Journal of Receptors and Signal Transduction最新文献_第7页

circ-PSD3 promoted proliferation and invasion of papillary thyroid cancer cells via regulating the miR-7-5p/METTL7B axis. circ-PSD3通过调节miR-7-5p/METTL7B轴促进甲状腺乳头状癌细胞的增殖和侵袭。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-04-15 DOI: 10.1080/10799893.2021.1910706

Jialun Zhu, Yongbin Wang, Chuanzhou Yang, Zhiping Feng, Yanni Huang, Pengjie Liu, Fukun Chen, Zhiyong Deng

{"title":"circ-PSD3 promoted proliferation and invasion of papillary thyroid cancer cells via regulating the miR-7-5p/METTL7B axis.","authors":"Jialun Zhu, Yongbin Wang, Chuanzhou Yang, Zhiping Feng, Yanni Huang, Pengjie Liu, Fukun Chen, Zhiyong Deng","doi":"10.1080/10799893.2021.1910706","DOIUrl":"https://doi.org/10.1080/10799893.2021.1910706","url":null,"abstract":"Papillary thyroid cancer (PTC) is a common tumor malignancy of the endocrine system worldwide. Recently, circular RNAs (circRNAs) have been reported to participate in diverse pathological processes, especially in tumorigenesis. However, the functional role and mechanism of circRNA pleckstrin and Sec7 domain containing 3 (circ-PSD3) in PTC are still unclear. In this study, qRT-PCR results showed that circ-PSD3 was significantly upregulated in PTC tissues and cell lines. Meanwhile, circ-PSD3 overexpression was positively associated with larger tumor size, TNM stage, and lymph node metastasis. Knockdown of circ-PSD3 suppressed the proliferation and invasion of PTC cells. Besides, circ-PSD3 interacted with miR-7-5p to reduce its expression, and methyltransferase like 7B (METTL7B) was verified as a target gene of miR-7-5p. Functionally, inhibition of circ-PSD3 impeded PTC cell proliferation and invasion via targeting miR-7-5p to downregulate METTL7B expression. Taken together, silencing of circ-PSD3 hampered the proliferation and invasion of PTC cells via upregulating the inhibitory effect of miR-7-5p on METTL7B expression. Therefore, circ-PSD3 could be a potential diagnostic biomarker or molecular treatment target for PTC.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"251-260"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1910706","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38876196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Methylglyoxal stimulates endoplasmic reticulum stress in vascular smooth muscle cells. 甲基乙二醛刺激血管平滑肌细胞内质网应激。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-04-26 DOI: 10.1080/10799893.2021.1918167

Mustafa Kırça, Akın Yeşilkaya

{"title":"Methylglyoxal stimulates endoplasmic reticulum stress in vascular smooth muscle cells.","authors":"Mustafa Kırça, Akın Yeşilkaya","doi":"10.1080/10799893.2021.1918167","DOIUrl":"https://doi.org/10.1080/10799893.2021.1918167","url":null,"abstract":"Methylglyoxal (MGO) is considered responsible for the detrimental effects of high blood glucose. MGO is produced as a by-product of the glycolysis pathway. While the glyoxalase system removes it, the system fails in people with diabetes. MGO concentration is detected as elevated in these patients. Endoplasmic reticulum (ER) stress may play a role in atherosclerosis progression and vascular diseases. If ER stress persists, it may result in apoptosis of the cell. As a result, stabilized plaque structure by these cells may be ruptured and cause a stroke. This study aimed to investigate whether MGO can induce ER stress and apoptosis in vascular smooth muscle cells (VSMCs). Also, the effects of aminoguanidine hydrochloride (AGH), 4-phenylbutyric acid (4-PBA), and tauroursodeoxycholic acid (TUDCA) were scrutinized to relieve ER stress. VSMCs were isolated from rat aorta and cultured primary. PERK phosphorylation, IRE1α, ATF6, BiP (Grp78), and CHOP expressions were detected by the western blot technique. A caspase-3 assay kit measured the apoptosis. MGO could stimulate the main three ER stress pathways, PERK phosphorylation, IRE1α, and ATF6 expressions in a time- and concentration-dependent manner. Furthermore, AGH, 4-PBA, and TUDCA alleviated MGO-induced ER stress. However, we detected neither an increase in CHOP expression nor apoptosis in VSMCs. This study shows that MGO induces ER stress even at low concentrations in VSMCs. The impaired glyoxalase system may cause MGO accumulation and result in persisted ER stress. Supposing that ER stress is not mitigated, this table might be finalized in cell apoptosis, plaque rupture, and stroke.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"279-284"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1918167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38905960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Baicalin regulates the development of pediatric asthma via upregulating microRNA-103 and mediating the TLR4/NF-κB pathway. 黄芩苷通过上调microRNA-103和介导TLR4/NF-κB通路调控儿童哮喘的发生。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-17 DOI: 10.1080/10799893.2021.1900865

