Cells最新文献

{"title":"Peri-Implant Soft Tissue in Contact with Zirconium/Titanium Abutments from Histological and Biological Perspectives: A Concise Review.","authors":"Fatma A N Abouel Maaty, Mai A Ragab, Yasmin M El-Ghazawy, Fatma I Elfaiedi, Marwa M S Abbass, Israa Ahmed Radwan, Dina Rady, Sara El Moshy, Nahed Sedky Korany, Geraldine M Ahmed, Christof E Dörfer, Karim M Fawzy El-Sayed","doi":"10.3390/cells14020129","DOIUrl":"10.3390/cells14020129","url":null,"abstract":"<p><p>Dental implants are crucial in contemporary oral rehabilitation, necessitating optimal integration with the surrounding soft tissues for durable success. The attachment between the implant surface and peri-implant mucosa should establish a secure seal to prevent bacterial infiltration and subsequent tissue inflammation. This concise review examines the histological and biological perspectives of peri-implant soft tissue reactions to zirconium and titanium abutments, shedding light on their respective advantages and limitations. While titanium has been the gold standard, zirconia has gained attention due to its biocompatibility and aesthetic appeal. Histological studies show comparable soft tissue attachment and inflammatory responses between the two materials. Further research is needed to explore surface treatments and optimize outcomes in dental implant rehabilitation.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032315","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}

{"title":"Key Role of Phosphorylation in Small Heat Shock Protein Regulation via Oligomeric Disaggregation and Functional Activation.","authors":"Zachary B Sluzala, Angelina Hamati, Patrice E Fort","doi":"10.3390/cells14020127","DOIUrl":"10.3390/cells14020127","url":null,"abstract":"<p><p>Heat shock proteins (HSPs) are essential molecular chaperones that protect cells by aiding in protein folding and preventing aggregation under stress conditions. Small heat shock proteins (sHSPs), which include members from HSPB1 to HSPB10, are particularly important for cellular stress responses. These proteins share a conserved α-crystallin domain (ACD) critical for their chaperone function, with flexible N- and C-terminal extensions that facilitate oligomer formation. Phosphorylation, a key post-translational modification (PTM), plays a dynamic role in regulating sHSP structure, oligomeric state, stability, and chaperone function. Unlike other PTMs such as deamidation, oxidation, and glycation-which are often linked to protein destabilization-phosphorylation generally induces structural transitions that enhance sHSP activity. Specifically, phosphorylation promotes the disaggregation of sHSP oligomers into smaller, more active complexes, thereby increasing their efficiency. This disaggregation mechanism is crucial for protecting cells from stress-induced damage, including apoptosis, inflammation, and other forms of cellular dysfunction. This review explores the role of phosphorylation in modulating the function of sHSPs, particularly HSPB1, HSPB4, and HSPB5, and discusses how these modifications influence their protective functions in cellular stress responses.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032428","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}

{"title":"Interaction Between Malat1 and miR-499-5p Regulates Meis1 Expression and Function with a Net Impact on Cell Proliferation.","authors":"Salma A Fahim, Manon Ragheb, Ibrahim Hassan Fayed, Aya Osama, Ahmed Karam, Sameh Magdeldin, Rana Metwale, Mohamed Dief Allah Abdalmoneam Elsayed, Ahmed Abdellatif, Hesham A Sadek, Shereen Ahmed El Sobky, Nada El-Ekiaby, Injie Omar Fawzy, Ahmed Ihab Abdelaziz","doi":"10.3390/cells14020125","DOIUrl":"10.3390/cells14020125","url":null,"abstract":"<p><p>Meis1 is a transcription factor involved in numerous functions including development and proliferation and has been previously shown to harness cell cycle progression. In this study, we used in silico analysis to predict that miR-499-5p targets Meis1 and that Malat1 sponges miR-499-5p. For the first time, we demonstrated that the overexpression of miR-499-5p led to the downregulation of Meis1 mRNA and protein in C166 cells by directly binding to its 3'UTR. Moreover, knocking down Malat1 increased miR-499-5p expression, subsequently suppressing Meis1. Through BrdU incorporation assay, we showed that the knockdown of Malat1, Meis1, or mimicking with miR-499-5p promoted cell proliferation. Enrichment analyses on proteins identified via mass spectrometry after manipulating Malat1, miR-499-5p, or Meis1 revealed a multitude of differentially expressed proteins related to cell cycle, cell division, and key pathways like Wnt and mTOR, essential for cell proliferation. Collectively, our findings confirm that Malat1 sponges miR-499-5p, regulating Meis1, and that Malat1/miR-499-5p/Meis1 could potentially form an axis that has a pivotal influence on cellular proliferation.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032469","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}

