs. We previously also confirmed that Thiazolidinedione (TZD) has the inhibitory effect on LOX-1 in ox-LDL-induced endothelial cells. However, the underlying mechanism is unclear. Here we showed that Rosiglitazone treatment significantly attenuated the expressions of LOX-1, ICAM-1, VCAM-1, p47phox, and the atherosclerotic lesions in ApoE−/− mice with high-fat diet. In vitro, we revealed that Rosiglitazone inhibited LOX-1 by regulating miR-590-5p. Ox-LDL-mediated ICAM-1, VCAM-1, and p47phox were significantly reduced by Rosiglitazone, but all reversed after pretreating the cells with antagomiR-590-5p. Induction with Rosiglitazone activated PPAR-γ and promoted its nuclear translocation in cultured human umbilical vein endothelial cells (HUVECs). The nuclear PPAR-γ upregulated the miR-590-5p level through binding to its transcriptional promoter region. Retaining PPAR-γ in cytoplasm by transfecting with PPAR-γ⊿NLS plasmid in HUVECs failed to activate miR-590-5p. Mutation of the promoter region of PPAR-γ also reduced the miR-590-5p promoter luciferase activity. Collectively, these data indicated that PPAR-γ may have the therapeutic potential in atherosclerosis via the transcriptional regulation of miR-590-5p in endothelial cells.
{"title":"Peroxisome Proliferator-Activated Receptor-γ Antagonizes LOX-1-Mediated Endothelial Injury by Transcriptional Activation of miR-590-5p","authors":"Lei Xu, Gang Zhao, Hong Zhu, Shijun Wang, A. Sun, Y. Zou, J. Ge","doi":"10.1155/2019/2715176","DOIUrl":"https://doi.org/10.1155/2019/2715176","url":null,"abstract":"Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is one of the major receptors expressed on the endothelium of arterial wall with a key role in endothelial dysfunction and the development of atherosclerosis. Recent evidence suggested that LOX-1 is upregulated under the condition of insulin resistance and could be suppressed by the antidiabetic drugs. We previously also confirmed that Thiazolidinedione (TZD) has the inhibitory effect on LOX-1 in ox-LDL-induced endothelial cells. However, the underlying mechanism is unclear. Here we showed that Rosiglitazone treatment significantly attenuated the expressions of LOX-1, ICAM-1, VCAM-1, p47phox, and the atherosclerotic lesions in ApoE−/− mice with high-fat diet. In vitro, we revealed that Rosiglitazone inhibited LOX-1 by regulating miR-590-5p. Ox-LDL-mediated ICAM-1, VCAM-1, and p47phox were significantly reduced by Rosiglitazone, but all reversed after pretreating the cells with antagomiR-590-5p. Induction with Rosiglitazone activated PPAR-γ and promoted its nuclear translocation in cultured human umbilical vein endothelial cells (HUVECs). The nuclear PPAR-γ upregulated the miR-590-5p level through binding to its transcriptional promoter region. Retaining PPAR-γ in cytoplasm by transfecting with PPAR-γ⊿NLS plasmid in HUVECs failed to activate miR-590-5p. Mutation of the promoter region of PPAR-γ also reduced the miR-590-5p promoter luciferase activity. Collectively, these data indicated that PPAR-γ may have the therapeutic potential in atherosclerosis via the transcriptional regulation of miR-590-5p in endothelial cells.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/2715176","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44875453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
PPAR Research would like to express concern with the article titled “Testosterone Replacement Modulates Cardiac Metabolic Remodeling a erMyocardial Infarction by Upregulating PPARα” [1] published in PPAR Research in June 2016 due to flaws found in the quality of the article. eEditorial Board believed that the experimental design is not solid enough as the control groups are missing. ey thought that it is confusing that most of the data sets are labeled with n=3 in the legends which is extremely low for animal experiments. In addition, the board found that the authors described each group number in the methods which is not n=3 but slightly higher. ere is no explanation why not all animals were included in all analyses and how a selection of data sets was performed. In some data sets, the authors use n=6 but some animal data sets are missing. e authors explained that, in theMaterials andMethods, additional normal rats that underwent the same procedure without LDA occlusion were used as the control group. Moreover, the number of animals which were alive a er the myocardial infarction was mentioned in the Materials and Methods and the number of animals in figure legendswas less than that in theMaterials andMethods as the remaining alive rats were divided into several parts for different experiments. ey added that, during echocardiographic measurement, two rats of Cas group died from anesthesia, so they took four rats from different groups to evaluate cardiac indexes. A er echocardiographic studies, the rats were immediately executed in addition to collecting blood and heart samples. e minimum number of different groups was 6 (8 S-Cas, 6 Cas, 7 Cas+T, and 6 Cas+T+F). Accordingly, they measured ATP content and sexual hormones of six rats. ree rats were performed by histological analysis, and the other three were performed by western blotting and real-time PCR. e Editorial Board was concerned about the death of several animals which should be clearly defined by the authors as they should state why the n was 3-6 when each treatment is mentioned with an n = 8. Moreover, the board found that the statistical analysis was not done properly and they recommended repeating the study to increase the sample size.
