BMC Molecular and Cell Biology最新文献

{"title":"Simple, low-cost, and well-performing method, the outgrowth technique, for the isolation of cells from nasal polyps.","authors":"Jonghui Kim, Karla Hegener, Claudia Hagedorn, Daniel Weidinger, Kashin Jamal Jameel, Inga Marte Charlott Seuthe, Sabine Eichhorn, Florian Kreppel, Jonas Jae-Hyun Park, Jürgen Knobloch","doi":"10.1186/s12860-023-00493-2","DOIUrl":"10.1186/s12860-023-00493-2","url":null,"abstract":"<p><strong>Background: </strong>Epithelial cells are an important part of the pathomechanism in chronic rhinosinusitis with nasal polyps. It is therefore essential to establish a robust method for the isolation and culture of epithelial cells from nasal polyps to enable further research. In this study, the feasibility of the outgrowth technique for the isolation of the epithelial cells from the nasal polyps was evaluated.</p><p><strong>Results: </strong>Using the outgrowth technique, epithelial cells could be isolated from all tissue samples. Isolated epithelial cells showed a proliferation rate of approximately 7- to 23-fold every 6 days up to the 3rd passage. Over 97% of isolated cells were shown to be cytokeratin- and p63-positive, and over 86% of them were Ki-67-positive in flow cytometry. Interleukin-33 and periostin were detectable in the supernatant.</p><p><strong>Conclusions: </strong>We introduce a simple, low-cost, and well-performing method for isolating epithelial cells from nasal polyps with the outgrowth technique.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"31"},"PeriodicalIF":2.8,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41191062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive brain tissue metabolomics and biological network technology to decipher the mechanism of hydrogen-rich water on Radiation-induced cognitive impairment in rats.","authors":"Xiaoming Liu, Mengya Liu, Huan Liu, Hui Yuan, Yong Wang, Xiaoman Chen, Jianguo Li, Xiujun Qin","doi":"10.1186/s12860-023-00491-4","DOIUrl":"10.1186/s12860-023-00491-4","url":null,"abstract":"<p><strong>Background: </strong>Hydrogen-rich water (HRW) has been shown to prevent cognitive impairment caused by ionizing radiation. This study aimed to investigate the pharmacological effects and mechanisms of HRW on ionizing radiation by coupling the brain metabolomics and biological target network methods.</p><p><strong>Methods and results: </strong>HRW significantly improves the cognitive impairment in rats exposed to ionizing radiation. Based on metabolomics and biological network results, we identified 54 differential metabolites and 93 target genes. The KEGG pathway indicates that glutathione metabolism, ascorbic acid and aldehyde acid metabolism, pentose and glucuronic acid interconversion, and glycerophospholipid metabolism play important roles in ionizing radiation therapy.</p><p><strong>Conclusion: </strong>Our study has systematically elucidated the molecular mechanism of HRW against ionizing radiation, which can be mediated by modulating targets, pathways and metabolite levels. This provides a new perspective for identifying the underlying pharmacological mechanism of HRW.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"30"},"PeriodicalIF":2.8,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10523633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mineral elements and adiposity-related consequences in adolescents with intellectual disabilities.","authors":"Ahmad H Alghadir, Sami A Gabr, Amir Iqbal","doi":"10.1186/s12860-023-00490-5","DOIUrl":"10.1186/s12860-023-00490-5","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Patients with intellectual disabilities are shown to have a limited capacity for cooperation, communication,and other biological consequences, which significantly require a specialized interest in healthcare professionals worldwide.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Aim: &lt;/strong&gt;In this respect, the present study was designed to evaluate the levels mineral elements, and their correlation with oxidative stress markers and adiposity markers; leptin (L), adiponectin (A), and L/A ratio in adolescents with intellectual disabilities.