PPAR ResearchPub Date : 2019-06-11DOI: 10.1155/2019/5137020
PPAR Research
{"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}
PPAR ResearchPub 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
{"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}
PPAR ResearchPub Date : 2019-05-07eCollection Date: 2019-01-01DOI: 10.1155/2019/6403504
Weiyan Wang, Chunling Li, Zhiyi Zhang, Yue Zhang
{"title":"Arsenic Trioxide in Synergy with Vitamin D Rescues the Defective VDR-PPAR-<i>γ</i> Functional Module of Autophagy in Rheumatoid Arthritis.","authors":"Weiyan Wang, Chunling Li, Zhiyi Zhang, Yue Zhang","doi":"10.1155/2019/6403504","DOIUrl":"https://doi.org/10.1155/2019/6403504","url":null,"abstract":"<p><p>Dysregulated autophagy leads to autoimmune diseases including rheumatoid arthritis (RA). Arsenic trioxide (ATO) is a single agent used for the treatment of acute promyelocytic leukemia and is highly promising for other malignancies but is also attractive for RA, although its relationship with autophagy remains to be further clarified and its application optimized. For the first time, we report a defective functional module of autophagy comprising the Vitamin D receptor (VDR), PPAR-<i>γ</i>, microtubule-associated protein 1 light-chain 3 (LC3), and p62 which appears in RA synovial fibroblasts. ATO alleviated RA symptoms by boosting effective autophagic flux through significantly downregulating p62, the inflammation and catabolism protein. Importantly, low-dose ATO synergizes with Vitamin D in RA treatment.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 ","pages":"6403504"},"PeriodicalIF":2.9,"publicationDate":"2019-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/6403504","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37336898","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}
PPAR ResearchPub Date : 2019-04-17eCollection Date: 2019-01-01DOI: 10.1155/2019/2630232
Mohammad Alsalem, Mansour Haddad, Sara A Aldossary, Heba Kalbouneh, Belal Azab, Aala Dweik, Amer Imraish, Khalid El-Salem
{"title":"Effects of Dual Peroxisome Proliferator-Activated Receptors <i>α</i> and <i>γ</i> Activation in Two Rat Models of Neuropathic Pain.","authors":"Mohammad Alsalem, Mansour Haddad, Sara A Aldossary, Heba Kalbouneh, Belal Azab, Aala Dweik, Amer Imraish, Khalid El-Salem","doi":"10.1155/2019/2630232","DOIUrl":"https://doi.org/10.1155/2019/2630232","url":null,"abstract":"<p><p>Neuropathic pain is a growing healthcare problem causing a global burden. Currently used analgesics such as opioids are associated with adverse effects; urging the need for safer alternatives. Here we aimed to investigate the potential analgesic effects of tesaglitazar; dual peroxisome proliferator-activated receptors <i>α</i> and <i>γ</i> (PPAR<i>α</i> and <i>γ</i>) agonist in rat models of neuropathic pain. This study also aimed to investigate the modulation of the transient receptor potential vanilloid 1 (TRPV1) receptor activity by tesaglitazar which could provide a potential mechanism that underlie tesaglitazar antinociceptive effects. Von Frey filaments were used to determine the paw withdrawal threshold (PWT) in adult male Sprague Dawley rats (180-250g) following i.p. injection of streptozotocin (STZ) or cisplatin, which were used as models of neuropathic pain. Antinociceptive effects of tesaglitazar were determined 6 hours after drug administration. Cobalt influx assays in cultured dorsal root ganglia (DRG) neurons were used to study the effects of tesaglitazar preincubation on capsaicin-evoked cobalt influx. Both cisplatin and STZ produced a significant decrease in PWT. The higher dose of tesaglitazar (20<i>μ</i>g/kg) significantly restored PWT in both neuropathic pain models (P<0.05). 10<i>μ</i>M capsaicin produced a robust cobalt response in DRG neurons. Preincubation of DRG neurones with tesaglitazar 6 hours prior to stimulation with capsaicin significantly reduce capsaicin-evoked cobalt responses in a PPAR<i>α</i> and PPAR<i>γ</i> dependent fashion (P<0.05). In conclusion, tesaglitazar produced significant analgesic effects in STZ and cisplatin-induced neuropathy, possibly by modulating TRPV1 receptor activity. This may be of potential benefit in clinical practice dealing with peripheral neuropathy.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 ","pages":"2630232"},"PeriodicalIF":2.9,"publicationDate":"2019-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/2630232","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37006989","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}
