Journal of Cellular Physiology最新文献_第8页

Muscle PGC-1α Overexpression Drives Metabolite Secretion Boosting Subcutaneous Adipocyte Browning 肌肉 PGC-1α 过表达促进代谢物分泌，促进皮下脂肪细胞褐变

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-12-15 DOI: 10.1002/jcp.31480

Caterina Miro, Ciro Menale, Lucia Acampora, Annarita Nappi, Serena Sagliocchi, Federica Restolfer, Sepehr Torabinejad, Mariano Stornaiuolo, Monica Dentice, Annunziata Gaetana Cicatiello

{"title":"Muscle PGC-1α Overexpression Drives Metabolite Secretion Boosting Subcutaneous Adipocyte Browning","authors":"Caterina Miro, Ciro Menale, Lucia Acampora, Annarita Nappi, Serena Sagliocchi, Federica Restolfer, Sepehr Torabinejad, Mariano Stornaiuolo, Monica Dentice, Annunziata Gaetana Cicatiello","doi":"10.1002/jcp.31480","DOIUrl":"10.1002/jcp.31480","url":null,"abstract":"<p>Muscle and adipose tissue (AT) are in mutual interaction through the integration of endocrine and biochemical signals, thus regulating whole-body function and physiology. Besides a traditional view of endocrine relationships that imply the release of cytokines and growth factors, it is becoming increasingly clear that a metabolic network involving metabolites as signal molecules also exists between the two tissues. By elevating the number and functionality of mitochondria, a key role in muscle metabolism is played by the master regulator of mitochondrial biogenesis peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α), that induces a fiber type shift from glycolytic to oxidative myofibers. As a consequence, the upregulation of muscle respiratory rate might affect metabolite production and consumption. However, the underlying mechanisms have not yet been fully elucidated. Here, we used a muscle-specific PGC-1α overexpressing mouse model (MCK-PGC-1α) to analyze the metabolite secretion profile of serum and culture medium recovered from MCK-PGC-1α muscle fibers by NMR. We revealed modified levels of different metabolites that might be ascribed to the metabolic activation of the skeletal muscle fibers. Notably, the dysregulated levels of these metabolites affected adipocyte differentiation, as well as the browning process in vitro and in vivo. Interestingly such effect was exacerbated in the subcutaneous WAT, while only barely present in the visceral WAT. Our data confirm a prominent role of PGC-1α as a trigger of mitochondrial function in skeletal muscle and propose a novel function of this master regulator gene in modulating the metabolite production in turn affecting the activation of WAT and its conversion toward the browning.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828656","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

Regulation of the Cilia as a Potential Treatment for Senescence and Tumors: A Review 纤毛调控作为治疗衰老和肿瘤的潜在手段：综述。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-12-11 DOI: 10.1002/jcp.31499

Danping Zhu, Yuqin Pan, Yong Yang, Shukui Wang

{"title":"Regulation of the Cilia as a Potential Treatment for Senescence and Tumors: A Review","authors":"Danping Zhu, Yuqin Pan, Yong Yang, Shukui Wang","doi":"10.1002/jcp.31499","DOIUrl":"10.1002/jcp.31499","url":null,"abstract":"<div>\u0000 \u0000 <p>Millions of people worldwide die from malignant tumors every year, and the current clinical treatment is still based on radiotherapy and chemotherapy. Immunotherapy-adjuvant chemotherapy is widely applied, yet resistance to various factors persists in the management of advanced malignancies. Recently researchers have gradually discovered that the integrity of primary cilia is closely related to many diseases. The phenotypic changes in primary cilia are found in some cases of progeria, tumorigenesis, and drug resistance. Primary cilia seem to mediate signaling during these diseases. Hedgehog inhibitors have emerged in recent years to treat tumors by controlling signaling proteins on primary cilia. There is evidence for the use of anti-tumor drugs to treat senescence-related disease. Considering the close relationship between aging and obesity, as well as the obesity is the phenotype of many ciliopathies. Therefore, we speculate that some anti-tumor or anti-aging drugs can treat ciliopathies. Additionally, there is evidence suggesting that anti-aging drugs for tumor treatment, in which the process may be mediated by cilia. This review elucidates for the first time that cilia may be involved in the regulation of senescence, metabolic, tumorigenesis, and tumor resistance and hypothesizes that cilia can be regulated to treat these diseases in the future.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806804","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

