Journal of Cellular Physiology最新文献_第10页

Melatonin regulates endoplasmic reticulum stress in diverse pathophysiological contexts: A comprehensive mechanistic review. 褪黑激素在多种病理生理环境中调节内质网应激：机理综述。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-22 DOI: 10.1002/jcp.31383

Luiz Gustavo de Almeida Chuffa, Fábio Rodrigues Ferreira Seiva, Henrique S Silveira, Roberta Carvalho Cesário, Karolina da Silva Tonon, Vinicius Augusto Simão, Debora Aparecida P C Zuccari, Russel J Reiter

{"title":"Melatonin regulates endoplasmic reticulum stress in diverse pathophysiological contexts: A comprehensive mechanistic review.","authors":"Luiz Gustavo de Almeida Chuffa, Fábio Rodrigues Ferreira Seiva, Henrique S Silveira, Roberta Carvalho Cesário, Karolina da Silva Tonon, Vinicius Augusto Simão, Debora Aparecida P C Zuccari, Russel J Reiter","doi":"10.1002/jcp.31383","DOIUrl":"https://doi.org/10.1002/jcp.31383","url":null,"abstract":"The endoplasmic reticulum (ER) is crucial for protein quality control, and disruptions in its function can lead to various diseases. ER stress triggers an adaptive response called the unfolded protein response (UPR), which can either restore cellular homeostasis or induce cell death. Melatonin, a safe and multifunctional compound, shows promise in controlling ER stress and could be a valuable therapeutic agent for managing the UPR. By regulating ER and mitochondrial functions, melatonin helps maintain cellular homeostasis via reduction of oxidative stress, inflammation, and apoptosis. Melatonin can directly or indirectly interfere with ER-associated sensors and downstream targets of the UPR, impacting cell death, autophagy, inflammation, molecular repair, among others. Crucially, this review explores the mechanistic role of melatonin on ER stress in various diseases including liver damage, neurodegeneration, reproductive disorders, pulmonary disease, cardiomyopathy, insulin resistance, renal dysfunction, and cancer. Interestingly, while it alleviates the burden of ER stress in most pathological contexts, it can paradoxically stimulate ER stress in cancer cells, highlighting its intricate involvement in cellular homeostasis. With numerous successful studies using in vivo and in vitro models, the continuation of clinical trials is imperative to fully explore melatonin's therapeutic potential in these conditions.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

EXPRESSION OF CONCERN: Th17 and treg cells function in SARS-CoV2 patients compared with healthy controls. 忧虑的表达：与健康对照组相比，SARS-CoV2 患者体内 Th17 和 treg 细胞的功能。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-22 DOI: 10.1002/jcp.31380

引用次数: 0

RETRACTION: "Coinhibition of S1PR1 and GP130 by siRNA-loaded Alginate-conjugated Trimethyl Chitosan Nanoparticles Robustly Blocks Development of Cancer Cells". 转载：《siRNA负载的藻酸盐结合三甲基壳聚糖纳米颗粒对S1PR1和GP130的联合抑制可有效阻断癌细胞的发育》。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-22 DOI: 10.1002/jcp.31376

{"title":"RETRACTION: \"Coinhibition of S1PR1 and GP130 by siRNA-loaded Alginate-conjugated Trimethyl Chitosan Nanoparticles Robustly Blocks Development of Cancer Cells\".","authors":"","doi":"10.1002/jcp.31376","DOIUrl":"https://doi.org/10.1002/jcp.31376","url":null,"abstract":"Retraction: N. Rostami, A. Nikkhoo, Y. Khazaei-poul, S. Farhadi, M. Sadat Haeri, S. Moghadaszadeh Ardebili, N. Aghaei Vanda, F. Atyabi, A. Namdar, M. Baghaei, N. Haghnavaz, T. Kazemi, M. Yousefi, G. Ghalamfarsa, G. Sabz, F. Jadidi-Niaragh, \"Coinhibition of S1PR1 and GP130 by siRNA-loaded Alginate-conjugated Trimethyl Chitosan Nanoparticles Robustly Blocks Development of Cancer Cells,\" Journal of Cellular Physiology 235, no. 12 (2020): 9702-9717, https://doi.org/10.1002/jcp.29781. The above article, published online on 18 May 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, the spectra in Figure 2c and 2d display irregularities suggesting data manipulation or fabrication. The data provided by the corresponding author upon request was inadequate to address the concerns. Therefore, the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141734159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Hakai, a novel Runx2 interacting protein, augments osteoblast differentiation by rescuing Runx2 from Smurf2-mediated proteasome degradation Hakai是一种新型Runx2互作蛋白，它通过挽救Runx2免于Smurf2介导的蛋白酶体降解来促进成骨细胞分化。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-21 DOI: 10.1002/jcp.31388

Vishal Upadhyay, Shivani Sharma, Arppita Sethi, Anil Kumar Singh, Sangita Chowdhury, Swati Srivastava, Shivkant Mishra, Shyam Singh, Naibedya Chattopadhyay, Arun Kumar Trivedi

