The Kaohsiung journal of medical sciences最新文献_第9页

In vitro and in vivo effects of Galectin-3 inhibitor TD139 on inflammation and ERK/JNK/p38 pathway in gestational diabetes mellitus. Galectin-3抑制剂TD139对妊娠糖尿病患者炎症和ERK/JNK/p38通路的体外和体内影响

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-09-04 DOI: 10.1002/kjm2.12890

Ji Xia, Yan Wang, Bang-Ruo Qi

{"title":"In vitro and in vivo effects of Galectin-3 inhibitor TD139 on inflammation and ERK/JNK/p38 pathway in gestational diabetes mellitus.","authors":"Ji Xia, Yan Wang, Bang-Ruo Qi","doi":"10.1002/kjm2.12890","DOIUrl":"10.1002/kjm2.12890","url":null,"abstract":"This study aims to investigate the effects of the Galectin-3 (Gal-3) inhibitor TD139 on inflammation and the extracellular signal-regulated kinase (ERK)/c-Jun N-terminal kinase (JNK)/p38 pathway in gestational diabetes mellitus (GDM). Human placental tissues were treated with TD139 and TNF-α, assessing Gal-3, ERK/JNK/p38 activation, and inflammatory cytokines. GDM was induced in mice via subcutaneous injections of streptozotocin (STZ). After confirming GDM, mice were treated with 15 mg/kg TD139 on GD 10.5 12.5, 14.5, 16.5, and 18.5. Serum inflammatory cytokines were measured on GD 20.5, and post-delivery placental tissues were analyzed. Data were analyzed using one-way or two-way repeated measures ANOVA with post hoc tests. TD139 suppressed TNF-α-induced increases in Gal-3, IL-1β, IL-6, MCP-1, and ERK/JNK/p38 activation in placental tissues. In STZ-induced GDM mice, TD139 reduced glucose levels, weight loss, and food and water intake. TD139 significantly lowered TNF-α, IL-1β, IL-6, and MCP-1 in serum and placental tissues and inhibited the ERK/JNK/p38 pathway. TD139 improved pup numbers in GDM mice compared to untreated ones. TD139 reduces inflammation and inhibits the ERK/JNK/p38 pathway in TNF-α stimulated placental tissues and STZ-induced GDM mice, suggesting its therapeutic potential for managing GDM-related placental inflammation and improving pregnancy outcomes. The study used TNF-α to mimic GDM in placental tissues and an STZ-induced GDM mouse model, which may not fully represent human GDM complexity. Future research should explore alternative models, and broader signaling pathways, and thoroughly evaluate TD139's safety in pregnancy.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"916-925"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142127814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HLA-DR genotypes in patients with primary Sjögren's syndrome in Taiwan. 台湾原发性斯约格伦综合征患者的 HLA-DR 基因型。

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-08 DOI: 10.1002/kjm2.12885

Chang-Yi Yen, Pin-Yi Wang, Kuan-Yu Chen, Chia-Chun Tseng, Cheng-Chin Wu, Tsan-Teng Ou, Jeng-Hsien Yen

{"title":"HLA-DR genotypes in patients with primary Sjögren's syndrome in Taiwan.","authors":"Chang-Yi Yen, Pin-Yi Wang, Kuan-Yu Chen, Chia-Chun Tseng, Cheng-Chin Wu, Tsan-Teng Ou, Jeng-Hsien Yen","doi":"10.1002/kjm2.12885","DOIUrl":"10.1002/kjm2.12885","url":null,"abstract":"Different human leukocyte antigen (HLA) genotypes have been known to be associated with the risk of development of Sjögren's syndrome in different populations, but this association has never been reported in Taiwan. We enrolled 1044 subjects (673 patients, 371 controls) and tested their HLA-DR genotypes. We found an increased risk of Sjögren's syndrome in patients carrying HLA-DR8. DR1 and DR14 were associated with increased risk of eye involvement (uveitis, scleritis or optic neuritis), while DR15 was associated with increased risk of interstitial lung disease. DR8 was associated with increased risk of formation of multiple antibodies: anti-Ro, rheumatoid factor and antinuclear antibodies (ANA) reaching titer 1:80 or above. DR9 was associated with decreased risk of formation of anti-La antibodies and increased risk of formation of antithyroglobulin antibodies. DR10 was associated with risk of formation of anticyclic citrullinated peptide (anti-CCP) antibodies, and DR11 was associated with increased risk of formation of anti-La antibodies. Oral ulcer was found to be negatively associated with anti-Ro antibodies and with anti-ENA antibodies. Skin lesions were associated with ANA antibody titer elevation to 1:80 or above. Malignancies of any kind were associated with the presence of cryoglobulin. Females were more likely to be diagnosed at a younger age than males. There was no statistically significant relationship between HLA-DR genotype and age at disease diagnosis. In patients with Sjögren's syndrome in Taiwan, the presence of HLA-DR8 appeared to be a risk factor. In addition, we found several associations between HLA-DR genotype, clinical presentation, and autoantibody status among them.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"934-941"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141904112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

