Molecular Biology Research Communications最新文献

{"title":"Clinical profile of <i>FTL3</i>-ITD mutation in West Algerian population with acute myeloid leukemia.","authors":"Fatima Zohra Moghtit, Wefa Boughrara, Samia Dorgham, Ilies Koriche, Imene Ouahba, Amina Ammour, Amine Bekadja, Meriem Samia Aberkane","doi":"10.22099/mbrc.2024.49437.1955","DOIUrl":"10.22099/mbrc.2024.49437.1955","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the abnormal and rapid growth of cells. The mutation of the Fms-like tyrosine kinase 3 ligand gene (<i>FLT3</i>-ITD) represents an important factor in the prognosis of AML. The objective of this study was to determine for the first time the prevalence of <i>FLT3</i>-ITD mutation in west Algerian AML patients. A total of 160 AML patients were genotyped for <i>FLT3</i>-ITD mutation by using polymerase chain reaction. <i>FLT3</i>-ITD mutation was detected in 13% of patients. Mutation rates show no significant difference in the distribution of sex and age. A positive association was found between this mutation and a higher leukocyte and blast cells counts. We also found that the M3 and M5 subtype were the commonest in the <i>FLT3</i> mutated group. This preliminary study provides first-time prevalence estimates for <i>FLT3</i>-ITD mutation in acute myeloid leukemia patients from the West region of Algeria.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"175-182"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural compounds solasonine and alisol B23-acetate target GLI3 signaling to block oncogenesis in MED12-altered breast cancer.","authors":"Shivani Akula, Cristian G Gonzalez, Sophia Kermet, Marieke Burleson","doi":"10.22099/mbrc.2024.49044.1915","DOIUrl":"10.22099/mbrc.2024.49044.1915","url":null,"abstract":"<p><p>Breast cancer remains to be the second leading cause of cancer deaths worldwide thereby highlighting the critical need to find superior treatment strategies for this disease. In the current era of cancer treatment, personalized medicine is garnering much attention as this type of treatment is more selective thereby minimizing harmful side effects. Personalized medicine is dependent upon knowing the underlying genetic landscape of the initial tumor. In our study, we focused our efforts on a specific subset of breast cancer that harbors genetic alterations in the Mediator subunit 12 (MED12). Our results show that loss of MED12 leads to enhanced cellular proliferation and colony formation of breast cancer cells through a mechanism that involves activation of GLI3-dependent SHH signaling, a pathway that is central to breast development and homeostasis. To find a personalized treatment option for this subset of breast cancer, we employed a natural compound screening strategy which uncovered a total of ten compounds that selectively target MED12 knockdown breast cancer cells. Our results show that two of these ten compounds, solasonine and alisol B23-acetate, block GLI3-dependent SHH signaling which leads to a reversal of enhanced cellular proliferation and colony formation ability. Thus, our findings provide promising insight into a novel personalized treatment strategy for patients suffering from MED12-altered breast cancer.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"127-135"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs targeting <i>CDKN2A</i> gene as a potential prognostic marker in head and neck squamous cell carcinoma.","authors":"Sivakumar Gopalakrishnan, Anitha Pandi, Paramasivam Arumugam, Vijayashree Priyadharsini Jayaseelan","doi":"10.22099/mbrc.2023.48081.1853","DOIUrl":"10.22099/mbrc.2023.48081.1853","url":null,"abstract":"<p><p>Epigenetic factors are known to markedly influence the functions of a gene by modification of transcripts, <i>via</i> methylation or acetylation and degradation of mRNA transcripts. The <i>CDKN2A</i> encodes cyclin-dependent kinase inhibitor 2A, a tumour suppressor protein. Genetic and epigenetic alterations in this gene have been demonstrated in several cancer types. The non-coding RNAs with a special emphasis on microRNAs have long been explored for their potential role in the epigenetic modification of gene expression. The present study aims to identify the microRNAs targeting <i>CDKN2A</i> gene transcripts and demonstrate their prognostic significance in head and neck squamous cell carcinoma (HNSCC). Computational approaches were employed to identify the microRNAs targeting <i>CDKN2A.