{"title":"Gonadal Hormone Changes with Aging and Their Impact on Chronic Pain.","authors":"Onella Athnaiel, Nicholas Davidson, Jaskaran Mangat, Ned F Nasr, Nebojsa Nick Knezevic","doi":"10.3390/cells14020123","DOIUrl":"10.3390/cells14020123","url":null,"abstract":"<p><p>Chronic pain, pain that lasts beyond three months, is a common finding in the elderly. It is often due to musculoskeletal conditions but can be precipitated by other factors as well. While physiological systems decline with aging, chronic pain is influenced by changes in hormone profiles as men and women enter into andropause and menopause, respectively. Research on gonadal hormones is limited, especially when it comes to their relationship with chronic pain. Women tend to experience less pain with aging compared to their premenopausal years, and this is partially explained by the fact that estrogen enhances pain sensitivity and its decline during menopause decreases it. However, hormone replacement therapy (HRT) seems to increase pain tolerance post-menopause. There is some evidence that testosterone plays a protective factor in pain perception. Men on the other hand, have higher pain tolerance as testosterone is considered to be a protective factor. With aging and decreasing testosterone, older men tend to be less tolerant to pain. This paper explores how hormonal changes with aging impact pain perception in both men and women, highlighting several pain conditions influenced by hormones. Although research remains limited, the potential of HRT as a treatment for common pain conditions is examined.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032446","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}

{"title":"Age-Dependent Effects of Butyl Benzyl Phthalate Exposure on Lipid Metabolism and Hepatic Fibrosis in Mice.","authors":"Min-Seo Park, Seonhwa Hwang, Hyun-Bon Kang, Minjeong Ha, Juyeon Park, So-Youn Park, Yong-Joo Park, Min-Hi Park","doi":"10.3390/cells14020126","DOIUrl":"10.3390/cells14020126","url":null,"abstract":"<p><p>Endocrine-disrupting chemicals (EDCs), including phthalates, have been implicated in the development of non-alcoholic fatty liver disease (NAFLD) and hepatic fibrosis. This study investigates the age-dependent effects of butyl benzyl phthalate (BBP) exposure on lipid metabolism in the livers of young and aged mice. Young (2-month-old) and aged (20-month-old) male C57BL/6 mice were exposed to BBP through drinking water at a dose of 169 μg/kg/day for 6 and 4 months, respectively. Young mice exposed to BBP showed fatty liver, with downregulation of key fatty acid oxidation genes (CPT1A, CPT1B, CPT2, and Acox1) and elevated pro-inflammatory cytokines (TNF-α and IL-6). In contrast, aged mice exhibited hepatic fibrosis, with increased collagen deposition and upregulation of genes related to fibrosis (Acta2, MMP2, TGF-ß1, and Col1a2), cirrhosis (CXCR4, SOX9, DCN, and MFAP4), and cancer (Bcl2, CDKN2a, c-Myc, and Fn1). Overall, these findings emphasize the importance of age when evaluating the risks of EDC exposure, such as BBP. Future research should focus on understanding the molecular mechanisms behind these age-related differences and explore Grem1 and SOCS3 as potential therapeutic targets for treating EDC-induced and age-related liver diseases.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031893","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}