{"title":"Expression of Concern on “Testosterone Replacement Modulates Cardiac Metabolic Remodeling after Myocardial Infarction by Upregulating PPARα”","authors":"PPAR Research","doi":"10.1155/2019/5137020","DOIUrl":"https://doi.org/10.1155/2019/5137020","url":null,"abstract":"PPAR Research would like to express concern with the article titled “Testosterone Replacement Modulates Cardiac Metabolic Remodeling a erMyocardial Infarction by Upregulating PPARα” [1] published in PPAR Research in June 2016 due to flaws found in the quality of the article. eEditorial Board believed that the experimental design is not solid enough as the control groups are missing. ey thought that it is confusing that most of the data sets are labeled with n=3 in the legends which is extremely low for animal experiments. In addition, the board found that the authors described each group number in the methods which is not n=3 but slightly higher. ere is no explanation why not all animals were included in all analyses and how a selection of data sets was performed. In some data sets, the authors use n=6 but some animal data sets are missing. e authors explained that, in theMaterials andMethods, additional normal rats that underwent the same procedure without LDA occlusion were used as the control group. Moreover, the number of animals which were alive a er the myocardial infarction was mentioned in the Materials and Methods and the number of animals in figure legendswas less than that in theMaterials andMethods as the remaining alive rats were divided into several parts for different experiments. ey added that, during echocardiographic measurement, two rats of Cas group died from anesthesia, so they took four rats from different groups to evaluate cardiac indexes. A er echocardiographic studies, the rats were immediately executed in addition to collecting blood and heart samples. e minimum number of different groups was 6 (8 S-Cas, 6 Cas, 7 Cas+T, and 6 Cas+T+F). Accordingly, they measured ATP content and sexual hormones of six rats. ree rats were performed by histological analysis, and the other three were performed by western blotting and real-time PCR. e Editorial Board was concerned about the death of several animals which should be clearly defined by the authors as they should state why the n was 3-6 when each treatment is mentioned with an n = 8. Moreover, the board found that the statistical analysis was not done properly and they recommended repeating the study to increase the sample size.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2019-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/5137020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41856444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-02eCollection Date: 2019-01-01DOI: 10.1155/2019/1932036
Izabela Wojtkowska, Tomasz A Bonda, Andrzej Tysarowski, Katarzyna Seliga, Janusz A Siedlecki, Maria M Winnicka, Janina Stępińska
TNFα and PPARγ are important modulators of metabolism, inflammation, and atherosclerosis. Coronary artery disease is the leading cause of heart failure (HF). The aim of the study was to assess whether polymorphisms of the TNFα (-308G>A) and PPARG2 (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. Methods. 122 patients without HF (aged 63 ± 8.8 years, 85% males) with confirmed coronary artery disease qualified for coronary bypass grafting were enrolled in the study. After the procedure, they were screened for cardiac parameters. Those with elevated NT-proBNP or diminished left ventricular ejection fraction during follow-up were assigned to the HF group (n=78), and the remaining ones to the non-HF group (n=44). The TNFα -308G>A and PPARG2 Pro12Ala polymorphisms were detected using the TaqMan method. Results. The distributions of TNFα -308G>A and PPARG2 Pro12Ala did not differ between the HF and non-HF groups (-308G>A: 16% vs. 11.4% of alleles; Pro12Ala: 23.9% vs. 20.5% of alleles, respectively). IL-6 concentration in the plasma of TNFα A-allele carriers at months 1 and 12 after CABG was higher in the HF group compared to the non-HF group (1 month after CABG: 5.3 ± 3.4 vs. 3.1 ± 2.9, p<0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p<0.01, respectively). Both polymorphisms were not related to changes in the plasma TNFα concentration or other parameters related to HF. Conclusions. Our study did not reveal any correlation between the PPARG2 Pro12Ala and TNFα -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.
