Cell Biology International最新文献_第5页

Chrysin attenuates epithelial prostatic hyperplasia in the ventral prostate of spontaneously hypertensive rats 蛹虫草素能减轻自发性高血压大鼠腹侧前列腺的上皮性前列腺增生。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-11 DOI: 10.1002/cbin.12218

Nathany R. L. dos Santos, Gessica C. de Sousa, Phâmella N. Lima, Bárbara C. M. Medeiros, Luana A. Manso, Cinthia R. B. Silva, Carla C. R. da Silveira, Paulo C. Ghedini, Hericles M. Campos, Matheus S. Costa, Isadora G. Fernandes, Elizabeth P. Mendes, Sebastião R. Taboga, Carlos H. de Castro, Fernanda C. A. dos Santos, Manoel F. Biancardi

{"title":"Chrysin attenuates epithelial prostatic hyperplasia in the ventral prostate of spontaneously hypertensive rats","authors":"Nathany R. L. dos Santos, Gessica C. de Sousa, Phâmella N. Lima, Bárbara C. M. Medeiros, Luana A. Manso, Cinthia R. B. Silva, Carla C. R. da Silveira, Paulo C. Ghedini, Hericles M. Campos, Matheus S. Costa, Isadora G. Fernandes, Elizabeth P. Mendes, Sebastião R. Taboga, Carlos H. de Castro, Fernanda C. A. dos Santos, Manoel F. Biancardi","doi":"10.1002/cbin.12218","DOIUrl":"10.1002/cbin.12218","url":null,"abstract":"The aim of this study was to evaluate the effects of chrysin on the ventral prostate of spontaneously hypertensive rats (SHR). Ten-week-old male Wistar and SHR rats received 100 mg/kg/day of chrysin (TW and TSHR) or 200 µL/day of the dilution vehicle (CW and CSHR) for 70 days. After the treatment, the animals were euthanized and the prostates were dissected out, fixed, and processed for further morphological, immunohistochemical, and biochemical analyses. Blood was collected for serological analysis. Chrysin did not interfere with the blood pressure. Morphologically, the epithelial height increased in TW and decreased in TSHR. Stereology showed an increase in the epithelial and stromal relative frequency, and a decrease in the lumen of TW, whereas the epithelium in TSHR was reduced. Normal alveoli decreased, and hyperplastic alveoli had an increment in TW, whereas in TSHR normal alveoli increased and intense hyperplasia decreased. The secretion area was reduced in TW. Immunohistochemical analysis showed a smaller number of PCNA-positive cells in TW. Finally, the biochemical analysis showed a reduction in malondialdehyde, carbonylated proteins, superoxide dismutase, and catalase in TW and TSHR. We concluded that the chrysin effect is dependent on the context in which this flavonoid is employed. In normal conditions, the anabolic potential of the chrysin was favored, disrupting the morphology of the prostate. However, when used in animals predisposed to develop hyperplasia, this flavonoid attenuates the hyperplastic status, improving the morphology of the gland.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Progranulin mitigates intestinal injury in a murine model of necrotizing enterocolitis by suppressing M1 macrophage polarization 在小鼠坏死性小肠结肠炎模型中，Progranulin 通过抑制 M1 巨噬细胞极化减轻肠道损伤。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-08 DOI: 10.1002/cbin.12209

Dandan Mo, Youjun Qiu, Bing Tian, Xinli Liu, Yujie Chen, Guotao Zou, Chunbao Guo, Chun Deng