Chuanhua Zhai, Debing Wang

{"title":"Baicalin regulates the development of pediatric asthma via upregulating microRNA-103 and mediating the TLR4/NF-κB pathway.","authors":"Chuanhua Zhai, Debing Wang","doi":"10.1080/10799893.2021.1900865","DOIUrl":"https://doi.org/10.1080/10799893.2021.1900865","url":null,"abstract":"Pediatric asthma seriously endangers the well-being and health of children worldwide. Baicalin (BA) protects against diverse disorders, including asthma. Therefore, this study explored the mechanism of BA in pediatric asthma. The ovalbumin (OVA)-induced asthmatic mouse model was established to evaluate BA efficacy from aspects of oxidative stress, inflammation, blood cells in bronchoalveolar lavage fluid (BALF) and collagen deposition. Differentially expressed microRNAs (miRs) in BA-treated mice were analyzed. Effects of BA on PDGF-BB-induced smooth muscle cells (SMCs) were assessed. miR downstream mRNA and the related pathway were predicted and verified, and their effects on asthmatic mice were evaluated. BA effectively reversed OVA-induced oxidative stress and inflammation, as well as decreased the number of total cells, eosinophils and neutrophils in BALF, and collagen deposition. miR-103 was significantly upregulated after BA treatment. BA inhibited the abnormal proliferation of PDGF-BB-induced SMCs, which was prevented by miR-103 knockdown. miR-103 targeted TLR4 and regulated the extent of NF-κB phosphorylation. In vivo, miR-103 inhibition weakened the alleviating effects of BA on asthma, which was then reversed after silencing of TLR4. We highlighted that BA has the potency to halt the pediatric asthma progression via miR-103 upregulation and the TLR4/NF-κB axis inhibition.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"230-240"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1900865","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25487684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Regulation of the apolipoprotein M signaling pathway: a review. 载脂蛋白M信号通路的调控研究进展。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-05-18 DOI: 10.1080/10799893.2021.1924203

Gangli Cheng, Lu Zheng

{"title":"Regulation of the apolipoprotein M signaling pathway: a review.","authors":"Gangli Cheng, Lu Zheng","doi":"10.1080/10799893.2021.1924203","DOIUrl":"https://doi.org/10.1080/10799893.2021.1924203","url":null,"abstract":"Apolipoprotein M (apoM), an apolipoprotein predominantly associated with high-density lipoprotein (HDL), is considered a mediator of the numerous roles of HDL, including reverse cholesterol transport, anti-atherosclerotic, anti-inflammatory and anti-oxidant, and mediates pre-β-HDL formation. ApoM expression is known to be regulated by a variety of in vivo and in vitro factors. The transcription factors farnesoid X receptor, small heterodimer partner, liver receptor homolog-1, and liver X receptor comprise the signaling cascade network that regulates the expression and secretion of apoM. Moreover, hepatocyte nuclear factor-1α and c-Jun/JunB have been demonstrated to exert opposing regulatory effects on apoM through competitive binding to the same sites in the proximal region of the apoM gene. Furthermore, as a carrier and modulator of sphingosine 1-phosphate (S1P), apoM binds to S1P within its hydrophobic-binding pocket. The apoM/S1P axis has been discovered to play a crucial role in the apoM signaling pathway through its ability to regulate glucose and lipid metabolism, vascular barrier homeostasis, inflammatory response and other pathological and physiological processes. Using the findings of previous studies, the present review aimed to summarize the regulation of apoM expression by various factors and its role in different physiological and pathological conditions, and provide a new perspective for the further treatment of these diseases.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"285-292"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1924203","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38995667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Early initiation of insulin attenuates histological and functional changes in the liver of streptozotocin-induced diabetic rats using ^99mTc-sulfur colloid functional imaging. 99mtc -硫胶体功能显像显示，早期注射胰岛素可减轻链脲佐菌素诱导的糖尿病大鼠肝脏的组织学和功能变化。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-04-15 DOI: 10.1080/10799893.2021.1912097