DMT1 Maintains Iron Homeostasis to Regulate Mitochondrial Function in Porcine Oocytes DMT1维持铁稳态调节猪卵母细胞线粒体功能。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-12-05 DOI: 10.1002/jcp.31494

Jin-Xin Zhang, Meng-Fan Lan, Jian-Zhou Shang, Xin-Le Lai, Li-Shu Li, Tong-Tong Duan, Ru-Hai Xu, Kun-Lin Chen, Xing Duan

{"title":"DMT1 Maintains Iron Homeostasis to Regulate Mitochondrial Function in Porcine Oocytes","authors":"Jin-Xin Zhang, Meng-Fan Lan, Jian-Zhou Shang, Xin-Le Lai, Li-Shu Li, Tong-Tong Duan, Ru-Hai Xu, Kun-Lin Chen, Xing Duan","doi":"10.1002/jcp.31494","DOIUrl":"10.1002/jcp.31494","url":null,"abstract":"<div>\u0000 \u0000 <p>Iron plays critical roles in many cellular functions, including energy production, metabolism, and cell proliferation. However, the role of iron in maintaining oocyte quality remains unclear. In this study, DMT1 was identified as a key iron transporter during porcine oocyte maturation. The results demonstrated that iron deficiency in porcine oocyte led to aberrant meiotic progression, accompanied by increased gene expression of <i>DMT1</i>. Inhibition of DMT1 resulted in the failure of cumulus cell expansion and oocyte maturation, along by the abnormal actin and microtubule assembly. Furthermore, loss of DMT1 function caused disruption in mitochondrial function and dynamics, resulting in oxidative stress and Ca<sup>2+</sup> dyshomeostasis. Additionally, the absence of DMT1 function activated PINK1/Parkin-dependent mitophagy in porcine oocyte. These findings suggested that DMT1 played a crucial role in safeguarding oocyte quality by protecting against iron-deficiency-induced mitochondrial dysfunction and autophagy. This study provided compelling evidence that DMT1 and iron homeostasis were crucial for maintaining the capacity of porcine oocyte maturation. Moreover, the results hinted at the potential of DMT1 as a novel therapeutic target for treating iron deficiency-related female reproductive disorders.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785416","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

Tumor-Derived GDF15 Induces Tumor Associated Fibroblast Transformation From BMSCs and Fibroblasts in Oral Squamous Cell Carcinoma 肿瘤来源的GDF15诱导口腔鳞状细胞癌中骨髓间充质干细胞和成纤维细胞的肿瘤相关成纤维细胞转化。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-12-05 DOI: 10.1002/jcp.31498

Jingjing Zhao, Yahui Li, Yingying Huang, Peng Su, Fujiao Nie, Pishan Yang, Chengzhe Yang