LncRNA NR2F2-AS1 inhibits the progression of oral squamous cell carcinoma by mediating the miR-32-5p/SEMA3A axis. LncRNA NR2F2-AS1 通过介导 miR-32-5p/SEMA3A 轴抑制口腔鳞状细胞癌的进展。

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-23 DOI: 10.1002/kjm2.12888

Shi-Yu Qin, Bo Li, Ji-Mu Liu, Qiu-Li Lv, Xiang-Lin Zeng

{"title":"LncRNA NR2F2-AS1 inhibits the progression of oral squamous cell carcinoma by mediating the miR-32-5p/SEMA3A axis.","authors":"Shi-Yu Qin, Bo Li, Ji-Mu Liu, Qiu-Li Lv, Xiang-Lin Zeng","doi":"10.1002/kjm2.12888","DOIUrl":"10.1002/kjm2.12888","url":null,"abstract":"Previous studies have supported a tumor-suppressive role of semaphorin 3A (SEMA3A) in several tumors including oral squamous cell carcinoma (OSCC). However, in-depth characterization of the role of SEMA3A in OSCC and the underlying molecular mechanisms is lacking. Gene and protein expressions were detected using quantitative real-time PCR, western blot assay, and immunohistochemistry. OSCC cell metastasis was evaluated using Transwell and angiogenesis of human umbilical vein endothelial cells (HUVECs) was determined using tube formation assay. The interactions among molecules were predicted using bioinformatics analysis and validated using luciferase activity experiment and RNA immunoprecipitation assay. Pulmonary metastasis was evaluated using hematoxylin and eosin staining after constructing a lung metastasis tumor model in mice. SEMA3A expression was decreased in OSCC cells and its overexpression led to suppression of epithelial-mesenchymal transition (EMT), migration, and invasion of OSCC cells and angiogenesis of HUVECs. miR-32-5p was identified as an upstream molecule of SEMA3A and long non-coding RNA NR2F2 antisense RNA 1 (NR2F2-AS1) was validated as an upstream gene of miR-32-5p. Further experiments revealed that the inhibitory effects of NR2F2-AS1 overexpression on EMT, migration, invasion of OSCC cells, and angiogenesis of HUVECs as well as tumor growth and metastasis in mice were mediated via the miR-32-5p/SEMA3A axis. To conclude, NR2F2-AS1 may attenuate OSCC cell metastasis and angiogenesis of HUVECs and suppress tumor growth and metastasis in mice via the miR-32-5p/SEMA3A axis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"877-889"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142038109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Emergence of clonal evolution with Philadelphia chromosome in acute myeloid leukemia after hypomethylation agents and BCL2 inhibitor treatment. 低甲基化药物和 BCL2 抑制剂治疗后，急性髓性白血病出现费城染色体克隆进化。

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-19 DOI: 10.1002/kjm2.12886

Shih-Yu Kao, Samuel Y Hsiao, Bi-Hua Du, Hui-Hua Hsiao

引用次数: 0

CMTM5 influences Hippo/YAP axis to promote ferroptosis in glioma through regulating WWP2-mediated LATS2 ubiquitination. CMTM5通过调节WWP2介导的LATS2泛素化影响Hippo/YAP轴，促进胶质瘤中的铁变态反应。

