BMC Molecular and Cell Biology最新文献

{"title":"CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity.","authors":"Yanming Wang,&nbsp;Chao Wang,&nbsp;Yan Zhu","doi":"10.1186/s12860-022-00447-0","DOIUrl":"https://doi.org/10.1186/s12860-022-00447-0","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer recurrence and chemotherapy resistance are still urgent issues, and exploring the mechanisms of metastasis and chemotherapy resistance is beneficial to the development of therapeutic methods. Caspase recruitment domain family member 9 (CARD9) and homeobox B5 (HOXB5) are related and both are upregulated in ovarian cancer. This study aimed to define their functions in ovarian cancer cell proliferation, migration, and cisplatin sensitivity.</p><p><strong>Results: </strong>The levels of CARD9 were detected in acquired ovarian cancer tissues and cell lines. CARD9 was indeed abnormally upregulated in them. CARD9 knockdown significantly suppressed cell proliferation, colony formation, migration, cycle arrest, and cisplatin sensitivity. HOXB5 bound to the CARD9 promoter, and HOXB5 overexpression reversed the regulation by CARD9 knockdown in cells, as well as the activation of NF-κB signaling. This indicated that CARD9 was positively regulated by HOXB5 in ovarian cancer cells.</p><p><strong>Conclusion: </strong>Together, CARD9 is involved in ovarian cancer cell proliferation, migration, and cisplatin sensitivity via NF-κB signaling after transcriptional activation by HOXB5.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10320729","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":"The role of the TGF-β/LIF signaling pathway mediated by SMADs during the cyst formation of Echinococcus in young children.","authors":"Shuang-Li Qin,&nbsp;Yun Guo,&nbsp;Shui-Xue Li,&nbsp;Ling Zhou,&nbsp;Azguli Maimaiti,&nbsp;Yusufu Akemu,&nbsp;Jun He,&nbsp;Hai-Xia Yao","doi":"10.1186/s12860-022-00452-3","DOIUrl":"https://doi.org/10.1186/s12860-022-00452-3","url":null,"abstract":"<p><strong>Objective: </strong>The present study aims to explore the correlation of the transforming growth factor β (TGF-β), drosophila mothers against decapentaplegic protein gene (SMAD) 2/3/4, and leukemia inhibitory factors (LIF) with the cyst formation of hepatic Echinococcus granulosus in young children.</p><p><strong>Methods: </strong>A total of 40 patients who met the diagnostic criteria for children's hydatid disease in people's Hospital of Xinjiang Uygur Autonomous Region between January 2020 and June 2021 were enrolled a s the study subjects. The cystic fluid of these children was collected as the case group and the corresponding infected viscera or pericystic tissue as the control group, with 40 cases in each group. In vitro cultured protoscolice of hydatid cyst, four groups including control group, LIF siRNA group, LIF factor group and SMAD4 siRNA group were divided by inhibiting TGF-β/SMADs signal pathway. Each assay was performed in triplicate. The expression of TGF-β, SMAD2/3/4 and LIF were detected.</p><p><strong>Results: </strong>The results of the clinical trial showed that the contents of SMAD2 and SMAD3 were increased in the case group compared with the control group; the differences were statistically significant (P < 0.05). The expression levels of TGF-β, Smad4, and LIF increased in the case group compared with the control group; however, the differences were not statistically significant. The results of further in vitro experiments, the expression levels of TGF-β, SMAD 2/3/4, and LIF after adding siRNA to interfere with Smad4 decreased in the case group compared with the control group; the differences were statistically significant (P < 0.05). Compared with the control group, the expression levels of TGF-β, SMAD2/3/4, and LIF increased after treatment with added LIF in the case group, and the expression levels of TGF-β, SMAD2/3/4, and LIF decreased after adding siRNA to interfere with LIF in the case group; the differences were all statistically significant (P < 0.05).