Experimental and molecular pathology最新文献

{"title":"Retraction notice to “Triptolide inhibits the growth and migration of colon carcinoma cells by down-regulation of miR-191” [Experimental and Molecular Pathology 107 (2019) 23–31]","authors":"Yuxi Qi , Jinliang Li","doi":"10.1016/j.yexmp.2022.104805","DOIUrl":"10.1016/j.yexmp.2022.104805","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104805"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000685/pdfft?md5=417726f3ffc46fc113718c5576701d5a&pid=1-s2.0-S0014480022000685-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40479496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “ Geniposide suppresses growth, migration and invasion of MKN45 cells by down-regulation of lncRNA HULC” [Experimental and Molecular Pathology 105/3 (2018) 252–259]","authors":"Ji Ma , Yong Ding","doi":"10.1016/j.yexmp.2022.104810","DOIUrl":"10.1016/j.yexmp.2022.104810","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104810"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000739/pdfft?md5=cc841f56d08a84f112fb132cbe80e4f3&pid=1-s2.0-S0014480022000739-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40492675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Anti-proliferation and anti-metastatic effects of sevoflurane on human osteosarcoma U2OS and Saos-2 cells” [Experimental and Molecular Pathology 108 (2019) 121–130]","authors":"Ke Gao , Zhen Su , Hailin Liu , Yan Liu","doi":"10.1016/j.yexmp.2022.104784","DOIUrl":"10.1016/j.yexmp.2022.104784","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104784"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000442/pdfft?md5=b0b16b37f8d2a04d120ebd141be9147e&pid=1-s2.0-S0014480022000442-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40478598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “ Triptolide inhibits viability and migration while promotes apoptosis in nephroblastoma cells by regulation of miR-193b-3p” [Experimental and Molecular Pathology 108 (2019) 80–88]","authors":"Shiying Hang , Xianghong Wang , Hai Li","doi":"10.1016/j.yexmp.2022.104799","DOIUrl":"10.1016/j.yexmp.2022.104799","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104799"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000624/pdfft?md5=f973563c4ddf3da4fe5164d5faf0149e&pid=1-s2.0-S0014480022000624-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40478600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ranolazine alleviated cardiac/brain dysfunction in doxorubicin-treated rats","authors":"Titikorn Chunchai ,&nbsp;Apiwan Arinno ,&nbsp;Benjamin Ongnok ,&nbsp;Patcharapong Pantiya ,&nbsp;Thawatchai Khuanjing ,&nbsp;Nanthip Prathumsap ,&nbsp;Chayodom Maneechote ,&nbsp;Nipon Chattipakorn ,&nbsp;Siriporn C. Chattipakorn","doi":"10.1016/j.yexmp.2022.104818","DOIUrl":"10.1016/j.yexmp.2022.104818","url":null,"abstract":"<div><p><span><span>Doxorubicin<span> (Dox), a powerful chemotherapeutic agent, has been shown to cause cardiotoxicity<span><span> and neurotoxicity. </span>Ranolazine, a </span></span></span>drug<span> that is commonly used to treat patients with chronic angina, has been shown to reduce toxicity from Dox therapy. Therefore, the present study aims to investigate the mechanisms behind the protective effects of ranolazine on the heart and brain in Dox-treatment. Twenty-four male Wistar rats received 6 doses of either 0.9% normal saline (0.9% NSS, i.p., </span></span><em>n</em> = 8) or Dox (3 mg/kg, i.p., <em>n</em><span><span> = 16). All Dox-treated rats were assigned into 2 groups to receive vehicle (0.9% NSS, orally; n = 8) or ranolazine (305 mg/kg/day, orally; n = 8) for 30 consecutive days. Following the treatments, left ventricular (LV) function and cognition were determined. Animals were euthanized, then the heart and brain were collected for further analysis. Dox induced systemic oxidative stress/inflammation, and cardiac injury evidenced by mitochondrial dysfunction, mitochondrial dynamic imbalance, and </span>apoptosis<span><span>, resulting in LV dysfunction. Ranolazine significantly improved LV function via attenuating cardiac injury. Dox also caused brain pathologies as indicated by increased brain inflammation, impaired blood-brain barrier integrity, brain mitochondrial dysfunction, microglial dysmorphology, hippocampal dysplasticity, and increased apoptosis, resulting in cognitive decline. Ranolazine exerted </span>neuroprotective effects by suppressing brain pathologies and restoring cognitive function. These findings suggest that ranolazine has a potential role in cardio- and neuro-protection against chemotherapy.