PPAR ResearchPub Date : 2019-02-03eCollection Date: 2019-01-01DOI: 10.1155/2019/1371758
María Sánchez-Aguilar, Luz Ibarra-Lara, Leonardo Del Valle-Mondragón, María Esther Rubio-Ruiz, Alicia G Aguilar-Navarro, Absalom Zamorano-Carrillo, Margarita Del Carmen Ramírez-Ortega, Gustavo Pastelín-Hernández, Alicia Sánchez-Mendoza
{"title":"Rosiglitazone, a Ligand to PPAR<i>γ</i>, Improves Blood Pressure and Vascular Function through Renin-Angiotensin System Regulation.","authors":"María Sánchez-Aguilar, Luz Ibarra-Lara, Leonardo Del Valle-Mondragón, María Esther Rubio-Ruiz, Alicia G Aguilar-Navarro, Absalom Zamorano-Carrillo, Margarita Del Carmen Ramírez-Ortega, Gustavo Pastelín-Hernández, Alicia Sánchez-Mendoza","doi":"10.1155/2019/1371758","DOIUrl":"https://doi.org/10.1155/2019/1371758","url":null,"abstract":"<p><p>Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor gamma (PPAR<i>γ</i>) ligand, has been reported to act as insulin sensitizer and exert cardiovascular actions. In this work, we hypothesized that RGZ exerts a PPAR<i>γ</i>-dependent regulation of blood pressure through modulation of angiotensin-converting enzyme (ACE)-type 2 (ACE2)/angiotensin-(1-7)/angiotensin II type-2 receptor (AT<sub>2</sub>R) axis in an experimental model of high blood pressure. We carried on experiments in normotensive (Sham) and aortic coarctation (AoCo)-induced hypertensive male Wistar rats. Both sham and AoCo rats were treated 7 days with vehicle (V), RGZ (5 mg/kg/day), or RGZ+BADGE (120 mg/kg/day) post-coarctation. We measured blood pressure and vascular reactivity on aortic rings, as well as the expression of renin-angiotensin system (RAS) proteins. We found that RGZ treatment in AoCo group decreases blood pressure values and improves vascular response to acetylcholine, both parameters dependent on PPAR<i>γ</i>-stimulation. RGZ lowered serum angiotensin II (AngII) but increased Ang-(1-7) levels. It also decreased 8-hydroxy-2'-deoxyguanosine (8-OH-2dG), malondialdehyde (MDA), and improved the antioxidant capacity. Regarding protein expression of RAS, RGZ decreases ACE and angiotensin II type 1 receptor (AT<sub>1</sub>R) and improved ACE2, AT<sub>2</sub>R, and Mas receptor in AoCo rats. Additionally, an <i>in silico</i> analysis revealed that 5'UTR regions of RAS and PPAR<i>γ</i> share motifs with a transcriptional regulatory role. We conclude that RGZ lowers blood pressure values by increasing the expression of RAS axis proteins ACE2 and AT<sub>2</sub>R, decreasing the levels of AngII and increasing levels of Ang-(1-7) in a PPAR<i>γ</i>-dependent manner. The <i>in silico</i> analysis is a valuable tool to predict the interaction between PPAR<i>γ</i> and RAS.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 ","pages":"1371758"},"PeriodicalIF":2.9,"publicationDate":"2019-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/1371758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37049104","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}
PPAR ResearchPub Date : 2019-01-01DOI: 10.1155/2019/5317126
Yong-Jik Lee, Yoo-Na Jang, Yoon-Mi Han, Hyun-Min Kim, Jong-Min Jeong, Min Jeoung Son, Chang Bae Jin, H. Kim, H. Seo
{"title":"Corrigendum: Caffeoylquinic Acid-Rich Extract of Aster glehni F. Schmidt Ameliorates Nonalcoholic Fatty Liver through the Regulation of PPAR δ and Adiponectin in ApoE KO Mice (PPAR Research (2017) 2017 (3912567) DOI: 10.1155/2017/3912567)","authors":"Yong-Jik Lee, Yoo-Na Jang, Yoon-Mi Han, Hyun-Min Kim, Jong-Min Jeong, Min Jeoung Son, Chang Bae Jin, H. Kim, H. Seo","doi":"10.1155/2019/5317126","DOIUrl":"https://doi.org/10.1155/2019/5317126","url":null,"abstract":"","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2019 1","pages":"5317126"},"PeriodicalIF":2.9,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2019/5317126","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64744955","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 ResearchPub Date : 2018-12-16eCollection Date: 2018-01-01DOI: 10.1155/2018/6485064
Yong-Jik Lee, Yoo-Na Jang, Yoon-Mi Han, Hyun-Min Kim, Hong Seog Seo