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A total of 350 schoolchildren aged (12-18 years) were randomly invited to participate in this prospective, observational study. Only 300 participants agreed to participate in this study. According to Intelligence quotients scores (IQ) measured by WISC-III, the participants were classified into two groups; the healthy control group (no = 180; IQ = 90-114); and the moderate intellectual disability (MID) group (no = 120; IQ = 35-49). Adiposity markers; body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), physical activity scores, adipokines biomarkers; leptin, adiponectin, L/A ratio, oxidative stress, and plasma mineral elements were evaluated by prevalidated questionnaires, inductively coupled plasma-mass spectrometry (ICP-MS), colorimetric, and immunoassay techniques.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Intellectual disability of moderate type was reported in 40% of the studied populations most of them are men aged 12-18 years (66.6% for men vs. 33.3 for females). Obesity was shown to be associated with the degree of intellectual disability of the students. There was a significant (P = 0.001) increase in the BMI, WHR, and WHtR scores as obesity markers with poor physical activity (P = 0.01) in students with poor disability compared to healthy controls (HC). The levels of leptin (P = 0.001), adiponectin (P = 0.01), and L/A ratio (P = 0.01) as adiposity biomarkers were significantly increased in students with MID compared to healthy controls. Also, oxidative stress measured by malondialdehyde (MDA) (P = 0.01) and total antioxidant capacity (TAC) (P = 0.01) were significantly increased in students with MID compared to healthy control subjects. In addition, mineral elements were shown to be linked with intellectual disability. The data showed that the levels of Fe, Mn, Zn, Hg, Pb, Ca, Cr, Mg, and Ni significantly (P = 0.001) increased, and the levels of Al, Na, K, Cu, and Zn/Cu ratio significantly (P = 0.001) decreased in subjects with MID compared to healthy controls. Correlation analysis concluded that changes in mineral elements significantly correlated with adiposity markers, oxidative stress, and the scores of intellectual disability (WISC III-IQ score).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The intellectual disability of moderate type (MID) was associated with abnormal changes in the levels of essential mineral elements and adipokines and increased levels of ","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"29"},"PeriodicalIF":2.8,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10512604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41123963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycyrrhizin inhibits LPS-induced inflammatory responses in goat ruminal epithelial cells in vitro.","authors":"Junfeng Liu, Bei Ma, Guang Hao, DuoDuo Su, Tianyang Wang, Ze Ding, Xuefeng Guo","doi":"10.1186/s12860-023-00489-y","DOIUrl":"10.1186/s12860-023-00489-y","url":null,"abstract":"<p><p>Inflammation plays a crucial role in the progression of Subacute Ruminal Acidosis (SARA). The experiment was designed to investigate anti-inflammatory effects of glycyrrhizin on goats ruminal epithelial cells (GREC) which were induced SARA by Lipopolysaccharide (LPS) in vitro. The GREC were induced SARA by adding LPS at the concentration of 5 μm and glycyrrhizin was added at different concentration of 0, 60, 90, 120, 150 μm. The structural integrity of LPS-induced GREC with the treatment of glycyrrhizin were observed by electron microscope; The levels of inflammatory factors TNF-α, IL-1β, IL-6, IL-8 and IL-12 were measured by ELISA; The number of Zo-1 and Occludin were measured, the expression of tight junction protein Occludin were measured by Western blot, and the mRNA expression of NF-κB, TNF-α, IL-1β, IL-6, IL-8 and IL-12 were measured in vitro. The results showed that higher concentration treatment of glycyrrhizin led to better morphology in LPS-induced GREC. Glycyrrhizin inhibited the growth of inflammatory factors TNF-α, IL-1β, IL-6, IL-8 and IL-12 in a dose-dependent manner. The number of ZO-1 and Occludin increased with the increase of adding of glycyrrhizin. Western blot analysis showed that the expression of tight junction protein Occludin in LPS-induced GREC increased with the adding of glycyrrhizin in a dose-dependent manner. Furthermore, the mRNA expression of NF-κB, TNF-α, IL-1β, IL-6, IL-8 and IL-12 decreased significantly with the increase treatment of glycyrrhizin. Glycyrrhizin significantly inhibits LPS-induced inflammatory mediators in GREC and the effects are better with the increase treatment of glycyrrhizin in vitro.