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-21 DOI: 10.1002/kjm2.12889

Ye Fan, He-Qin Zou

{"title":"CMTM5 influences Hippo/YAP axis to promote ferroptosis in glioma through regulating WWP2-mediated LATS2 ubiquitination.","authors":"Ye Fan, He-Qin Zou","doi":"10.1002/kjm2.12889","DOIUrl":"10.1002/kjm2.12889","url":null,"abstract":"Glioma, a common malignancy, is characterized by high morbidity and mortality. Promoting ferroptosis can delay tumor progression. Here, we aimed to explore the underlying mechanism of ferroptosis in glioma. In vitro and in vivo experiments were conducted using glioma cells and nude mice. The expression of genes and proteins was evaluated by RT-qPCR, Western blot assay, and immunohistochemical staining. Malignant activities of glioma cells were evaluated using MTT, EdU, and Transwell assays. The levels of Fe2+, lipid reactive oxygen species, and malondialdehyde were determined using commercial kits. The interplays among CMTM5, WWP2, and LATS2 were validated using Co-immunoprecipitation assay. The UALCAN database predicted downregulation of CMTM5 expression in glioma, and low expression of CMTM5 was associated with poor survival outcomes. CMTM5 overexpression inhibited cell growth and invasion and promoted ferroptosis of glioma cells. Besides, CMTM5 protein interacted with WWP2 protein and decreased WWP2 expression. WWP2 silencing attenuated LATS2 ubiquitination to enhance LATS2 expression and phosphorylation of YAP1. CMTM5 exerted a suppressive effect on cell growth and invasion and promoted ferroptosis of glioma cells by regulating the WWP2/LATS2 pathway. In the in vivo experiments, CMTM5 overexpression suppressed tumor growth and enhanced ferroptosis. CMTM5 regulated Hippo/YAP signaling to inhibit cell growth and invasion and to promote ferroptosis in glioma by regulating WWP2-mediated LATS2 ubiquitination, thereby attenuating glioma progression.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"890-902"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142020053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction: 'ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer'. Zhen-Ya Gao, Fang Yu, Huan-Xia Jia, Zhuo Ye, Shi-Jie Yao, Kaohsiung J Med Sci. 2020; 36: 1021-1029 (https://doi.org/10.1002/kjm2.12284). 撤稿：《ASPM预测膀胱癌不良预后并调控细胞增殖》。Zhen-Ya Gao, Fang Yu, Huan-Xia Jia, Zhuo Ye, Shi-Jie Yao, Kaohsiung J Med Sci. 2020; 36: 1021-1029 (https://doi.org/10.1002/kjm2.12284).

The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-03-28 DOI: 10.1002/kjm2.12825

引用次数: 0

Correction to “miR‐199a/214 cluster enhances prostate cancer sensitiveness to nimotuzumab via targeting TBL1XR1” 对 "miR-199a/214基因簇通过靶向TBL1XR1增强前列腺癌对尼莫妥珠单抗的敏感性 "的更正

The Kaohsiung journal of medical sciences Pub Date : 2024-09-19 DOI: 10.1002/kjm2.12897

引用次数: 0

Molecular mechanism of ALKBH5‐mediated m6A demethylation regulating lipopolysaccharide‐induced epithelial–mesenchymal transition in sepsis‐induced acute kidney injury ALKBH5 介导的 m6A 去甲基化调控脂多糖诱导的脓毒症急性肾损伤上皮-间质转化的分子机制

The Kaohsiung journal of medical sciences Pub Date : 2024-09-17 DOI: 10.1002/kjm2.12892