TNFα和PPARγ是代谢、炎症和动脉粥样硬化的重要调节剂。冠状动脉疾病是导致心力衰竭的主要原因。该研究的目的是评估TNFα (-308G>A)和PPARG2 (Pro12Ala)基因多态性是否与缺血性心脏病患者发生HF的风险相关。方法:122例无心衰患者(年龄63±8.8岁，男性85%)经证实有冠状动脉病变，符合冠状动脉搭桥术条件。手术后，他们接受了心脏参数的筛查。随访期间NT-proBNP升高或左室射血分数降低的患者被分配到HF组(n=78)，其余患者被分配到非HF组(n=44)。TaqMan法检测TNFα -308G>A和PPARG2 Pro12Ala多态性。结果。TNFα -308G>A和PPARG2 Pro12Ala在HF组和非HF组之间的分布无差异(-308G>A: 16% vs. 11.4%;Pro12Ala: 23.9% vs. 20.5%)。在CABG术后1、12个月，HF组TNFα a等位基因携带者血浆IL-6浓度高于非HF组(CABG术后1个月:5.3±3.4 vs 3.1±2.9)，pα浓度或其他与HF相关的参数。结论。我们的研究未发现PPARG2 Pro12Ala和TNFα -308G>A多态性与缺血性心脏病患者冠状动脉搭桥术后HF的发生之间存在相关性。
{"title":"PPARG2 Pro12Ala and TNF<i>α</i> -308G>A Polymorphisms Are Not Associated with Heart Failure Development in Patients with Ischemic Heart Disease after Coronary Artery Bypass Grafting.","authors":"Izabela Wojtkowska, Tomasz A Bonda, Andrzej Tysarowski, Katarzyna Seliga, Janusz A Siedlecki, Maria M Winnicka, Janina Stępińska","doi":"10.1155/2019/1932036","DOIUrl":"https://doi.org/10.1155/2019/1932036","url":null,"abstract":"<p><p>TNF<i>α</i> and PPAR<i>γ</i> are important modulators of metabolism, inflammation, and atherosclerosis. Coronary artery disease is the leading cause of heart failure (HF). The aim of the study was to assess whether polymorphisms of the <i>TNFα</i> (-308G>A) and <i>PPARG2</i> (Pro12Ala) genes are associated with the risk of developing HF by patients with ischemic heart disease. <i>Methods</i>. 122 patients without HF (aged 63 ± 8.8 years, 85% males) with confirmed coronary artery disease qualified for coronary bypass grafting were enrolled in the study. After the procedure, they were screened for cardiac parameters. Those with elevated NT-proBNP or diminished left ventricular ejection fraction during follow-up were assigned to the HF group (n=78), and the remaining ones to the non-HF group (n=44). The <i>TNFα</i> -308G>A and <i>PPARG</i>2 Pro12Ala polymorphisms were detected using the TaqMan method. <i>Results</i>. The distributions of <i>TNFα</i> -308G>A and <i>PPARG</i>2 Pro12Ala did not differ between the HF and non-HF groups (-308G>A: 16% vs. 11.4% of alleles; Pro12Ala: 23.9% vs. 20.5% of alleles, respectively). IL-6 concentration in the plasma of <i>TNFα</i> A-allele carriers at months 1 and 12 after CABG was higher in the HF group compared to the non-HF group (1 month after CABG: 5.3 ± 3.4 vs. 3.1 ± 2.9, p<0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p<0.01, respectively). Both polymorphisms were not related to changes in the plasma TNF<i>α</i> concentration or other parameters related to HF. <i>Conclusions</i>. Our study did not reveal any correlation between the <i>PPARG2</i> Pro12Ala and <i>TNFα</i> -308G>A polymorphisms and development of HF in patients with ischemic heart disease after coronary bypass grafting.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 ","pages":"1932036"},"PeriodicalIF":2.9,"publicationDate":"2019-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/1932036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37392487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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