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"28"},"PeriodicalIF":2.8,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10507872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41111126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"D-galactose-induced mitochondrial oxidative damage and apoptosis in the cochlear stria vascularis of mice.","authors":"Zhe Peng, Chunli Zhao, Zijing Yang, Shusheng Gong, Zhengde Du","doi":"10.1186/s12860-023-00480-7","DOIUrl":"10.1186/s12860-023-00480-7","url":null,"abstract":"<p><strong>Background: </strong>Age-related hearing loss, known as presbycusis, is the result of auditory system degeneration. Numerous studies have suggested that reactive oxygen species (ROS) and mitochondrial oxidative damage play important roles in the occurrence and progression of aging. The D-galactose (D-gal)-induced aging model is well known and widely utilized in aging research. Our previous studies demonstrate that administration of D-gal causes mitochondrial oxidative damage and causes subsequent dysfunction in the cochlear ribbon synapses, which in turn leads to hearing changes and early stage presbycusis. Stria vascularis (SV) cells are vital for hearing function. However, it is unclear to what extent D-gal induces oxidative damage and apoptosis in the cochlear SV of mice. In addition, the source of the causative ROS in the cochlear SV has not been fully investigated.</p><p><strong>Methods: </strong>In this study, we investigated ROS generation in the cochlear SV of mice treated with D-gal. Hearing function was measured using the auditory brainstem response (ABR). Immunofluorescence was used to examine apoptosis and oxidative damage. Transmission electron microscopy was also used to investigate the mitochondrial ultrastructure. DNA fragmentation was determined using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) assay. Mitochondrial membrane potential (MMP) and ATP were also measured.</p><p><strong>Results: </strong>We found that D-gal-treated mice exhibited a significant shift in the mean amplitude and latency of the ABR; a remarkable increase in the levels of NADPH oxidase (NOX-2), Uncoupling protein 2 (UCP2) and cleaved caspase-3 (c-Cas3) was observed, as well as an increase in the number of TUNEL-positive cells were observed in the SV of mice. Both the expression of the DNA oxidative damage biomarker 8-hydroxy-2-deoxyguanosine (8-OHdG) and a commonly occurring mitochondrial DNA deletion were markedly elevated in the SV of mice that had been treated with D-gal to induce aging. Conversely, the ATP level and MMP were significantly reduced in D-gal-induced aging mice. We also found alterations in the mitochondrial ultrastructure in the SV of aging mice, which include swollen and distorted mitochondrial shape, shortened and thickened microvilli, and the accumulation of lysosomes in the SV.</p><p><strong>Conclusion: </strong>Our findings suggest that the impairment of cochlear SV during presbycusis may be caused by mitochondrial oxidative damage and subsequent apoptosis.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"27"},"PeriodicalIF":2.8,"publicationDate":"2023-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10441755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10056175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer.","authors":"Arwa Fallatah, Dimitrios G Anastasakis, Amirhossein Manzourolajdad, Pooja Sharma, Xiantao Wang, Alexis Jacob, Sarah Alsharif, Ahmed Elgerbi, Pierre A Coulombe, Markus Hafner, Byung Min Chung","doi":"10.1186/s12860-023-00488-z","DOIUrl":"10.1186/s12860-023-00488-z","url":null,"abstract":"<p><strong>Background: </strong>Heterogeneous nuclear ribonucleoprotein K (HNRNPK) regulates pre-mRNA processing and long non-coding RNA localization in the nucleus. It was previously shown that shuttling of HNRNPK to the cytoplasm promotes cell proliferation and cancer metastasis. However, the mechanism of HNRNPK cytoplasmic localization, its cytoplasmic RNA ligands, and impact on post-transcriptional gene regulation remain uncharacterized.