</p><p><strong>Conclusion: </strong>SMAD2 and SMAD3 have a certain clinical relevance with hydatidosis in young children. The LIF expression level may be related to the cystic transformation of protoscoleces. It has been suggested that the TGF-β/Smads/LIF signaling pathway may be present in the process of protoscoleces cyst formation; this provides a research basis for the prevention and treatment of post-infection parasitism of E. multilocularis eggs in young children.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9706881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40490141","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":"Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway.","authors":"Huahua Zhang,&nbsp;Junli Liu,&nbsp;Qingqing Dang,&nbsp;Xueru Wang,&nbsp;Jie Chen,&nbsp;Xiaoyin Lin,&nbsp;Na Yang,&nbsp;Juan Du,&nbsp;Haiyan Shi,&nbsp;Yong Liu,&nbsp;Jiming Han","doi":"10.1186/s12860-022-00448-z","DOIUrl":"https://doi.org/10.1186/s12860-022-00448-z","url":null,"abstract":"<p><strong>Background: </strong>Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear.</p><p><strong>Methods: </strong>Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting.</p><p><strong>Results: </strong>The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway.</p><p><strong>Conclusion: </strong>RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9670436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40688744","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":"High levels of follicular fluid testosterone could impair oocyte developmental competency via affecting aryl hydrocarbon receptor pathway in PCOS patients.","authors":"Fatemeh Eini,&nbsp;Maryam Azizi Kutenaei,&nbsp;Tahereh Foroutan,&nbsp;Ensieh Salehi","doi":"10.1186/s12860-022-00449-y","DOIUrl":"https://doi.org/10.1186/s12860-022-00449-y","url":null,"abstract":"<p><strong>Background: </strong>Although hormonal and metabolic dysfunction have been recognized as a possible cause of polycystic ovarian syndrome (PCOS), the associations between hyperandrogenism and aryl hydrocarbon receptor (Ahr) signaling pathway remains controversial. The current study aimed to investigate the effect of hyperandrogenism on oocyte developmental competency via regarding Ahr signaling downstream pathway in granulosa cells.</p><p><strong>Materials and methods: </strong>Granulosa cells were collected from 45 PCOS patients under assisted reproductive technique (ART). Gene expression of Ahr downstream pathway was evaluated based on Reverse Transcription Q-PCR assay. Moreover the correlation was investigated between gene expression and hyperandrogenism, and oocyte developmental competency in PCOS.</p><p><strong>Results: </strong>From the 45 PCOS patients, 26 (64.44%) had a high level of follicular fluid testosterone (FFT). Based on the FFT level, two groups of PCOS: HFT (high level of FFT) and non-HFT, were shown significant differences in oocyte and embryo quality, and fertilization and cleavage rates. Moreover, the mean relative expressions of Ahr and Arnt genes were significantly higher in HFT -PCOS group (p < 0.01 and p < 0.01) respectively. Also, the significant positive correlations were obtained for Ahr, Arnt, Cyp1A1, and Cyp1B1 with incidence of clinical hyperandrogenism and FFT level. Besides, our results showed that Ahr, Cyp1A1, and Cyp1B1 gene expression was correlated significantly with fertilization rate.</p><p><strong>Conclusion: </strong>The present study suggested that hyperandrogenism could impair oocyte developmental competency via affecting Ahr signaling downstream pathway.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9650820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40700130","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":"Downregulation of miR-451 in cholangiocarcinoma help the diagnsosi and promotes tumor progression.","authors":"Dengfang Guo,&nbsp;Qingling Wang,&nbsp;Jiancheng Huang,&nbsp;Zhanglin Hu,&nbsp;Chun Chen,&nbsp;Chun Zhang,&nbsp;Feng Lin","doi":"10.1186/s12860-022-00445-2","DOIUrl":"https://doi.org/10.1186/s12860-022-00445-2","url":null,"abstract":"<p><strong>Background: </strong>Cholangiocarcinoma is a kind of invasive malignant tumor followed by hepatocellular carcinoma. miR-451 was suggested to function as regulator in various human tumors, but its role in mediating tumor progression and predicting the prognosis of cholangiocarcinoma remains unknown. The clinical significance and biological function of miR-451 in cholangiocarcinoma were assessed in this study.