Fatma J Al-Saeedi, Salah Kh Al-Waheeb, Peramaiyan Rajendran, Khalid M Khan, Moudhi Sadan

{"title":"Early initiation of insulin attenuates histological and functional changes in the liver of streptozotocin-induced diabetic rats using 99mTc-sulfur colloid functional imaging.","authors":"Fatma J Al-Saeedi, Salah Kh Al-Waheeb, Peramaiyan Rajendran, Khalid M Khan, Moudhi Sadan","doi":"10.1080/10799893.2021.1912097","DOIUrl":"https://doi.org/10.1080/10799893.2021.1912097","url":null,"abstract":"This study aimed to investigate the effect of insulin on the reticuloendothelial system (RES) in the liver and spleen in diabetic rats. Sprague Dawley rats were divided into control, diabetic rats (DM) and diabetic rats treated with insulin (IDM) for 2 weeks. Rats were imaged with technetium-99m-sulfur colloid (99mTc-SC) tracer to determine regional distributions of the tracer for all groups by drawing regions of interest and then obtained the ratios as the cumulative counts of heart, liver, and spleen to the whole body (WB). Liver tissue from sacrificed rats from each group was examined by light and electron microscopy. 99mTc-SC uptake ratios showed a lower liver to WB uptake ratio in the DM rats compared to both controls and IDM rats. Electron microscopy showed severe vacuolization of the hepatocytes of DM rats. The IDM rats show complete resolution of the vacuolization. The early administration of insulin for 2 weeks to diabetic rats could significantly resolve the phagocytic RES function and histological changes in the liver.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"261-267"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1912097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25591936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MicroRNA-320a-containing exosomes from human umbilical cord mesenchymal stem cells curtail proliferation and metastasis in lung cancer by binding to SOX4. 含microrna -320a的人脐带间充质干细胞外泌体通过与SOX4结合抑制肺癌的增殖和转移。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-06-07 DOI: 10.1080/10799893.2021.1918166

Huan Xie, Jie Wang

{"title":"MicroRNA-320a-containing exosomes from human umbilical cord mesenchymal stem cells curtail proliferation and metastasis in lung cancer by binding to SOX4.","authors":"Huan Xie, Jie Wang","doi":"10.1080/10799893.2021.1918166","DOIUrl":"https://doi.org/10.1080/10799893.2021.1918166","url":null,"abstract":"Exosomes from human umbilical cord mesenchymal stem cells (HUCMSCs) containing microRNAs (miRNAs) have been underscored as possible therapeutic options for cancers. Hence, our goal here was to investigate the relevance of miR-320a-containing exosomes from HUCMSCs to lung cancer. First, H1299 and H460 cells were co-cultured with the exosomes overexpressing miR-320a from HUCMSCs. The data displayed that HUCMSCs-secreted exosomes expressing miR-320a exerted anti-tumor effects in vitro and in vivo. Online analysis available at TargetScan database revealed that miR-320a bound to sex-determining region Y-box 4 (SOX4), and the luciferase reporter gene assay clarified this targeting relationship. Next, a β-catenin-specific agonist WAY-262611 was delivered into the H1299 and H460 cells to assess the effects of the Wnt/β-catenin pathway on lung cancer cellular processes. The results demonstrated that WAY-262611 potentiated lung cancer cell viability, invasion, and migration, but inhibited cell apoptosis. Altogether, exosomes carrying miR-320a from HUCMSCs might suppress lung cancer cell growth via the SOX4/Wnt/β-catenin axis, which highpoints the potency of exosomes expressing miR-320a as a possible therapeutic option for lung cancer treatment.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"268-278"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1918166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39086076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

Curcumin restrains hepatocellular carcinoma progression depending on the regulation of the circ_0078710/miR-378b/PRIM2 axis. 姜黄素通过调节circ_0078710/miR-378b/PRIM2轴抑制肝细胞癌的进展。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-06-18 DOI: 10.1080/10799893.2021.1936554