</p><p><strong>Results: </strong>Here we show that the intermediate filament protein Keratin 19 (K19) directly interacts with HNRNPK and sequesters it in the cytoplasm. Correspondingly, in K19 knockout breast cancer cells, HNRNPK does not localize in the cytoplasm, resulting in reduced cell proliferation. We comprehensively mapped HNRNPK binding sites on mRNAs and showed that, in the cytoplasm, K19-mediated HNRNPK-retention increases the abundance of target mRNAs bound to the 3' untranslated region (3'UTR) at the expected cytidine-rich (C-rich) sequence elements. Furthermore, these mRNAs protected by HNRNPK in the cytoplasm are typically involved in cancer progression and include the p53 signaling pathway that is dysregulated upon HNRNPK knockdown (HNRNPK KD) or K19 knockout (KRT19 KO).</p><p><strong>Conclusions: </strong>This study identifies how a cytoskeletal protein can directly regulate gene expression by controlling the subcellular localization of RNA-binding proteins to support pathways involved in cancer progression.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"26"},"PeriodicalIF":2.8,"publicationDate":"2023-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10433649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10421813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A computational peptide model induces cancer cells' apoptosis by docking Kringle 5 to GRP78.","authors":"Ibrahim Khater, Aaya Nassar","doi":"10.1186/s12860-023-00484-3","DOIUrl":"10.1186/s12860-023-00484-3","url":null,"abstract":"<p><strong>Background: </strong>Cells can die through a process called apoptosis in both pathological and healthy conditions. Cancer development and progression may result from abnormal apoptosis. The 78-kDa glucose-regulated protein (GRP78) is increased on the surface of cancer cells. Kringle 5, a cell apoptosis agent, is bound to GRP78 to induce cancer cell apoptosis. Kringle 5 was docked to GRP78 using ClusPro 2.0. The interaction between Kringle 5 and GRP78 was investigated.</p><p><strong>Results: </strong>The interacting amino acids were found to be localized in three areas of Kringle 5. The proposed peptide is made up of secondary structure amino acids that contain Kringle 5 interaction residues. The 3D structure of the peptide model amino acids was created using the PEP-FOLD3 web tool.</p><p><strong>Conclusions: </strong>The proposed peptide completely binds to the GRP78 binding site on the Kringle 5, signaling that it might be effective in the apoptosis of cancer cells.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"25"},"PeriodicalIF":2.8,"publicationDate":"2023-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10019395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BMP9 maintains the phenotype of HTR-8/Svneo trophoblast cells by activating the SDF1/CXCR4 pathway.","authors":"Xue Yang, Lingling Ren, Xiang Chen, Ying Pang, Baoxia Jia, Jing Sun, Xiaofang Quan","doi":"10.1186/s12860-023-00487-0","DOIUrl":"10.1186/s12860-023-00487-0","url":null,"abstract":"<p><strong>Background: </strong>Bone morphogenetic protein 9 (BMP9) has been shown to regulate processes such as angiogenesis, endothelial dysfunction, and tumorigenesis. However, the role of BMP9 in preeclampsia (PE) is unclear. The purpose of this study was to investigate the role and mechanism of BMP9 in PE.</p><p><strong>Methods: </strong>The effects of BMP9 on the viability, migration and invasion of HTR-8/Svneo cells were investigated by CCK-8 assay, wound healing assay and Transwell invasion assay. The effect of BMP9 on apoptosis of HTR-8/Svneo cells was detected by flow cytometry. Plasma levels of BMP9, SDF1 and CXCR4 were detected by ELISA kit. qRT-PCR and Western blot were used to detect the expression levels of each gene in the cells.</p><p><strong>Results: </strong>Overexpression of BMP9 promoted the proliferation and migration of trophoblast cells and inhibited apoptosis. Knockdown of BMP9 had the opposite effect. The levels of BMP9, SDF1 and CXCR4 in the plasma of PE patients were down-regulated, and BMP9 was positively correlated with the levels of SDF1 and CXCR4. BMP9 also significantly upregulated the mRNA and protein levels of SDF1 and CXCR4 in HTR-8/SVneo cells. Further mechanistic studies found that BMP9 promoted the migration and invasion of HTR-8/SVneo cells and inhibited apoptosis by activating the SDF1/CXCR4 pathway.</p><p><strong>Conclusion: </strong>We demonstrate for the first time that BMP9 promoted the migration and invasion of HTR-8/SVneo cells and inhibits apoptosis by activating the SDF1/CXCR4 pathway. This suggests that BMP9 may be a biomarker molecule for PE.