</span></span></p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104818"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40650356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The PI3K/AKT signaling pathway in cancer: Molecular mechanisms and possible therapeutic interventions","authors":"Mohammad Rafi Khezri ,&nbsp;Reza Jafari ,&nbsp;Keyvan Yousefi ,&nbsp;Naime Majidi Zolbanin","doi":"10.1016/j.yexmp.2022.104787","DOIUrl":"https://doi.org/10.1016/j.yexmp.2022.104787","url":null,"abstract":"<div><p>The human body consists of countless cells with the possibility of excessive and uncontrolled proliferation under certain dysregulated circumstances that could cause abnormal states such as cancer. Phosphatidylinositol<span> 3 kinase (PI3K) and its downstream target, Protein kinase B<span> or AKT, play a critical role in cell survival, proliferation, differentiation, migration, and metabolism. Research studies have examined the aberrant expression of signaling molecules that regulate PI3K/AKT pathway with the purpose of target discovery. The present review aims to recapitulate the relationship between the PI3K/AKT signaling pathway and factors contributing to initiation and development of various cancers. In addition, therapeutic interventions regulating this signaling pathway have been summarized.</span></span></p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104787"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71787921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The temporal impact of erythropoietin administration on mitochondrial function and dynamics in cardiac ischemia/reperfusion injury","authors":"Juthipong Benjanuwattra ,&nbsp;Nattayaporn Apaijai ,&nbsp;Titikorn Chunchai ,&nbsp;Kodchanan Singhanat ,&nbsp;Busarin Arunsak ,&nbsp;Kannaporn Intachai ,&nbsp;Siriporn C. Chattipakorn ,&nbsp;Nipon Chattipakorn","doi":"10.1016/j.yexmp.2022.104802","DOIUrl":"https://doi.org/10.1016/j.yexmp.2022.104802","url":null,"abstract":"<div><p><span><span>Erythropoietin (EPO) has been shown to provide protection against ischemia/reperfusion (I/R) injury in various experimental models. However, </span>clinical trials<span><span> revealed unsatisfactory results when EPO was given to patients with myocardial infarction following reperfusion. The timing of EPO administration and its relation to mitochondrial function may largely involve in this controversy. We hypothesized that EPO given at different time points exert varying cardioprotective effects in terms of myocardial infarct size, left ventricular (LV) function, arrhythmia, </span>apoptosis<span><span>, mitochondrial function, and mitochondrial dynamics in rats with cardiac I/R injury. Male </span>Wistar rats were subjected to either sham (</span></span></span><em>n</em> = 6) or cardiac I/R operation (<em>n</em><span> = 48). Rats undergoing cardiac I/R operation (30-min ischemia, followed by 120-min reperfusion) were allotted into 4 subgroups (</span><em>n</em><span><span> = 12/group): vehicle, EPO pretreatment, EPO given during ischemia, and EPO given at reperfusion. EPO was administered intravenously at 5000 unit/kg. Arrhythmia and LV function were monitored throughout the protocol. Next, the hearts were collected to determine infarct size, mitochondrial function, mitochondrial dynamics, gap junction protein, and apoptosis. Cardiac I/R promoted arrhythmias, LV dysfunction, infarct size expansion, apoptosis, mitochondrial dysfunction and increased </span>mitochondrial fission<span>. EPO given either before or during ischemia, but not at reperfusion, attenuated arrhythmia scores, LV