{"title":"Progranulin mitigates intestinal injury in a murine model of necrotizing enterocolitis by suppressing M1 macrophage polarization","authors":"Dandan Mo, Youjun Qiu, Bing Tian, Xinli Liu, Yujie Chen, Guotao Zou, Chunbao Guo, Chun Deng","doi":"10.1002/cbin.12209","DOIUrl":"10.1002/cbin.12209","url":null,"abstract":"Neonatal necrotizing enterocolitis (NEC) is a critical digestive disorder frequently affecting premature infants. Characterized by intestinal inflammation caused by activated M1 macrophages, modulation of macrophage polarization is considered a promising therapeutic strategy for NEC. It has been demonstrated that the growth factor-like protein progranulin (PGRN), which plays roles in a number of physiological and pathological processes, can influence macrophage polarization and exhibit anti-inflammatory characteristics in a number of illnesses. However, its role in NEC is yet to be investigated. Our research showed that the levels of PGRN were markedly elevated in both human and animal models of NEC. PGRN deletion in mice worsens NEC by encouraging M1 polarization of macrophages and escalating intestinal damage and inflammation. Intravenous administration of recombinant PGRN to NEC mice showed significant survival benefits and protective effects, likely due to PGRN's ability to inhibit M1 polarization and reduce the release of pro-inflammatory factors. Our findings shed new light on PGRN's biological role in NEC and demonstrate its potential as a therapeutic target for the disease.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to “Stem cells technology as a platform for generating reproductive system organoids and treatment of infertility-related diseases” 更正 "干细胞技术作为生成生殖系统器官组织和治疗不孕不育相关疾病的平台"。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-04 DOI: 10.1002/cbin.12217

引用次数: 0

Transcriptome-wide profiling for melanocytes derived from newborn and adult human epidermis with enhanced proliferation 从新生儿和成人表皮中提取的黑素细胞的全转录组图谱，其增殖能力增强。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-03 DOI: 10.1002/cbin.12214

Ai Orimoto, Sayo Kashiwagi, Ayaka Funakoshi, Takashi Shimizu, Tsuyoshi Ishii, Tohru Kiyono, Tomokazu Fukuda

{"title":"Transcriptome-wide profiling for melanocytes derived from newborn and adult human epidermis with enhanced proliferation","authors":"Ai Orimoto, Sayo Kashiwagi, Ayaka Funakoshi, Takashi Shimizu, Tsuyoshi Ishii, Tohru Kiyono, Tomokazu Fukuda","doi":"10.1002/cbin.12214","DOIUrl":"10.1002/cbin.12214","url":null,"abstract":"The senescence-associated protein p16INK4A acts as a limiter element in cell-cycle progression. The loss of p16INK4A function is causally related to cellular immortalization. The increase in p16INK4A levels with advancing age was demonstrated in melanocytes. However, the characteristic difference between young and senescent melanocytes affecting immortalization of melanocytes remains unclear. In this study, we generated 10 different cell lines in total from newborn (NB) and adult (AD) primary normal human epidermal melanocytes (NHEM) using four different methods, transduction of CDK4R24C and cyclin D1 (K4D), K4D with TERT (K4DT), SV40 T-antigen (SV40T), and HPV16 E6 and E7 (E6/E7) and performed whole transcriptome sequencing analysis (RNA-Seq) to elucidate the differences of genome-wide expression profiles among cell lines. The analysis data revealed distinct differences in expression pattern between cell lines from NB and AD although no distinct biological differences were detected in analyses such as comparison of cell morphology, evaluation of cell proliferation, and cell cycle profiles. This study may provide useful in vitro models to benefit the understanding of skin-related diseases.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Golgi protein ACBD3 downregulation sensitizes cells to ferroptosis 下调高尔基体蛋白 ACBD3 可使细胞对铁变态反应敏感。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-02 DOI: 10.1002/cbin.12213

Ying Qian, Shanchuan Ma, Rong Qiu, Zhiyang Sun, Wei Liu, Fan Wu, Sin Man Lam, Zhengguo Xia, Kezhen Wang, Linshen Fang, Guanghou Shui, Xinwang Cao

{"title":"Golgi protein ACBD3 downregulation sensitizes cells to ferroptosis","authors":"Ying Qian, Shanchuan Ma, Rong Qiu, Zhiyang Sun, Wei Liu, Fan Wu, Sin Man Lam, Zhengguo Xia, Kezhen Wang, Linshen Fang, Guanghou Shui, Xinwang Cao","doi":"10.1002/cbin.12213","DOIUrl":"10.1002/cbin.12213","url":null,"abstract":"Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, is emerging as a promising target in cancer therapy. It is regulated by a network of molecules and pathways that modulate lipid metabolism, iron homeostasis and redox balance, and related processes. However, there are still numerous regulatory molecules intricately involved in ferroptosis that remain to be identified. Here, we indicated that suppression of Golgi protein acyl-coenzyme A binding domain A containing 3 (ACBD3) increased the sensitivity of Henrieta Lacks and PANC1 cells to ferroptosis. ACBD3 knockdown increases labile iron levels by promoting ferritinophagy. This increase in free iron, coupled with reduced levels of glutathione peroxidase 4 due to ACBD3 knockdown, leads to the accumulation of reactive oxygen species and lipid peroxides. Moreover, ACBD3 knockdown also results in elevated levels of polyunsaturated fatty acid-containing glycerophospholipids through mechanisms that remain to be elucidated. Furthermore, inhibition of ferrtinophagy in ACBD3 downregulated cells by knocking down the nuclear receptor co-activator 4 or Bafilomycin A1 treatment impeded ferroptosis. Collectively, our findings highlight the pivotal role of ACBD3 in governing cellular resistance to ferroptosis and suggest that pharmacological manipulation of ACBD3 levels is a promising strategy for cancer therapy.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