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"24"},"PeriodicalIF":2.8,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10405378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10318932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emodin and aloe-emodin, two potential molecules in regulating cell migration of skin cells through the MAP kinase pathway and affecting Caenorhabditis elegans thermotolerance.","authors":"Aysenur Gunaydin-Akyildiz,&nbsp;Rabia Sare Yanikoglu,&nbsp;Meltem Gulec,&nbsp;Gulbahar Ozge Alim-Toraman,&nbsp;Ebru Didem Kuran,&nbsp;Sezen Atasoy,&nbsp;Abdullah Olgun,&nbsp;Gulacti Topcu","doi":"10.1186/s12860-023-00486-1","DOIUrl":"https://doi.org/10.1186/s12860-023-00486-1","url":null,"abstract":"<p><strong>Background: </strong>Emodin and aloe-emodin are two anthraquinones having positive effects in wound healing. However, their mechanism of action of wound healing is not fully understood. The MAP kinase family, which plays an active role in wound healing, is a well-characterized large family of serine/threonine kinases and regulates processes such as proliferation, oncogenesis, differentiation, and inflammation in the cell. The aim of this study is to comparatively elucidate the mechanisms of action of emodin and aloe-emodin, which are potential agents in wound healing.</p><p><strong>Methods: </strong>The mechanism of the effects of emodin and aloe-emodin on cell viability and cell migration was examined using the human skin fibroblast (CCD-1079Sk) cell line. The gene expression levels of the MAP kinases (JNK, P38, ERK) in the skin fibroblast cells along with a molecular docking study analyzing their interaction potential were evaluated. Furthermore, the molecules' effects on the lifespan of Caenorhabditis elegans were studied.</p><p><strong>Results: </strong>Emodin and aloe-emodin inhibited the ATP content of the cells in a concentration dependent manner and accelerated cell migration at the lower concentrations while inhibiting cell migration in the higher concentration treatment groups. The expressions of JNK and P38 were upregulated at the low concentrations and downregulated at the higher concentrations. The molecular docking studies of the molecules gave high docking scores indicating their interaction potential with JNK and P38. C. elegans lifespan under heat stress was observed longer after 75 µM emodin and was significantly reduced after 150 µM aloe-emodin treatment.</p><p><strong>Conclusion: </strong>Aloe-emodin was found to be more potent on cell viability, cell migration, gene expression levels of the MAP kinases in healthy fibroblastic skin cells, and on the lifespan of C. elegans. This study reveals the functional effects and the biological factors that interact in the wound healing process of emodin and aloe-emodin, and give a possible treatment alternative to shorten the duration of wound care.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"23"},"PeriodicalIF":2.8,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10367395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9875467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress.","authors":"Li Li,&nbsp;Shunying Wang,&nbsp;Wenming Wang","doi":"10.1186/s12860-023-00485-2","DOIUrl":"10.1186/s12860-023-00485-2","url":null,"abstract":"<p><strong>Background: </strong>Renal ischemia/reperfusion (I/R) injury is a major cause of acute kidney injury (AKI). Dysfunction of E74-like ETS transcription factor 4 (ELF4) leads to inflammation. This research intended to look into the function and mechanisms of ELF4 in I/R and oxygen-glucose deprivation/reperfusion (OGD/R) model.</p><p><strong>Results: </strong>In I/R and OGD/R model, ELF4 expression was downregulated. ELF4 knockout aggravated I/R-induced kidney injury, oxidative stress (OS), endoplasmic reticulum stress (ERS), apoptosis, inflammation, and pyroptosis in mice. In HK-2 cells treated with OGD/R, suppression of ELF4 expression inhibited cell proliferation and promoted cell apoptosis, OS, ERS, inflammation, and pyroptosis. Moreover, ELF4 overexpression led to the opposite results.</p><p><strong>Conclusion: </strong>ELF4 deficiency aggravated I/R induced AKI, which was involved in apoptosis, OS, ERS, inflammation, and pyroptosis. Targeting ELF4 may be a promising new therapeutic strategy for preventing inflammation after IR-AKI.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"22"},"PeriodicalIF":2.8,"publicationDate":"2023-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10360327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9911606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}