Qian Chen, Hai Guo, Yan Zong, Xiaofeng Zhao

{"title":"Curcumin restrains hepatocellular carcinoma progression depending on the regulation of the circ_0078710/miR-378b/PRIM2 axis.","authors":"Qian Chen, Hai Guo, Yan Zong, Xiaofeng Zhao","doi":"10.1080/10799893.2021.1936554","DOIUrl":"https://doi.org/10.1080/10799893.2021.1936554","url":null,"abstract":"Purpose: Curcumin has shown anti-tumor activity in multiple malignancies. The aim of our study was to explore the molecular mechanism behind the anti-tumor activity of curcumin in hepatocellular carcinoma (HCC).Methods: The proliferation, migration, invasion, and apoptosis were analyzed by 5-ethynyl-2'-deoxyuridine (EDU) assay, transwell migration assay, transwell invasion assay, and flow cytometry. Western blot assay and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) were conducted to analyze protein and RNA expression. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay, and RNA-pull down assay were performed to confirm the interaction between microRNA-378b (miR-378b) and circular RNA_0078710 (circ_0078710) or DNA primase, polypeptide 2 (PRIM2). Tumor xenograft assay was conducted to assess the roles of curcumin and circ_0078710 in vivo.Results: Curcumin stimulation restrained the proliferation, migration, and invasion, and triggered the apoptosis of HCC cells. Curcumin down-regulated the expression of circ_0078710 in HCC cells in a dose-dependent manner. Circ_0078710 knockdown aggravated curcumin-mediated anti-tumor effects in HCC cells. Circ_0078710 acted as a molecular sponge for miR-378b. Circ_0078710 interference-induced effects in curcumin-stimulated HCC cells were partly abolished by the silence of miR-378b. MiR-378b bound to the 3' untranslated region (3'UTR) of PRIM2. PRIM2 overexpression partly reversed circ_0078710 interference-mediated influences in curcumin-treated HCC cells. Circ_0078710 silencing aggravated curcumin-mediated suppressive effect in tumor growth in vivo.Conclusions: Circ_0078710 silencing aggravated curcumin-mediated anti-tumor effects through mediating the miR-378b/PRIM2 signaling in HCC cells.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"313-324"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1936554","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39243224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

FAM19A5/S1PR1 signaling pathway regulates the viability and proliferation of mantle cell lymphoma. FAM19A5/S1PR1信号通路调控套细胞淋巴瘤的生存和增殖。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-09 DOI: 10.1080/10799893.2021.1895220

Yanfang Wang, Zhenhao Zhang, Wei Wan, Yan Liu, Hongmei Jing, Fei Dong

{"title":"FAM19A5/S1PR1 signaling pathway regulates the viability and proliferation of mantle cell lymphoma.","authors":"Yanfang Wang, Zhenhao Zhang, Wei Wan, Yan Liu, Hongmei Jing, Fei Dong","doi":"10.1080/10799893.2021.1895220","DOIUrl":"https://doi.org/10.1080/10799893.2021.1895220","url":null,"abstract":"Several intracellular pathological processes have been reported to be regulated by the FAM19A5/S1PR1 signaling pathway. However, the role of FAM19A5/S1PR1 signaling pathway in the viability and proliferation of mantle cell lymphoma is not been completely understood. The task of this study is to explore the influence of FAM19A5/S1PR1 signaling pathway in affecting the survival and growth of mantle cell lymphoma. shRNAs against FAM19A5 or S1PR1 were transfected into mantle cell lymphom. Cell viability and proliferation were measured through MTT assay and CCK8 assay, respectively. Our results demonstrated that loss of FAM19A5 significantly reduced the viability of mantle cell lymphom, an effect that was followed by a drop in cell proliferation capacity. Besides, inhibition of S1PR1 also impairs cell survival and interrupt mantle cell lymphom proliferation in vitro. Taken together, our results illustrate that FAM19A5/S1PR1 signaling pathway is associated with the regulation of mantle cell lymphom viability and proliferation. This finding will provide a potential target for the treatment of malignant lymphoma in the clinical practice.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"225-229"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1895220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25449130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

SIRT1/NFκB pathway mediates anti-inflammatory and anti-apoptotic effects of rosmarinic acid on in a mouse model of nonalcoholic steatohepatitis (NASH). SIRT1/NFκB 通路介导了迷迭香酸在非酒精性脂肪性肝炎（NASH）小鼠模型中的抗炎和抗凋亡作用。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-03-31 DOI: 10.1080/10799893.2021.1905665