{"title":"Tumor-Derived GDF15 Induces Tumor Associated Fibroblast Transformation From BMSCs and Fibroblasts in Oral Squamous Cell Carcinoma","authors":"Jingjing Zhao, Yahui Li, Yingying Huang, Peng Su, Fujiao Nie, Pishan Yang, Chengzhe Yang","doi":"10.1002/jcp.31498","DOIUrl":"10.1002/jcp.31498","url":null,"abstract":"<div>\u0000 \u0000 <p>Cancer associated fibroblasts (CAFs) are the predominant stromal cell-type in the solid tumor microenvironment, originating from various cell types and playing a crucial role in promoting tumor progression and metastasis The generation of CAFs is influenced by complex factors secreted by tumor cells, with particular emphasis on transforming growth factor-β (TGF-β). However, it remains largely unknown whether growth/differentiation factor-15 (GDF15), as a member of the TGF-β superfamily, exerts similar effects to TGF-β in oral squamous cell carcinoma (OSCC). In this study, we investigated the impact of GDF15 derived from tumor cells on CAF transformation and elucidated the underlying mechanisms. Exogenous GDF15 and OSCC cells induced the transformation of bone marrow mesenchymal stem cells (BMSCs) and human gingival fibroblasts (HGFs) into CAFs, as evidenced by α-smooth muscle actin (α-SMA) as a phenotypic marker and TGF-β, interleukin 6 (IL-6), and vascular endothelial-derived growth factor (VEGF) as functional markers. Conversely, knockdown of GDF15 in OSCC cells reversed CAF transformation. Mechanistically, extracellular signal-regulated kinases 1/2(ERK1/2) pathway was associated with GDF15-mediated promotion of CAF transformation. Furthermore, OSCC-induced CAFs enhanced migration and invasion abilities of OSCC cells; but this pro-cancer effect was abolished upon knockdown of GDF15 in OSCC cells. Subcutaneous coinjection of OSCC cells with BMSCs or HGFs into mice revealed the promoted tumor growth along with increased expression levels of α-SMA and Ki67 compared with alone OSCC cells injection; these effects were attenuated when GDF15 was knocked down in OSCC cells. Collectively, our findings suggest that tumor-derived GDF15 contributes to the progression of OSCC by promoting CAF transformation through activation of the ERK1/2 pathway.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785503","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

Maintenance of Cardiac Microenvironmental Homeostasis: A Joint Battle of Multiple Cells 心脏微环境稳态的维持：多细胞的联合战斗。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-12-04 DOI: 10.1002/jcp.31496

Jiayu Yao, Youtao Zhang, Ziwen Wang, Yuejun Chen, Xingjuan Shi

引用次数: 0

METTL3-Dependent YTHDF2 Mediates TSC1 Expression to Regulate Alveolar Epithelial Mesenchymal Transition and Promote Idiopathic Pulmonary Fibrosis 依赖 METTL3 的 YTHDF2 介导 TSC1 的表达，从而调节肺泡上皮间充质转化并促进特发性肺纤维化。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-11-28 DOI: 10.1002/jcp.31473

Min Liu, Yingying Sheng, Mengyu Li, Tianyu Pan, Wei Jiang, Yafei Zhang, Xin Pan, Cheng Huang, Jun Li, Yuanyuan Wang

{"title":"METTL3-Dependent YTHDF2 Mediates TSC1 Expression to Regulate Alveolar Epithelial Mesenchymal Transition and Promote Idiopathic Pulmonary Fibrosis","authors":"Min Liu, Yingying Sheng, Mengyu Li, Tianyu Pan, Wei Jiang, Yafei Zhang, Xin Pan, Cheng Huang, Jun Li, Yuanyuan Wang","doi":"10.1002/jcp.31473","DOIUrl":"10.1002/jcp.31473","url":null,"abstract":"<div>\u0000 \u0000 <p>Diffuse, progressive interstitial lung disease with few treatment options and low survival rates is known as idiopathic pulmonary fibrosis (IPF). Alveolar epithelial cell damage and dysfunction are the main features of IPF. TSC1 has been documented to exert a pivotal function in governing cellular growth, proliferation, and ontogenesis. This work investigated TSC1's function and mechanism in IPF. Mice were given BLM to cause pulmonary fibrosis, and A549 cells underwent epithelial mesenchymal transition (EMT) in response to TGF-β1. According to the data, TSC1 expression was reduced in IPF. Overexpression of TSC1 was established by adenopathy-associated virus in vivo and adenovirus in vitro to significantly block the EMT process. Besides, the findings from the RNA-sequencing analysis indicate that overexpression of TSC1 mitigated the EMT process by suppressing the activation of the AKT/mTOR pathway via downregulation of ACTN4 expression. To examine the upstream regulatory mechanism, we employed the SRAMP database to predict m<sup>6</sup>A modification of TSC1 mRNA, followed by verification of m<sup>6</sup>A modification levels and expression using MERIP-qPCR, Dot blot, RT-qPCR, and WB. The results indicated a high degree of m<sup>6</sup>A modification in TSC1 mRNA in pulmonary fibrosis. The expression of METTL3 was further found to be significantly elevated. METTL3 knockdown impeded EMT progression. METTL3 inhibits TSC1 expression by increasing TSC1 m<sup>6</sup>A modification through the reading protein YTHDF2. In conclusion, our study elucidated that the METTL3/YTHDF2/TSC1 signaling axis activates the AKT/mTOR pathway to promote the development of IPF. This study provides potential molecular-level therapeutic targets for IPF disease.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739532","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