Hai‐Hong Zhao, Chun‐Ling Chen, Fen‐Fang Chen, Lu‐Lu Zhang, Mei‐Mei Li, Ze‐Bao He

{"title":"Molecular mechanism of ALKBH5‐mediated m6A demethylation regulating lipopolysaccharide‐induced epithelial–mesenchymal transition in sepsis‐induced acute kidney injury","authors":"Hai‐Hong Zhao, Chun‐Ling Chen, Fen‐Fang Chen, Lu‐Lu Zhang, Mei‐Mei Li, Ze‐Bao He","doi":"10.1002/kjm2.12892","DOIUrl":"https://doi.org/10.1002/kjm2.12892","url":null,"abstract":"This study explored the mechanism by which the m6A demethylase ALKBH5 mediates epithelial–mesenchymal transition (EMT) in sepsis‐associated acute kidney injury (SA‐AKI) and AKI‐chronic kidney disease (CKD) transition. HK‐2 cells were stimulated with lipopolysaccharide (LPS) to establish an in vitro model of SA‐AKI. ALKBH5 expression was reduced through the transfection of si‐ALKBH5. Cell viability, apoptosis, and migration were detected by CCK‐8 assay, TUNEL staining, and Transwell. The levels of TNF‐α, IL‐1β, and IL‐6 were measured by enzyme‐linked immunosorbent assay. Quantitative real‐time polymerase chain reaction or Western blotting was performed to determine the expressions of ALKBH5, miR‐205‐5p, DDX5, E‐cadherin, and α‐SMA. The m6A level was quantitatively analyzed. The expression of pri‐miR‐205 bound to DGCR8 and m6A‐modified pri‐miR‐205 after intervention with ALKBH5 expression was detected by RNA immunoprecipitation. A dual‐luciferase assay confirmed the binding between miR‐205‐5p and DDX5. ALKBH5 was highly expressed in LPS‐induced HK‐2 cells. Inhibition of ALKBH5 increased cell viability, repressed apoptosis, and reduced EMT. Inhibition of ALKBH5 increased the m6A modification level, thereby promoting DGCR8 binding to pri‐miR‐205 to increase miR‐205‐5p expression and eventually targeting DDX5 expression. Low expression of miR‐205‐5p or overexpression of DDX5 partially abolished the inhibitory effect of ALKBH5 silencing on EMT. In conclusion, ALKBH5 represses miR‐205‐5p expression by removing m6A modification to upregulate DDX5 expression, thereby promoting EMT and AKI‐CKD transition after SA‐AKI.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142257965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MicroRNA‐223 alleviates inflammatory response in renal ischemia‐reperfusion injury by targeting NLRP3 MicroRNA-223 通过靶向 NLRP3 减轻肾缺血再灌注损伤的炎症反应

The Kaohsiung journal of medical sciences Pub Date : 2024-09-06 DOI: 10.1002/kjm2.12883

Jun Ye, Xiaoli Tang, Ming Li, Yutian Liao, Yiqian Zeng, Furong Tang, Eryue Qiu

{"title":"MicroRNA‐223 alleviates inflammatory response in renal ischemia‐reperfusion injury by targeting NLRP3","authors":"Jun Ye, Xiaoli Tang, Ming Li, Yutian Liao, Yiqian Zeng, Furong Tang, Eryue Qiu","doi":"10.1002/kjm2.12883","DOIUrl":"https://doi.org/10.1002/kjm2.12883","url":null,"abstract":"We investigated the potential correlation between miR‐223 and NAcHT, LRR, and PYd domain‐containing protein 3 (NLRP3) in the context of renal ischemia‐reperfusion injury (RIRI), which is a leading cause of acute renal failure with significant mortality rates. Additionally, miR‐223 has been implicated in renal inflammation, further highlighting its relevance to this study. C57BL/6 male mice were used as RIRI models. After successful modeling, pathological examinations and serum creatinine and miR‐223 levels were tested. Pro‐inflammatory cytokine (IL‐1β, IL‐6, IL‐8, NLPR3, TLR4) expression was detected in mice by western blot (kidney tissue) and enzyme‐linked immunosorbent assay (serum). HK‐2 cells were used for in vitro experiments. A hypoxia/reoxygenation (H/R) model was used, and miR‐223 and pro‐inflammatory cytokine levels were detected using PCR and western blot assays, respectively. A dual‐luciferase reporter assay was conducted to confirm the binding of miR‐223 to NLPR3. Next, NLRP3 was knocked down to determine whether the anti‐inflammatory function of miR‐223 is dependent on NLRP3. MiR‐223 expression was lower in RIRI mice than in the sham operation group. The level of miR‐223 negatively correlated with serum creatinine levels and the severity of tubule injury. Increased proinflammatory cytokine levels in RIRI mice were observed. In vitro, miR‐223 alleviated the inflammatory response in H/R treated cells by inhibiting proinflammatory cytokines. Dual‐luciferase reporter and western blot assays confirmed the binding of miR‐223 to NLRP3. NLRP3 knockdown reversed the anti‐inflammatory effects of miR‐223 in HK‐2 cells. MiR‐223 plays an anti‐inflammatory role in RIRI by targeting NLRP3 to repress pro‐inflammatory factors.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142202809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Self-knotted feeding jejunostomy tube in an esophageal cancer patient: A case report and review of the literature. 食管癌患者的自结进食空肠造口管：病例报告和文献综述。

The Kaohsiung journal of medical sciences Pub Date : 2024-09-01 Epub Date: 2024-06-11 DOI: 10.1002/kjm2.12869

Po-Hsuan Wu, Pei-Shan Weng

引用次数: 0