</i> The gene and protein expression profile of <i>CDKN2A</i> was analyzed using UALCAN. A significant upregulation of <i>CDKN2A</i> was observed in the primary tumour tissues (p=<10^-12). Interestingly, the protein expression, although found to be statistically significant (p=0.0129) did not correlate well with the gene expression profile. The microRNAs targeting <i>CDKN2A</i> were further analyzed to identify the possible reason for the decrease in protein expression. Among the 44 microRNAs targeting <i>CDKN2A</i> gene transcripts, hsa-miR-3681-3p, hsa-miR-542-5p, hsa-miR-4519 were found to be upregulated and hsa-miR-134-5p was found to be downregulated with a significant association with survival status of HNSCC patients. The hsa-miR-542-5p was found to correlate well with the survival and hence can be considered as the key microRNA associated with HNSCC. However, further validation of this microRNA is warranted to confirm its role in the process of carcinogenesis.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 1","pages":"21-27"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valproic acid and/or rapamycin preconditioning protects hair follicle stem cells from oxygen glucose serum deprivation-induced oxidative injury via activating Nrf2 pathway.","authors":"Fatemeh Keshavarzi, Mohammad Saied Salehi, Sareh Pandamooz, Razieh Zare, Mozhdeh Zamani, Zohreh Mostafavi-Pour, Pooneh Pooneh Mokarram","doi":"10.22099/mbrc.2024.49302.1922","DOIUrl":"10.22099/mbrc.2024.49302.1922","url":null,"abstract":"<p><p>Among leading causes of the ischemic stroke pathogenesis, oxidative stress strongly declines rate of stem cell engraftment at the injury site, and disables stem cell-based therapy as a key treatment for ischemia stroke. To overcome this therapeutic limitation, preconditioning has been represented a possible approach to augment the adaptation and viability of stem cells to oxidative stress. Here, we illustrated protective impacts of valproic acid (VPA) and/or rapamycin (RAPA) preconditioning unto oxygen glucose and serum deprivation (OGSD)-stimulated cell damage in hair follicle-derived stem cells (HFSCs) and surveyed the plausible inducement mechanisms. OGSD, as an <i>in vitro</i> cell injury model, was established and HFSCs viability was observed using MTT assay after VPA, RAPA, and VPA-RAPA preconditioning under OGSD. ROS and MDA production was assessed to reflect oxidative stress. Real-time PCR and western blotting were employed to investigate Nrf2 expression. The activity of Nrf2-related antioxidant enzymes including NQO1, GPx and GSH level were examined. <i>VEGF</i> and <i>BDNF</i> mRNA expression levels were analyzed. Our results showed that VPA and/or RAPA preconditioning ameliorated OGSD-induced decline in HFSCs viability. In addition, they considerably prohibited ROS and MDA generation in the OGSD-treated HFSCs. Furthermore, VPA and/or RAPA preconditioning stimulated Nrf2 nuclear repositioning and NQO1 and GPx activity and GSH amount, as well as expression of paracrine factors <i>VEGF</i> and <i>BDNF</i> in OGSD-treated HFSCs. Thus, the protective effects afforded by VPA and/or RAPA preconditioning, which involved Nrf2-modulated oxidant stress and regulation of <i>VEGF</i> and <i>BDNF</i> expression, display a simple strategy to augment cell-transplantation efficiency for ischemic stroke.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"103-116"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Allele and genotype frequencies of β-lactoglobulin gene using PCR-RFLP in Algerian local cattle populations.","authors":"Nadjet Boushaba, Nacera Tabet-Aoul","doi":"10.22099/mbrc.2023.47661.1841","DOIUrl":"10.22099/mbrc.2023.47661.1841","url":null,"abstract":"<p><p>Milk protein genetic polymorphisms are associated with economically important traits in dairy cattle. The objective of this study is to genotype a single nucleotide polymorphism (SNP) responsible for the amino acid changes in the beta-lactoglobulin (β-Lg) variants A and B on 85 unrelated DNA representing Algerian cattle populations: Chelifienne (28), Cheurfa (31) and Guelmoise (26). The method used is the PCR-RFLP (Polymerase Chain Reaction-Restriction Fragment Length Polymorphism). Genetic polymorphism was detected by digestion of PCR products amplified of exon II of β-Lg gene by with the endonuclease <i>Hae</i>III enzyme. The results revealed that the amplified product was observed as 247 bp. Restriction digestion with <i>Hae</i>III revealed three genotypes: AA, AB and BB. The genotypic frequencies of AA, AB and BB genotypes were 0.08, 0.41, 0.50; 0.08, 0.41, 0.50 and 0.01, 0.19, 0.56 in Chelifienne, Cheurfa and Guelmoise and respectively. Frequency of AA genotype was absent in Guelmoise population. Frequencies of A and B alleles were 0.29 and 0.71 in both Chelifienne and Cheurfa and 0.25 and 0.75 Guelmoise population. These results further confirm that Bos torus cattle are predominantly of β-Lactoglobulin B type. The Chi-square test at <i>p</i>-value < 0.05 results revealed that the Chelifienne and Cheurfa populations were in Hardy-Weinberg equilibrium and the results are not significant for the Guelmoise. This genetic information could be useful to estimate the effect of polymorphism on different milk production of Algerian bovine populations.