Osteoclast Secretes Stage-Specific Key Molecules for Modulating Osteoclast–Osteoblast Communication 破骨细胞分泌特定阶段的关键分子，调节破骨细胞与成骨细胞之间的交流

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-11-28 DOI: 10.1002/jcp.31484

Yi-fei Fu, Shu-wen Shi, Jun-jie Wu, Zheng-dong Yuan, Lei-sheng Wang, Hao Nie, Zheng-yu Zhang, Xian Wu, Yue-chun Chen, Hui-bo Ti, Ke-yue Zhang, Dong Mao, Jun-xing Ye, Xia Li, Feng-lai Yuan

{"title":"Osteoclast Secretes Stage-Specific Key Molecules for Modulating Osteoclast–Osteoblast Communication","authors":"Yi-fei Fu, Shu-wen Shi, Jun-jie Wu, Zheng-dong Yuan, Lei-sheng Wang, Hao Nie, Zheng-yu Zhang, Xian Wu, Yue-chun Chen, Hui-bo Ti, Ke-yue Zhang, Dong Mao, Jun-xing Ye, Xia Li, Feng-lai Yuan","doi":"10.1002/jcp.31484","DOIUrl":"10.1002/jcp.31484","url":null,"abstract":"<div>\u0000 \u0000 <p>In most cases of bone metabolic disorders, such as osteoporosis and osteomalacia, these conditions are often attributed to dysfunctional osteoclasts, leading to their common characterization as “destructors.” In addition to the widely documented regulatory process where osteoblasts direct osteoclastic bone resorption, there is increasing evidence suggesting that osteoclasts also in turn influence osteoblastic bone formation through direct and indirect mechanisms. It is well-known that differentiation of osteoclasts involves several stages, each characterized by specific cellular features and functions. Stage-specific key molecules secreted during these stages play a critical role in mediating osteoclast–osteoblast communication. In this review, we described the different stages of osteoclast differentiation and reviewed stage-specific key molecules involved in osteoclasts-osteoblasts communication. We highlighted that a detailed understanding of these processes and molecular mechanism could facilitate the development of novel treatments for bone metabolic disorders.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739535","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

Spontaneously Immortalised Nonhuman Primate Müller Glia Cell Lines as Source to Explore Retinal Reprogramming Mechanisms for Cell Therapies 自发永生化的非人灵长类 Müller 神经胶质细胞系是探索细胞疗法视网膜重编程机制的来源。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-11-28 DOI: 10.1002/jcp.31482

Ahmed Salman, Arantxa Bolinches-Amorós, Tina Storm, Daniela Moralli, Paulina Bryika, Angela J. Russell, Stephen G. Davies, Alun R. Barnard, Robert E. MacLaren