{"title":"Dysregulation of Metabolic Peptides Precedes Hyperinsulinemia and Inflammation Following Exposure to Rotenone in Rats.","authors":"Vandana Zaman, Denise Matzelle, Naren L Banik, Azizul Haque","doi":"10.3390/cells14020124","DOIUrl":"10.3390/cells14020124","url":null,"abstract":"<p><p>Rotenone, a naturally occurring compound derived from the roots of tropical plants, is used as a broad-spectrum insecticide, piscicide, and pesticide. It is a classical, high-affinity mitochondrial complex I inhibitor that causes not only oxidative stress, α-synuclein phosphorylation, DJ-1 (Parkinson's disease protein 7) modifications, and inhibition of the ubiquitin-proteasome system but it is also widely considered an environmental contributor to Parkinson's disease (PD). While prodromal symptoms, such as loss of smell, constipation, sleep disorder, anxiety/depression, and the loss of dopaminergic neurons in the substantia nigra of rotenone-treated animals, have been reported, alterations of metabolic hormones and hyperinsulinemia remain largely unknown and need to be investigated. Whether rotenone and its effect on metabolic peptides could be utilized as a biomarker for its toxic metabolic effects, which can cause long-term detrimental effects and ultimately lead to obesity, hyperinsulinemia, inflammation, and possibly gut-brain axis dysfunction, remains unclear. Here, we show that rotenone disrupts metabolic homeostasis, altering hormonal peptides and promoting infiltration of inflammatory T cells. Specifically, our results indicate a significant decrease in glucagon-like peptide-1 (GLP-1), C-peptide, and amylin. Interestingly, levels of several hormonal peptides related to hyperinsulinemia, such as insulin, leptin, pancreatic peptide (PP), peptide YY (PYY), and gastric inhibitory polypeptide (GIP), were significantly upregulated. Administration of rotenone to rats also increased body weight and activated macrophages and inflammatory T cells. These data strongly suggest that rotenone disrupts metabolic homeostasis, leading to obesity and hyperinsulinemia. The potential implications of these findings are vast, given that monitoring these markers in the blood could not only provide a crucial tool for assessing the extent of exposure and its relevance to obesity and inflammation but could also open new avenues for future research and potential therapeutic strategies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032364","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}

{"title":"Discovery of Evolutionary Loss of the Ubiquitin-like Autophagy-Related ATG12 System in a Lineage of Apicomplexa.","authors":"Xiaoxia X Lin, Yun D Bai, Sichang T Wang, Akira Nozawa, Tatsuya Sawasaki, Tatsunori Masatani, Kenji Hikosaka, Masahito Asada, Hirokazu Sakamoto","doi":"10.3390/cells14020121","DOIUrl":"10.3390/cells14020121","url":null,"abstract":"<p><p>The autophagy-related ubiquitin-like conjugation systems, the ATG8 and ATG12 systems, are universally conserved in eukaryotes. However, the covalent bond in the ATG12 system has recently been shown to be evolutionarily lost in Apicomplexa. Here, we show that all genes associated with the ATG12 system are absent in piroplasmida, a lineage within Apicomplexa. Comparative genomics of ATGs further shows that piroplasm ATG3 has lost the region necessary for ATG12 binding. However, our in vitro functional analysis using recombinant proteins demonstrated that ATG3 retained the ability to interact with ATG8 in <i>Babesia bovis</i>, a model species in piroplasmida. These findings provide evidence that the ATG8 system is functional, while the ATG12 system is completely lost in the common ancestor of piroplasmida and highlight the evolutionary flexibility of the ATG12 system in Apicomplexa.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11764061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032361","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}

{"title":"Effect of Kinases in Extracellular Vesicles from HIV-1-Infected Cells on Bystander Cells.","authors":"Gifty A Mensah, Anastasia Williams, Pooja Khatkar, Yuriy Kim, James Erickson, Alexandra Duverger, Heather Branscome, Kajal Patil, Hafsa Chaudhry, Yuntao Wu, Olaf Kutsch, Fatah Kashanchi","doi":"10.3390/cells14020119","DOIUrl":"10.3390/cells14020119","url":null,"abstract":"<p><p>As of 2023, there were 39.9 million people living with Human Immunodeficiency Virus type 1 (HIV-1). Although great strides have been made in treatment options for HIV-1, and our understanding of the HIV-1 life cycle has vastly improved since the start of this global health crisis, a functional cure remains elusive. One of the main barriers to a cure is latency, which allows the virus to persist despite combined antiretroviral therapy (cART). Recently, we have found that exosomes, which are small, membrane-enclosed particles released by virtually all cell types and known to mediate intercellular communication, caused an increase in RNA Polymerase II loading onto the HIV-1 promoter. This resulted in the production of both short- and long-length viral transcripts in infected cells under cART. This current study examines the effects of exosome-associated kinases on bystander cells. The phospho-kinase profiling of exosomes revealed differences in the kinase payload of exosomes derived from uninfected and HIV-1-infected cells, with CDK10, GSK3β, and MAPK8 having the largest concentration differences. These kinases were shown to be biologically active and capable of phosphorylating substrates, and they modulated changes in the cell cycle dynamics of exposed cells. Given the relevance of such effects for the immune response, our results implicate exosome-associated kinases as new possible key contributors to HIV-1 pathogenesis that affect bystander cells. These findings may guide new therapeutic avenues to improve the current antiretroviral treatment regimens.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032368","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}