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 1","pages":"43-49"},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10644313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of silymarin as adjuvant drug on serum levels of CTRP3, anti-cyclic citrullinated peptide (CCP), and high-sensitivity C-reactive protein (hs-CRP) in rheumatoid arthritis patients.","authors":"Mohammad Ehsan Elahi, Daniel Elieh-Ali-Komi, Farjam Goudarzi, Ehsan Mohammadi Noori, Shirin Assar, Mehrdad Shavandi, Amir Kiani, Homayoin Elahi","doi":"10.22099/mbrc.2024.48466.1876","DOIUrl":"10.22099/mbrc.2024.48466.1876","url":null,"abstract":"<p><p>Silymarin is known for its anti-inflammatory and antioxidant properties. We investigated these effects on serum levels of CTRP3, Anti-CCP, and hs-CRP in individuals with Rheumatoid arthritis (RA). In this study, 42 individuals with RA were recruited and their serum specimens were collected, serum levels of hs-CRP, AntiCCP antibodies, and CTRP3 were measured using ELISA. DNA was extracted and investigated for the existence of possible new mutations in the gene encoding CTRP3 using the PCR technique; the desired fragments were then amplified and sequenced. Another blood sample was collected from the case group after taking <i>livergol</i> for three months (3 doses of 140 mg/day) and the tests were repeated. Anti-CCP Abs levels in the postintervention responding group decreased compared to preintervention (p<0.001) while in the non-responding group, the levels increased after the intervention compared to the levels before the intervention (p=0.019). Additionally, CTRP3 levels in the responding group increased postintervention (p=0.003), however, in the non-responding group the levels decreased postintervention when compared to preintervention (p=0.02). The responding group had significantly lower levels of hs-CRP when compared to that of preintervention (p=0.005) whereas the non-responding group had significantly higher levels of postintervention (p<0.001). Moreover, the results of sequencings of exon 6 on <i>CTRP3</i> gene showed the presence of mutations in exon 6 (position 215:C>T, 338:G>A, 359:A>C, and 153:T>C). Silymarin could be used as an adjuvant in the treatment of rheumatoid arthritis.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"137-145"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The hepatoprotective effects of sitagliptin against cyclophosphamide-induced hepatotoxicity in rat.","authors":"Reza Maleki, Mohammad Foad Noorbakhsh, Nasrin Kazemipour, Maliheh Masoudian, Fatemeh Namazi, Saeed Nazifi","doi":"10.22099/mbrc.2024.49925.1964","DOIUrl":"10.22099/mbrc.2024.49925.1964","url":null,"abstract":"<p><p>Hepatotoxicity is a serious side effects of cyclophosphamide. Thus, the present research investigates the protective properties of sitagliptin against cyclophosphamide-induced hepatotoxicity. Fifty male rats were randomly divided into five groups. They were pre-treated with either sitagliptin or normal saline once a day for the first ten days of the study. To induce acute hepatotoxicity, cyclophosphamide (200 mg/kg, i.p) was injected only one time and 45 min after the last dose of sitagliptin. The rats were sacrificed on the 11th day, and their blood and liver were collected for biochemical, gene expression, and histopathological assessments. Our results showed that cyclophosphamide induced obvious liver toxicity as marked by an increase in serum levels of alanine transaminase and aspartate transaminase, reduced serum albumin and total protein levels, in addition to histopathological changes. The malondialdehyde, tumor necrosis factor-α, and interleukin-6 levels were also elevated and total antioxidant capacity declined in serum and hepatic homogenates. Sitagliptin magnificently attenuated the cylophosphamide-induced histological alterations, improved liver function tests, enhanced total antioxidant capacity, and decreased malondialdehyde, tumor necrosis factor-α, and interleukin-6 in the blood and hepatic tissues. These findings suggest that sitagliptin has hepatoprotective activity against cyclophosphamide toxicity, which may be due to its antioxidant and anti-inflammatory effects.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 4","pages":"193-200"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In silico analysis for SARS-CoV-2 detection in the context of genetic variability of the Algerian omicron variant.","authors":"Chahinez Amira Dahmani, Asmaa Azzoune, Abdallah Boudjema","doi":"10.22099/mbrc.2024.50192.1985","DOIUrl":"10.22099/mbrc.2024.50192.1985","url":null,"abstract":"<p><p>The risk to public health conferred by the Omicron variant is still not completely clear, although its numerous gene mutations have raised concerns regarding its potential for increased transmissibility and immune escape. In this study, we test the compatibility of the different primers and probes available in different commercial kits sold internationally with all the sequences of SARS-CoV-2 analyzed