</p><p><strong>Results: </strong>The tissue and serum expression of miR-451 was decreased in cholangiocarcinoma compared with corresponding normal samples. The downregulation of miR-451 was associated with the progressive TNM stage and positive lymph node metastasis of patients. miR-451 was identified to be an indicator of the diagnosis and prognosis of cholangiocarcinoma distinguishing cholangiocarcinoma patients from healthy volunteers and predicting the poor outcome of patients. miR-451 also served as a tumor suppressor negatively regulating the cellular processes of cholangiocarcinoma.</p><p><strong>Conclusions: </strong>miR-451 played a vital role in the early detection and risk prediction of cholangiocarcinoma. miR-451 also suppressed the progression of cholangiocarcinoma, which provides a potential therapeutical target for cholangiocarcinoma treatment.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9647969/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40453694","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":"Acetaminophen changes the RNA m⁶A levels and m⁶A-related proteins expression in IL-1β-treated chondrocyte cells.","authors":"Jie Gao,&nbsp;Yan Li,&nbsp;Zijin Liu,&nbsp;Dong Wang,&nbsp;Huawu Zhang","doi":"10.1186/s12860-022-00444-3","DOIUrl":"https://doi.org/10.1186/s12860-022-00444-3","url":null,"abstract":"<p><strong>Background: </strong>Acetaminophen is commonly recommended for the early analgesia of osteoarthritis. However, the molecular mechanism by which it acts remains unknown. The aim of this study is to investigate the effect of acetaminophen on inflammation and extracellular matrix degradation in human chondrocytes, and the possible molecular mechanisms involved in its effect.</p><p><strong>Methods: </strong>The normal chondrocyte cell line C28/I2 was treated with interleukin-1β to mimic the inflammatory state. Acetaminophen and the methylation inhibitor (cycloleucine) were used to treat interleukin-1β-induced C28/I2 cells. The expression of RNA N⁶-methyladenosine -related proteins was detected by RT-qPCR and western blot. The total RNA N⁶-methyladenosine level was measured by dot blot analysis and enzyme linked immunosorbent assay. The levels of interleukin-6, interleukin-8 and anti-tumor necrosis factor-α were measured by enzyme linked immunosorbent assay. The extracellular matrix synthesis and degradation were examined by western blot.</p><p><strong>Results: </strong>After interleukin-1β stimulated C28/I2 cells, the intracellular RNA N⁶-methyladenosine level increased, and the expression of regulatory proteins also changed, mainly including the increased expression of methyltransferase like 3 and the downregulated expression of AlkB family member 5. The use of cycloleucine inhibited interleukin-1β-induced inflammation and extracellular matrix degradation by inhibiting RNA N⁶-methyladenosine modification. In contrast, acetaminophen treatment counteracted interleukin-1β-induced changes in RNA N⁶-methyladenosine levels and regulatory protein expression. Furthermore, acetaminophen treatment of interleukin-1β-induced C28/I2 cells inhibited the secretion of interleukin-6, interleukin-8 and anti-tumor necrosis factor-α, down-regulated the expression of matrix metalloproteinase-13 and Collagen X, and up-regulated the expression of collagen II and aggrecan. In addition, AlkB family member 5 overexpression activated interleukin-1β-induced chondrocyte viability and suppressed inflammation and extracellular matrix degradation.</p><p><strong>Conclusion: </strong>Acetaminophen affects inflammatory factors secretion and extracellular matrix synthesis of human chondrocytes by regulating RNA N⁶-methyladenosine level and N⁶-methyladenosine-related protein expression. Stimulation of the normal chondrocyte cell line C28/I2 with the cytokine IL-1β (10 μM) mimics the inflammatory state in vitro. Acetaminophen (Ace, 50 μg/mL) changes the m⁶A related proteins expression and the total RNA m⁶A levels in IL-1β-treated chondrocyte cells. Furthermore, regulation of RNA m⁶A levels (by methylation inhibitor Cyc and/or Ace) affects IL-1β-induced inflammatory cytokines secretion and extracellular matrix synthesis in C28/I2 cells.