dysfunction, infarct size, and apoptosis. Only EPO given either before or during ischemia alleviated mitochondrial swelling, mitochondrial depolarization, and reduced the levels of p-Drp1</span></span>^ser616<span>/Drp1. Data from in vitro study also confirmed that EPO directly attenuated mitochondrial dysfunction in H9c2 cells subjected to hypoxia/reoxygenation. In conclusion, the EPO administration, either before or during ischemia, exerted cardioprotection against I/R injury by attenuating mitochondrial dynamic imbalance, mitochondrial dysfunction, and apoptosis, leading to reduced infarct size and improved LV function.</span></p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104802"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71787922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “The role of cardiac fibroblasts in post-myocardial heart tissue repair” [Experimental and Molecular Pathology 101/2 (2016) 231–240]","authors":"Dimitry A. Chistiakov ,&nbsp;Alexander N. Orekhov ,&nbsp;Yuri V. Bobryshev","doi":"10.1016/j.yexmp.2022.104783","DOIUrl":"https://doi.org/10.1016/j.yexmp.2022.104783","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104783"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000430/pdfft?md5=1fac1471fccdc167926526f581cb8c0c&pid=1-s2.0-S0014480022000430-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71787923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurogranin regulates calcium-dependent cardiac hypertrophy","authors":"Ashton N. Jorgensen ,&nbsp;Chowdhury S. Abdullah ,&nbsp;Md. Shenuarin Bhuiyan ,&nbsp;Megan Watt ,&nbsp;Paari Dominic ,&nbsp;Gopi K. Kolluru ,&nbsp;Christopher G. Kevil ,&nbsp;Hyung W. Nam","doi":"10.1016/j.yexmp.2022.104815","DOIUrl":"10.1016/j.yexmp.2022.104815","url":null,"abstract":"<div><p>Intracellular Ca²⁺-calmodulin (CaM) signaling plays an important role in Ca²⁺<span><span>-CaM-dependent kinase (CaMKII) and calcineurin (CaN)-mediated cardiac biology. While </span>neurogranin (Ng) is known as a major Ca</span>²⁺<span>-CaM modulator in the brain, its pathophysiological role in cardiac hypertrophy has never been studied before. In the present study, we report that Ng is expressed in the heart and depletion of Ng dysregulates Ca</span>²⁺<span><span> homeostasis and promotes cardiac failure in mice. 10-month-old Ng </span>null mice demonstrate significantly increased heart-to-body weight ratios compared to wild-type. Using histological approaches, we identified that depletion of Ng increases cardiac hypertrophy, fibrosis, and collagen deposition near perivascular areas in the heart tissue of Ng null mice. Ca</span>²⁺<span> spark experiments revealed that cardiac myocytes isolated from Ng null mice have decreased spark frequency and width, while the duration of sparks is significantly increased. We also identified that a lack of Ng increases CaMKII</span>_δ<span> signaling and periostin<span> protein expression in these mouse hearts. Overall, we are the first study to explore how Ng expression in the heart plays an important role in Ca</span></span>²⁺<span> homeostasis in cardiac myocytes as well as the pathophysiology of cardiac hypertrophy and fibrosis.</span></p></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104815"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10211459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Quercetin ameliorates lipopolysaccharide-caused inflammatory damage via down-regulation of miR-221 in WI-38 cells”: [Experimental and Molecular Pathology 108 (2019) 1–8]","authors":"Chong Wang,&nbsp;Zhenghai Qu,&nbsp;Lingpeng Kong,&nbsp;Lei Xu,&nbsp;Mengxue Zhang,&nbsp;Jianke Liu,&nbsp;Zhaochuan Yang","doi":"10.1016/j.yexmp.2022.104809","DOIUrl":"10.1016/j.yexmp.2022.104809","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"127 ","pages":"Article 104809"},"PeriodicalIF":3.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014480022000727/pdfft?md5=e3a24dfdbf5d62bba931373c218a9280&pid=1-s2.0-S0014480022000727-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40492674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}