JRK binds satellite III DNA and is necessary for the heat shock response JRK 与卫星 III DNA 结合，是热休克反应所必需的。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-01 DOI: 10.1002/cbin.12216

Rosalie Waldron, Maria de los Angeles Becerra Rodriguez, John M. Williams, Zhenfei Ning, Abrar Ahmed, Andrew Lindsay, Tom Moore

{"title":"JRK binds satellite III DNA and is necessary for the heat shock response","authors":"Rosalie Waldron, Maria de los Angeles Becerra Rodriguez, John M. Williams, Zhenfei Ning, Abrar Ahmed, Andrew Lindsay, Tom Moore","doi":"10.1002/cbin.12216","DOIUrl":"10.1002/cbin.12216","url":null,"abstract":"JRK is a DNA-binding protein of the pogo superfamily of transposons, which includes the well-known centromere binding protein B (CENP-B). Jrk null mice exhibit epilepsy, and growth and reproductive disorders, consistent with its relatively high expression in the brain and reproductive tissues. Human JRK DNA variants and gene expression levels are implicated in cancers and neuropsychiatric disorders. JRK protein modulates β-catenin–TCF activity but little is known of its cellular functions. Based on its homology to CENP-B, we determined whether JRK binds centromeric or other satellite DNAs. We show that human JRK binds satellite III DNA, which is abundant at the chromosome 9q12 juxtacentromeric region and on Yq12, both sites of nuclear stress body assembly. Human JRK-GFP overexpressed in HeLa cells strongly localises to 9q12. Using an anti-JRK antiserum we show that endogenous JRK co-localises with a subset of centromeres in non-stressed cells, and with heat shock factor 1 following heat shock. Knockdown of JRK in HeLa cells proportionately reduces heat shock protein gene expression in heat-shocked cells. A role for JRK in regulating the heat shock response is consistent with the mouse Jrk null phenotype and suggests that human JRK may act as a modifier of diseases with a cellular stress component.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466423","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}

引用次数: 0

Correction to “potential role of heat shock proteins in neural differentiation of murine embryonal carcinoma stem cells (P19)” 更正 "热休克蛋白在小鼠胚胎癌干细胞（P19）神经分化中的潜在作用"。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-30 DOI: 10.1002/cbin.12193

引用次数: 0

TCF12 induces ferroptosis by suppressing OTUB1-mediated SLC7A11 deubiquitination to promote cisplatin sensitivity in oral squamous cell carcinoma TCF12通过抑制OTUB1介导的SLC7A11去泛素化诱导铁变态反应，从而促进口腔鳞状细胞癌对顺铂的敏感性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-30 DOI: 10.1002/cbin.12211