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9609262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40433185","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":"CLCA2 overexpression suppresses epithelial-to-mesenchymal transition in cervical cancer cells through inactivation of ERK/JNK/p38-MAPK signaling pathways.","authors":"Wenhu Xin,&nbsp;Jian Zhang,&nbsp;Haibin Zhang,&nbsp;Xueyao Ma,&nbsp;Yunzhong Zhang,&nbsp;Yufeng Li,&nbsp;Fang Wang","doi":"10.1186/s12860-022-00440-7","DOIUrl":"https://doi.org/10.1186/s12860-022-00440-7","url":null,"abstract":"<p><p>Cervical cancer is an important malignant tumor threatening the physical and mental health of women in the world. As a new calcium activated chloride channel protein, calcium activated chloride channel (CLCA2) plays an important role in tumorigenesis and development. But its role and exact regulatory mechanism in cervical cancer are still unclear. In our study, we found CLCA2 was significantly decreased in cervical cancer cells, and overexpression of CLCA2 inhibited the proliferation, migration and invasion, and promotes apoptosis of cervical cancer cells, and CLCA2 inhibited EMT (Epithelial-mesenchymal transition) through an p38 / JNK / ERK pathway. The results in vivo were consistent with those in vitro. In conclusion, overexpression of CLCA2 inhibited the progression of cervical cancer in vivo and in vitro. This may provide a theoretical basis for CLCA2 as a new indicator of clinical diagnosis and prognosis of cervical cancer or as a potential target of drug therapy.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9594891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40586659","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":"The role of proteoglycan form of DMP1 in cranial repair.","authors":"Yang Liu,&nbsp;Pingping Niu,&nbsp;Mengqi Zhou,&nbsp;Hui Xue","doi":"10.1186/s12860-022-00443-4","DOIUrl":"https://doi.org/10.1186/s12860-022-00443-4","url":null,"abstract":"<p><strong>Background: </strong>The cranial region is a complex set of blood vessels, cartilage, nerves and soft tissues. The reconstruction of cranial defects caused by trauma, congenital defects and surgical procedures presents clinical challenges. Our previous data showed that deficiency of the proteoglycan (PG) form of dentin matrix protein 1 (DMP1-PG) could lead to abnormal cranial development. In addition, DMP1-PG was highly expressed in the cranial defect areas. The present study aimed to investigate the potential role of DMP1-PG in intramembranous ossification in cranial defect repair.</p><p><strong>Methods: </strong>Mouse cranial defect models were established by using wild- type (WT) and DMP1-PG point mutation mice. Microcomputed tomography (micro-CT) and histological staining were performed to assess the extent of repair. Immunofluorescence assays and real-time quantitative polymerase chain reaction (RT‒qPCR) were applied to detect the differentially expressed osteogenic markers. RNA sequencing was performed to probe the molecular mechanism of DMP1-PG in regulating defect healing.</p><p><strong>Results: </strong>A delayed healing process and an abnormal osteogenic capacity of primary osteoblasts were observed in DMP1-PG point mutation mice. Furthermore, impaired inflammatory signaling pathways were detected by using RNA transcription analysis of this model.</p><p><strong>Conclusions: </strong>Our data indicate that DMP1-PG is an indispensable positive regulator during cranial defect healing.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9524138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40383271","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":"Effects of growth hormone/estrogen/androgen on COVID-19-type proinflammatory responses in normal human lung epithelial BEAS-2B cells.","authors":"Zemin Zhu,&nbsp;Zhijian Zhao,&nbsp;Xun Chen,&nbsp;Zhou Chu,&nbsp;Yi He,&nbsp;Yingzheng Tan,&nbsp;Juan Zhou,&nbsp;Caixi Tang","doi":"10.1186/s12860-022-00442-5","DOIUrl":"https://doi.org/10.1186/s12860-022-00442-5","url":null,"abstract":"<p><strong>Background: </strong>COVID-19 is a disease caused by SARS-CoV-2, which can cause mild to serious infections in humans. We aimed to explore the effect of growth hormone (GH)/estrogen/androgen in normal human lung epithelial BEAS-2B cells on COVID-19-type proinflammatory responses.