{"title":"6-Gingerol Normalizes the Expression of Biomarkers Related to Hypertension via PPAR<i>δ</i> in HUVECs, HEK293, and Differentiated 3T3-L1 Cells.","authors":"Yong-Jik Lee, Yoo-Na Jang, Yoon-Mi Han, Hyun-Min Kim, Hong Seog Seo","doi":"10.1155/2018/6485064","DOIUrl":"https://doi.org/10.1155/2018/6485064","url":null,"abstract":"<p><p>Hypertension is a disease with a high prevalence and high mortality rates worldwide. In addition, various factors, such as genetic predisposition, lifestyle factors, and the abnormality of organs related to blood pressure, are involved in the development of hypertension. However, at present, there are few available drugs for hypertension that do not induce side effects. Although the therapeutic effects of ginger on hypertension are well established, the precise mechanism has not been elucidated. Therefore, this study was designed to evaluate the antihypertensive mechanism of 6-gingerol, one of the main ingredients of ginger, and to assist in the development of new drugs for hypertension without side effects. The antihypertensive effects and mechanism of 6-gingerol were identified through reverse transcription polymerase chain reaction (RT-PCR), western blotting, and immunocytochemical staining for biomarkers involved in hypertension in human umbilical vein endothelial cells (HUVECs), human embryonal kidney cells (HEK293 cells), and mouse preadipocytes (3T3-L1 cells). The lipid accumulation in differentiated 3T3-L1 cells was evaluated by using Oil Red O staining. 6- Gingerol increased the level of phosphorylated endothelial nitric oxide synthase (eNOS) protein but decreased that of vascular cell adhesion protein 1 (VCAM1) and tumor necrosis factor alpha (TNF<i>α</i>) in HUVECs. In HEK293 cells, the expression of the epithelial sodium channel (ENaC) protein was reduced by 6-gingerol. Lipid accumulation was attenuated by 6-gingerol treatment in differentiated 3T3-L1 cells. These effects were regulated via peroxisome proliferator-activated receptor delta (PPAR<i>δ</i>). 6-Gingerol ameliorated the expression of biomarkers involved in the development of hypertension through PPAR<i>δ</i> in HUVECs, HEK293, and differentiated 3T3-L1 cells.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"6485064"},"PeriodicalIF":2.9,"publicationDate":"2018-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/6485064","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36863388","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}
PPAR ResearchPub Date : 2018-12-05eCollection Date: 2018-01-01DOI: 10.1155/2018/8530371
Yin-Feng Zhang, Hai-Ming Xu, Fei Yu, Man Wang, Meng-Yang Li, Tao Xu, Yan-Yan Gao, Jian-Xun Wang, Pei-Feng Li
{"title":"Crosstalk between MicroRNAs and Peroxisome Proliferator-Activated Receptors and Their Emerging Regulatory Roles in Cardiovascular Pathophysiology.","authors":"Yin-Feng Zhang, Hai-Ming Xu, Fei Yu, Man Wang, Meng-Yang Li, Tao Xu, Yan-Yan Gao, Jian-Xun Wang, Pei-Feng Li","doi":"10.1155/2018/8530371","DOIUrl":"https://doi.org/10.1155/2018/8530371","url":null,"abstract":"<p><p>Peroxisome proliferator-activated receptors (PPARs) play vital roles in cardiovascular pathophysiology, such as energy balance, cell proliferation/apoptosis, inflammatory response, and adipocyte differentiation. These vital roles make PPARs potential targets for therapeutic prevention of cardiovascular diseases (CVDs). Emerging evidence indicates that the crosstalk of microRNAs (miRNAs) and PPARs contributes greatly to CVD pathogenesis. PPARs are inhibited by miRNAs at posttranscriptional mechanisms in the progress of pulmonary hypertension and vascular dysfunction involving cell proliferation/apoptosis, communication, and normal function of endothelial cells and vascular smooth muscle cells. In the development of atherosclerosis and stroke, the activation of PPARs could change the transcripts of target miRNA through miRNA signalling. Furthermore, the mutual regulation of PPARs and miRNAs involves cell proliferation/apoptosis, cardiac remodeling, and dysfunction in heart diseases. In addition, obesity, an important cardiovascular risk, is modulated by the regulatory axis of PPARs/miRNAs, including adipogenesis, adipocyte dysfunction, insulin resistance, and macrophage polarization in adipose tissue. In this review, the crosstalk of PPARs and miRNAs and their emerging regulatory roles are summarized in the context of CVDs and risks. This provides an understanding of the underlying mechanism of the biological process related to CVD pathophysiology involving the interaction of PPARs and miRNAs and will lead to the development of PPARs/miRNAs as effective anti-CVD medications.</p>","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"8530371"},"PeriodicalIF":2.9,"publicationDate":"2018-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/8530371","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36889906","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}