Yanchun Liu, Qin Bai, Nan Pang, Jun Xue

{"title":"TCF12 induces ferroptosis by suppressing OTUB1-mediated SLC7A11 deubiquitination to promote cisplatin sensitivity in oral squamous cell carcinoma","authors":"Yanchun Liu, Qin Bai, Nan Pang, Jun Xue","doi":"10.1002/cbin.12211","DOIUrl":"10.1002/cbin.12211","url":null,"abstract":"Chemotherapy resistance is a major obstacle to effective cancer treatment, and promotion of ferroptosis can suppress cisplatin resistance in tumor cells. TCF12 plays a suppressive role in oral squamous cell carcinoma (OSCC), but whether it participates in the regulation of cisplatin resistance by modulating ferroptosis remains unclear. Here, we found that TCF12 expression was decreased in OSCC cells compared with normal oral cells, and it was reduced in cisplatin (DDP)-resistant OSCC cells compared with parental cells. Moreover, overexpression of TCF12 sensitized DDP-resistant cells to DDP by promoting ferroptosis. Intriguingly, silencing TCF12 reversed the promotion effect of the ferroptosis activator RSL3 on ferroptosis and DDP sensitivity, and overexpressing TCF12 antagonized the effect of the ferroptosis inhibitor liproxstatin-1 on ferroptosis and DDP resistance. Mechanically, TCF12 promoted ubiquitination of SLC7A11 and decreased SLC7A11 protein stability through transcriptional repression of OTUB1, thereby facilitating ferroptosis. Consistently, SLC7A11 overexpression neutralized the promotion effect of TCF12 on ferroptosis and DDP sensitivity. Additionally, upregulation of TCF12 hindered the growth of mouse OSCC xenografts and enhanced the DDP sensitivity of xenografts by inducing ferroptosis. In conclusion, TCF12 enhanced DDP sensitivity in OSCC cells by promoting ferroptosis, which was achieved through modulating SLC7A11 expression via transcriptional regulation of OTUB1.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular mechanisms of diabetic nephropathy: A narrative review 糖尿病肾病的分子机制：叙述性综述。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-30 DOI: 10.1002/cbin.12212

Tian Sun, Yina Guo, Yanting Su, Shigang Shan, Wenbin Qian, Feixue Zhang, Mengxi Li, Zhenwang Zhang

引用次数: 0

Osteoking prevents bone loss and enhances osteoblastic bone formation by modulating the AGEs/IGF-1/β-catenin/OPG pathway in type 2 diabetic db/db mice Osteoking 通过调节 AGEs/IGF-1/β-catenin/OPG 通路，防止 2 型糖尿病 db/db 小鼠骨质流失并促进成骨细胞骨形成。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-27 DOI: 10.1002/cbin.12215

Yi Yang, Rong Li, Peijin Wang, Yulan Zhao, Jintao Li, Jianlin Jiao, Hong Zheng

{"title":"Osteoking prevents bone loss and enhances osteoblastic bone formation by modulating the AGEs/IGF-1/β-catenin/OPG pathway in type 2 diabetic db/db mice","authors":"Yi Yang, Rong Li, Peijin Wang, Yulan Zhao, Jintao Li, Jianlin Jiao, Hong Zheng","doi":"10.1002/cbin.12215","DOIUrl":"10.1002/cbin.12215","url":null,"abstract":"Type 2 diabetic osteoporosis (T2DOP) is a skeletal metabolic syndrome characterized by impaired bone remodeling due to type 2 diabetes mellitus, and there are drawbacks in the present treatment. Osteoking (OK) is widely used for treating fractures and femoral head necrosis. However, OK is seldom reported in the field of T2DOP, and its role and mechanism of action need to be elucidated. Consequently, this study investigated whether OK improves bone remodeling and the mechanisms of diabetes-induced injury. We used db/db mice as a T2DOP model and stimulated MC3T3-E1 cells (osteoblast cell line) with high glucose (HG, 50 mM) and advanced glycation end products (AGEs, 100 µg/mL), respectively. The effect of OK on T2DOP was assessed using a combined 3-point mechanical bending test, hematoxylin and eosin staining, and enzyme-linked immunosorbent assay. The effect of OK on enhancing MC3T3-E1 cell differentiation and mineralization under HG and AGEs conditions was assessed by an alkaline phosphatase activity assay and alizarin red S staining. The AGEs/insulin-like growth factor-1(IGF-1)/β-catenin/osteoprotegerin (OPG) pathway-associated protein levels were assayed by western blot analysis and immunohistochemical staining. We found that OK reduced hyperglycemia, attenuated bone damage, repaired bone remodeling, increased tibial and femoral IGF-1, β-catenin, and OPG expression, and decreased receptor activator of nuclear kappa B ligand and receptor activator of nuclear kappa B expression in db/db mice. Moreover, OK promoted the differentiation and mineralization of MC3T3-E1 cells under HG and AGEs conditions, respectively, and regulated the levels of AGEs/IGF-1/β-catenin/OPG pathway-associated proteins. In conclusion, our results suggest that OK may lower blood glucose, alleviate bone damage, and attenuate T2DOP, in part through activation of the AGEs/IGF-1/β-catenin/OPG pathway.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0