{"title":"Hakai, a novel Runx2 interacting protein, augments osteoblast differentiation by rescuing Runx2 from Smurf2-mediated proteasome degradation","authors":"Vishal Upadhyay, Shivani Sharma, Arppita Sethi, Anil Kumar Singh, Sangita Chowdhury, Swati Srivastava, Shivkant Mishra, Shyam Singh, Naibedya Chattopadhyay, Arun Kumar Trivedi","doi":"10.1002/jcp.31388","DOIUrl":"10.1002/jcp.31388","url":null,"abstract":"Runt-related transcription factor 2 (Runx2) is a key regulator of osteoblast differentiation and bone formation. In Runx2-deficient embryos, skeletal development ceases at the cartilage anlage stage. These embryos die of respiratory failure upon birth and display a complete absence of bone and cartilage mineralization. Here, we identified Hakai, a type of E3 ubiquitin ligase as a potential Runx2 interacting partner through affinity pulldown-based proteomic approach. Subsequently, we observed that similar to Runx2, Hakai was downregulated in osteopenic ovariectomized rats, suggesting its involvement in bone formation. Consistent with this observation, Hakai overexpression significantly enhanced osteoblast differentiation in mesenchyme-like C3H10T1/2 as well as primary rat calvaria osteoblast (RCO) cells in vitro. Conversely, overexpression of a catalytically inactive Hakai mutant (C109A) exhibited minimal to no effect, whereas Hakai depletion markedly reduced endogenous Runx2 levels and impaired osteogenic differentiation in both C3H10T1/2 and RCOs. Mechanistically, Hakai physically interacts with Runx2 and enhances its protein turnover by rescuing it from Smad ubiquitination regulatory factor 2 (Smurf2)-mediated proteasome degradation. Wild-type Hakai but not Hakai-C109A inhibited Smurf2 protein levels through proteasome-mediated degradation. These findings underscore Hakai's functional role in bone formation, primarily through its positive modulation of Runx2 protein turnover by protecting it from Smurf2-mediated ubiquitin-proteasomal degradation. Collectively, our results demonstrate Hakai as a promising novel therapeutic target for osteoporosis.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141734158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Clusterin enhances AKT2-mediated motility of normal and cancer prostate cells through a PTEN and PHLPP1 circuit 更正为Clusterin通过PTEN和PHLPP1回路增强AKT2介导的正常和癌前列腺细胞的运动能力

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-21 DOI: 10.1002/jcp.31377

引用次数: 0

Adapting STEMM in Hawaiʻi: Necessary actions for one of the most diverse places in the United States 调整夏威夷的 STEMM：为美国最多样化的地方之一采取必要行动。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-19 DOI: 10.1002/jcp.31336

Kit Neikirk

{"title":"Adapting STEMM in Hawaiʻi: Necessary actions for one of the most diverse places in the United States","authors":"Kit Neikirk","doi":"10.1002/jcp.31336","DOIUrl":"10.1002/jcp.31336","url":null,"abstract":"Hawaiʻi's diverse population prime it to be an exemplary environment to study representation in science, technology, engineering, mathematics, and medicine (STEMM). In actuality, Hawaiʻi has low STEMM enrollment and therefore, low representation in STEMM. What primarily inhibits Hawaiʻi from having a strong STEMM workforce is the lack of education in STEMM, resources allocated to STEMM, and mentorship to succeed in STEMM. Other factors such as cultural values, high costs of living, and geographical barriers also contribute to Hawaiʻi's low STEMM enrollment. To combat these issues, I offer suggestions to encourage STEMM enrollment, such as directing funds toward after-school education. I also suggest combatting the lack of resources by providing more online opportunities for students and workers. As for Hawaiʻi's low mentorship, I suggest that more programs be created within communities and universities to create a platform for mentors and mentees to network. This manuscript seeks to highlight these areas of improvement and recognize lessons to be learned from Hawaiʻi, thus serving as a resource for individuals internationally.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31336","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141731149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 "Postnatal growth retardation is associated with deteriorated intestinal mucosal barrier function using a porcine model". 更正 "利用猪模型研究产后生长迟缓与肠粘膜屏障功能退化的关系"。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-19 DOI: 10.1002/jcp.31386

引用次数: 0

RETRACTION. 回收。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-19 DOI: 10.1002/jcp.31357

{"title":"RETRACTION.","authors":"","doi":"10.1002/jcp.31357","DOIUrl":"https://doi.org/10.1002/jcp.31357","url":null,"abstract":"Retraction: S. Mukherjee, S. Manna, D. Pal, P. Mukherjee, C. K. Panda, Sequential loss of cell cycle checkpoint control contributes to malignant transformation of murine embryonic fibroblasts induced by 20-methylcholanthrene, Journal of Cellular Physiology 224, no. 1 (2010): 49-58, https://doi.org/10.1002/jcp.22089. The above article, published online on 23 April 2010 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between journal Editor in Chief, Alexander Hutchison; and Wiley Periodicals LLC. Concerns were raised by a third party regarding image manipulation and duplication in the above article. An investigation by the publisher has confirmed the following image-related concerns: duplication and splicing of western blots in Figure 3B(i); rotation, resizing, and duplication of cellular sections in Figure 4; duplication of cellular sections between Figure 4 and Figure 6 C; duplication of western blots in Figure 5B; duplication of western blots in Figure 6 A; and duplication of cellular sections in Figure 6 C. Because the evidence of image manipulation is extensive and impacts several figures, the journal has determined that the results are fundamentally compromised, and so the journal must retract the article. The authors disagree with the retraction.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141731155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Corrigendum to "PDGFB as a vascular normalization agent in an ovarian cancer model treated with a gamma-secretase inhibitor". 更正："PDGFB 作为一种血管正常化剂，用于接受伽马分泌酶抑制剂治疗的卵巢癌模型"。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-18 DOI: 10.1002/jcp.31354

引用次数: 0

Correction to: “O-GlcNAcylation promotes the migratory ability of hepatocellular carcinoma cells via regulating FOXA2 stability and transcriptional activity” 更正："O-GlcNAcylation通过调节FOXA2的稳定性和转录活性促进肝癌细胞的迁移能力"。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-07-18 DOI: 10.1002/jcp.31381

引用次数: 0