</p><p><strong>Methods: </strong>A BEAS-2B COVID-19-like proinflammatory cell model was constructed. After that, the cells were treated with GH, 17β-estradiol (E2), and testosterone (Tes) for 24 h. CCK-8 assays were utilized to evaluate cell viability. The mRNA expression of ACE2, AGTR1, TMRRSS2, and ISG15 and the protein expression of ACE2, AGTR1, TMRRSS2, and ISG15 were measured by qRT‒PCR and Western blotting, respectively. ELISAs were performed to determine IL-6, MCP-1, MDA and SOD expression. Flow cytometry was used to measure ROS levels. Finally, MAPK/NF-κB pathway-related factor expression was evaluated.</p><p><strong>Results: </strong>The COVID-19-type proinflammatory model was successfully constructed, and 1000 ng/mL RBD treatment for 24 h was selected as the condition for the model group for subsequent experiments. After RBD treatment, cell viability decreased, the mRNA expression of ACE2, AGTR1, TMRRSS2, and ISG15 and the protein expression of ACE2, AGTR1, TMRRSS2, and ISG15 increased, IL-6, MCP-1, MDA and ROS levels increased, and MDA levels decreased. The mRNA levels of MAPK14 and RELA increased, but the protein levels did not change significantly. In addition, phospho-MAPK14 and phospho-RELA protein levels were also increased. Among the tested molecules, E2 had the most pronounced effect, followed by GH, while Tes showed the opposite effect.</p><p><strong>Conclusion: </strong>GH/E2 alleviated inflammation in a COVID-19-type proinflammatory model, but Tes showed the opposite effect.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9520119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40382325","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":"Optimization of differentiation protocols of dental tissues stem cells to pancreatic β-cells.","authors":"Riham M Aly,&nbsp;Hadeer A Aglan,&nbsp;Ghada Nour Eldeen,&nbsp;Hanaa H Ahmed","doi":"10.1186/s12860-022-00441-6","DOIUrl":"https://doi.org/10.1186/s12860-022-00441-6","url":null,"abstract":"<p><strong>Background: </strong>Despite the recent progress in the differentiation strategies of stem cells into pancreatic beta cell lineage, current protocols are not optimized for different cell types. The purpose of this study is to investigate and compare the ability of stem cells derived from dental pulp (DPSCs) and periodontal ligament (PDLSCs) as two anatomically different dental tissues to differentiate into pancreatic beta cells while assessing the most suitable protocol for each cell type.</p><p><strong>Methods: </strong>DPSCs & PDLSCs were isolated and characterized morphologically and phenotypically and then differentiated into pancreatic beta cells using two protocols. Differentiated cells were assessed by qRT-PCR for the expression of pancreatic related markers Foxa-2, Sox-17, PDX-1, Ngn-3, INS and Gcg. Functional assessment of differentiation was performed by quantification of Insulin release via ELISA.</p><p><strong>Results: </strong>Protocol 2 implementing Geltrex significantly enhanced the expression levels of all tested genes both in DPSCs & PDLSCs. Both DPSCs & PDLSCs illustrated improved response to increased glucose concentration in comparison to undifferentiated cells. Moreover, DPSCs demonstrated an advanced potency towards pancreatic lineage differentiation over PDLSCs under both protocols.</p><p><strong>Conclusion: </strong>In conclusion, the current study reports the promising potential of dental derived stem cells in differentiating into pancreatic lineage through selection of the right protocol.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.8,"publicationDate":"2022-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9487116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40371895","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}