{"title":"Advancing Neuroscience and Therapy: Insights into Genetic and Non-Genetic Neuromodulation Approaches.","authors":"Weijia Zhi, Ying Li, Lifeng Wang, Xiangjun Hu","doi":"10.3390/cells14020122","DOIUrl":"10.3390/cells14020122","url":null,"abstract":"<p><p>Neuromodulation stands as a cutting-edge approach in the fields of neuroscience and therapeutic intervention typically involving the regulation of neural activity through physical and chemical stimuli. The purpose of this review is to provide an overview and evaluation of different neuromodulation techniques, anticipating a clearer understanding of the future developmental trajectories and the challenges faced within the domain of neuromodulation that can be achieved. This review categorizes neuromodulation techniques into genetic neuromodulation methods (including optogenetics, chemogenetics, sonogenetics, and magnetogenetics) and non-genetic neuromodulation methods (including deep brain stimulation, transcranial magnetic stimulation, transcranial direct current stimulation, transcranial ultrasound stimulation, photobiomodulation therapy, infrared neuromodulation, electromagnetic stimulation, sensory stimulation therapy, and multi-physical-factor stimulation techniques). By systematically evaluating the principles, mechanisms, advantages, limitations, and efficacy in modulating neuronal activity and the potential applications in interventions of neurological disorders of these neuromodulation techniques, a comprehensive picture is gradually emerging regarding the advantages and challenges of neuromodulation techniques, their developmental trajectory, and their potential clinical applications. This review highlights significant advancements in applying these techniques to treat neurological and psychiatric disorders. Genetic methods, such as sonogenetics and magnetogenetics, have demonstrated high specificity and temporal precision in targeting neuronal populations, while non-genetic methods, such as transcranial magnetic stimulation and photobiomodulation therapy, offer noninvasive and versatile clinical intervention options. The transformative potential of these neuromodulation techniques in neuroscience research and clinical practice is underscored, emphasizing the need for integration and innovation in technologies, the optimization of delivery methods, the improvement of mediums, and the evaluation of toxicity to fully harness their therapeutic potential.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031959","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}

{"title":"Phosphodiesterase Type 5 Inhibitors in Male Reproduction: Molecular Mechanisms and Clinical Implications for Fertility Management.","authors":"Aris Kaltsas, Fotios Dimitriadis, Athanasios Zachariou, Nikolaos Sofikitis, Michael Chrisofos","doi":"10.3390/cells14020120","DOIUrl":"10.3390/cells14020120","url":null,"abstract":"<p><p>Phosphodiesterases, particularly the type 5 isoform (PDE5), have gained recognition as pivotal regulators of male reproductive physiology, exerting significant influence on testicular function, sperm maturation, and overall fertility potential. Over the past several decades, investigations have expanded beyond the original therapeutic intent of PDE5 inhibitors for erectile dysfunction, exploring their broader reproductive implications. This narrative review integrates current evidence from in vitro studies, animal models, and clinical research to clarify the roles of PDEs in effecting the male reproductive tract, with an emphasis on the mechanistic pathways underlying cyclic nucleotide signaling, the cellular specificity of PDE isoform expression, and the effects of PDE5 inhibitors on Leydig and Sertoli cell functions. Although certain findings suggest potential improvements in sperm motility, semen parameters, and a more favorable biochemical milieu for spermatogenesis, inconsistencies in study design, limited sample sizes, and inadequate long-term data temper definitive conclusions. Addressing these gaps through standardized protocols, larger and more diverse patient cohorts, and explorations of mechanistic biomarkers could pave the way for incorporating PDE5 inhibitors into evidence-based fertility treatment strategies. In the future, such targeted approaches may inform individualized regimens, optimize male reproductive outcomes, and refine the clinical application of PDE5 inhibitors as part of comprehensive male fertility management.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 2","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11763789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032319","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}