in Algeria until March 2023. The Algerian SARS-CoV-2 Omicron variant sequences were aligned with the Muscle tool using Genious software. We also used primers and probes sequences of seven international RT-qPCR kits; CDC China, Charite Germany, HKU Hong Kong, NIH Thailand, NIID Japan, CDC US, and Pasteur Institute. We used the primer check v2.0 developed by VIROSCIENCE LAB, To identify the different mutations located at the level of primers and probes about the Algerian sequences of SARS-CoV2. Statistical tests were carried out by calculating the <math> <msup> <mrow><mrow><mi>x</mi></mrow> </mrow> <mrow><mrow><mn>2</mn></mrow> </mrow> </msup> </math> test. We found regarding the Forward primer sequences that the two Thailand and Japan kits are less specific to the Algerian version of the SARS-CoV-2 Omicron variant genome compared to the other kits (<i>p</i>=10^-6). Furthermore, regarding the Reverse primers and fluorescent Probes, the three kits; Thailand, Japan, and CDC US; are less effective (<i>p</i>=10^-6). Regarding all primers and probes, this work allowed us to conclude that the four RT-qPCR kits: CDC China, Charite Germany, NHD Hong Kong, and Pasteur Institute seem to be more specific for the Algerian omicron genome detection and therefore for diagnosis of COVID-19 in Algeria.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 4","pages":"223-234"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between rs3761548 polymorphism of <i>FOXP3</i> and the risk of gastric cancer: a case-control study.","authors":"Shamimeh Validi, Iraj Saadat","doi":"10.22099/mbrc.2024.49125.1989","DOIUrl":"10.22099/mbrc.2024.49125.1989","url":null,"abstract":"<p><p>Gastric cancer is one of the most prevalent malignancies in the world. Various factors play a role in the development of this disease as risk factors. One of these genes is the <i>FOXP3</i>, which is located on the short arm of the X chromosome (Xp11.23). The rs3761548 polymorphism in the promoter region of this gene increases cell proliferation. In the current study, the association between this genetic polymorphism and the risk of gastric cancer was investigated. This study included 147 patients (55 women, 92 men) with gastric cancer and 147 healthy individuals (53 women, 94 men). The PCR-RFLP method is used for genotyping. Statistical analysis showed that there was no significant association between this polymorphism and the risk of gastric cancer. However, the analysis of genotype, family history and smoking risk factors simultane-oussly revealed a significant relationship between simultaneous occurrence of two (OR=3.79, 95% CI=1.77-8.09, p=0.001) and three risk factors (OR=6.44, 95% CI=1.76-23.5, p=0.017) and the risk of gastric cancer.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 4","pages":"247-252"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142308168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of <i>NLRP3</i> rs10754558 and rs4612666 polymorphisms on preeclampsia susceptibility, onset, and severity: a case-control study and in silico analysis.","authors":"Mahnaz Rezaei, Marzieh Ghasemi, Mohsen Saravani, Rahele Ghasemian- Moghadam, Hossein Shahraki-Ghadimi, Mahtab Norouzi, Saeedeh Salimi","doi":"10.22099/mbrc.2024.49510.1936","DOIUrl":"10.22099/mbrc.2024.49510.1936","url":null,"abstract":"<p><p>Preeclampsia (PE) is one of the serious complications of pregnancy and its exact etiology is unknown. Inflammasomes are multiportion complexes whose relation with PE has been described. Evidence showed the effect of NLRP3 inflammasome in PE pathogenesis. In the current study, we investigated the possible impacts of <i>NLRP3</i> polymorphisms on PE. A total of 252 PE and 258 control pregnant women were selected for the study. The PCR-RFLP method was employed to genotype rs10754558 and rs4612666 polymorphisms. The RNAsnp and SpliceAid 2 software were used for in silico analysis. There was no relationship between <i>NLRP3</i> polymorphisms and PE. In comparison to control women, the <i>NLRP3</i> rs10754558 could increase the risk of severe PE in codominant and dominant models (OR=1.89, 95% CI=1.19-3.01, P=0.012, OR=1.95, 95% CI=1.24-3.06, P=0.0037, respectively). The findings of the in silico analysis revealed the effects of rs10754558 C to G and rs4612666 C to T substitutions on protein binding sites and rs10754558 C to G substitution on secondary RNA structure. These findings could confirm the finding those studies reported the impacts of these variants on various diseases. In conclusion, the <i>NLRP3</i> rs10754558 variant was associated with an increased risk of EOPE and severe PE.</p>","PeriodicalId":19025,"journal":{"name":"Molecular Biology Research Communications","volume":"13 3","pages":"165-173"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11194025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141446620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}