{"title":"Spontaneously Immortalised Nonhuman Primate Müller Glia Cell Lines as Source to Explore Retinal Reprogramming Mechanisms for Cell Therapies","authors":"Ahmed Salman, Arantxa Bolinches-Amorós, Tina Storm, Daniela Moralli, Paulina Bryika, Angela J. Russell, Stephen G. Davies, Alun R. Barnard, Robert E. MacLaren","doi":"10.1002/jcp.31482","DOIUrl":"10.1002/jcp.31482","url":null,"abstract":"<p>Cell replacement therapies for ocular diseases characterised by photoreceptors degeneration are challenging due to poor primary cell survival in culture. A stable retinal cell source to replace lost photoreceptors holds promise. Müller glia cells play a pivotal role in retinal homoeostasis by providing metabolic and structural support to retinal neurons, preventing aberrant photoreceptors migration, and facilitating safe glutamate uptake. In fish and amphibians, injured retinas regenerate due to Müller-like glial stem cells, a phenomenon absent in the mammalian retina for unknown reasons. Research on Müller cells has been complex due to difficulties in obtaining pure cell population and their rapid de-differentiation in culture. While various Müller glia cell lines from human and rats are described, no nonhuman primate Müller glia cell line is currently available. Here, we report spontaneously immortalised Müller glia cell lines derived from macaque neural retinas that respond to growth factors and expand indefinitely in culture. They exhibit Müller cells morphology, such as an elongated shape and cytoplasmic projections, express Müller glia markers (VIMENTIN, GLUTAMINE SYNTHASE, glutamate-aspartate transporter, and CD44), and express stem cell markers such as PAX6 and SOX2. In the presence of factors that induce photoreceptor differentiation, these cells show a shift in gene expression patterns suggesting a state of de-differentiation, a phenomenon known in reprogrammed mammalian Müller cells. The concept of self-renewing retina might seem unfeasible, but not unprecedented. While vertebrate Müller glia have a regeneration potential absent in mammals, understanding the mechanisms behind reprogramming of Müller glia in mammals could unlock their potential for treating retinal degenerative diseases.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739550","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

CCL2-CCR2 Axis Inhibition in Osteosarcoma Cell Model: The Impact of Oxygen Level on Cell Phenotype 骨肉瘤细胞模型中的 CCL2-CCR2 轴抑制：氧含量对细胞表型的影响

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-11-25 DOI: 10.1002/jcp.31489

Agne Petrosiute, Justina Musvicaitė, Donatas Petroška, Alvilė Ščerbavičienė, Sascha Arnold, Jurgita Matulienė, Aurelija Žvirblienė, Daumantas Matulis, Asta Lučiūnaitė

{"title":"CCL2-CCR2 Axis Inhibition in Osteosarcoma Cell Model: The Impact of Oxygen Level on Cell Phenotype","authors":"Agne Petrosiute, Justina Musvicaitė, Donatas Petroška, Alvilė Ščerbavičienė, Sascha Arnold, Jurgita Matulienė, Aurelija Žvirblienė, Daumantas Matulis, Asta Lučiūnaitė","doi":"10.1002/jcp.31489","DOIUrl":"10.1002/jcp.31489","url":null,"abstract":"<p>Treatment of osteosarcoma is hampered by tumor hypoxia and requires alternative approaches. Although the CCL2-CCR2 axis is indispensable in tumor-induced inflammation and angiogenesis, its blockade has not been effective to date. This study aimed to characterize how CCR2 inhibition affects the crosstalk of osteosarcoma cells with immune cells to better delineate tumor resistance mechanisms that help withstand such treatment. In this study, 143B cells were exposed to healthy donor PBMC supernatants in a transwell assay lacking direct cell-to-cell contact and subjected to different oxygen concentrations. In addition, mice bearing orthotopic 143B tumors were subjected to CCR2 antagonist treatment. Our findings show that hypoxic conditions alter cytokine and cancer- related protein expression on cells and impair CCR2 antagonist effects in the experimental osteosarcoma model. CCL2-CCR2 axis blockade in the 143B xenografts, which are positive for hypoxia marker CAIX, did not slow 143B tumor growth or metastasis but altered tumor microenvironment by VEGFR downregulation and shift in the CD44-positive cell population towards high CD44 expression. This study highlights differential responses of tumor cells to CCR2 antagonists in the presence of different oxygen saturations and expands our knowledge of compensatory mechanisms leading to CCL2-CCR2 treatment resistance.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11747949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716296","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

Signaling Regulation of FAM134-Dependent ER-Phagy in Cells 细胞中 FAM134 依赖性 ER 吞噬的信号调控

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-11-25 DOI: 10.1002/jcp.31492

Alessandro Palma, Alessio Reggio

引用次数: 0