Tahereh Komeili-Movahhed, Mahdi Bassirian, Zahra Changizi, Azam Moslehi

{"title":"SIRT1/NFκB pathway mediates anti-inflammatory and anti-apoptotic effects of rosmarinic acid on in a mouse model of nonalcoholic steatohepatitis (NASH).","authors":"Tahereh Komeili-Movahhed, Mahdi Bassirian, Zahra Changizi, Azam Moslehi","doi":"10.1080/10799893.2021.1905665","DOIUrl":"10.1080/10799893.2021.1905665","url":null,"abstract":"Nonalcoholic steatohepatitis (NASH) is considered as a common liver disease. SIRT1, a pivotal sensor, controls activation of metabolic, inflammatory and apoptotic pathways. Rosmarinic acid (RA) has positive effects on the liver injuries; nevertheless, its mechanisms are not completely studied. The aim of this study was to explore the role of rosmarinic acid on the pathways involved by SIRT1 for amelioration of a mouse model of NASH. To do this, C57/BL6 mice were divided into four equal groups (6 in each group). Animals received saline and rosmarinic acid as the control groups. NASH was induced by methionine-choline-deficient (MCD) diet. In the NASH + RA group, Rosmarinic acid was injected daily in mice fed on an MCD diet. Rosmarinic acid decreased plasma triglyceride, cholesterol, liver Steatosis and oxidative stress. Rosmarinic acid administration also increased SIRT1, Nrf2 and PPARα and decreased SREBP1c, FAS, NFκB and caspase3 expressions. Moreover, TNFα, IL6, P53, Bax/Bcl2 ratio and caspase3 expressions decreased. Our study demonstrated that remarkable effects of rosmarinic acid on the mice with NASH might be due to activation of SIRT1/Nrf2, SIRT1/NFκB and SIRT1/PPARα pathways, which alleviate hepatic steatosis, oxidative stress, inflammation and apoptosis.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"241-250"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1905665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25533285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death. 尿酸可通过控制线粒体和caspase依赖性细胞死亡，增强MAPK途径介导的大鼠血管平滑肌细胞增殖。

IF 2.8 4区生物学

Journal of Receptors and Signal Transduction Pub Date : 2022-06-01 Epub Date: 2021-05-30 DOI: 10.1080/10799893.2021.1931320

Segün Doğru, Ekrem Yaşar, Akın Yeşilkaya

{"title":"Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death.","authors":"Segün Doğru, Ekrem Yaşar, Akın Yeşilkaya","doi":"10.1080/10799893.2021.1931320","DOIUrl":"https://doi.org/10.1080/10799893.2021.1931320","url":null,"abstract":"Hyperuricemia may be a risk factor for cardiovascular diseases such as hypertension and atherosclerosis, but the mechanisms underlying uric acid-induced pathological conditions remain unknown. In this study, we investigated the effect of short time and long-term administration of increasing uric acid concentrations on cell viability, proliferative and apoptotic pathways in vascular smooth muscle cells (VSMCs). Cell viability/proliferation was determined with WST-1 assay. Expression levels of mitogen-activated protein kinases (MAPKs) (phosphorylated (p)-p38 and p-p44/42 MAPK), extrinsic (caspase 3, caspase 8), and intrinsic (B-cell lymphoma-extra-large (Bcl-xL)) apoptotic pathway proteins were measured by Western blotting. In order to assess the proliferative effects of uric acid incubations on VSMCs, we monitored the proliferative/apoptosis signaling pathways for up to 24 h. Our results indicated that uric acid increases cell viability at time and dose-dependently in VSMCs. Immunoblotting results showed that uric acid treatment elevated the expression level of p-p38 MAPK but did markedly reduce the protein levels of p-p44/42, compared with all the uric acid doses-treated VSMCs, especially at 1 h. Uric acid stimulation increased caspase-3 protein levels and decreased Bcl-xL, but did not alter caspase-8 protein expression at the same dose and time. Furthermore, low uric acid incubations (0-7.5 mg/dL) did not affect any signaling pathways for long time points (6-24 h). In conclusion, our study demonstrates for the first time that VSMCs induced with uric acid can affect cell viability, proliferative, and apoptosis pathways at the widest time and dose range. These findings provide a better understanding of the uric acid effects related to vascular impairments.","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 3","pages":"293-301"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2021.1931320","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38955208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5