JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Intradiscal Delivery of Notoginsenoside R1-Loaded PLGA Nanoparticles Attenuates Intervertebral Disc Degeneration in Rats","authors":"Baichuan Zheng,&nbsp;Haotian Zhong,&nbsp;Zhengwei Wang,&nbsp;Junyu Qin,&nbsp;Ziying Xie,&nbsp;Rong Tang,&nbsp;Chengshang Hu,&nbsp;Xiuming Zhang,&nbsp;Jianwen Li,&nbsp;Songbo Li","doi":"10.1111/jcmm.71378","DOIUrl":"10.1111/jcmm.71378","url":null,"abstract":"<p>Intervertebral disc degeneration (IVDD) contributes to persistent low back pain, but existing treatments focus on symptom relief rather than addressing the degeneration. Notoginsenoside R1 (NR1), a bioactive saponin derived from Panax notoginseng, has exhibited protective effects in experimental models of disc injury. However, its clinical application is limited by poor bioavailability and rapid clearance. Here, NR1 was encapsulated into poly(lactic-co-glycolic acid) nanoparticles (NR1@PLGA) to improve local drug retention. NR1@PLGA showed uniform particle characteristics, prolonged NR1 release, and time-dependent uptake by nucleus pulposus cells (NPCs). Under H₂O₂-induced oxidative stress, NR1@PLGA reduced SA-β-gal-positive cells, preserved aggrecan and collagen II (Col-2) expression, and improved cell viability compared with free NR1 at the same concentration. In a rat caudal puncture model, intradiscal administration of NR1@PLGA preserved T2-weighted MRI signals, improved histological outcomes, increased aggrecan expression, and decreased MMP-13 levels. No obvious abnormalities were observed in major organs or serum biochemical indicators related to liver and kidney function during the 4-week observation period. These results demonstrate that NR1@PLGA is a potential treatment for IVDD, with PLGA encapsulation enhancing the efficacy of NR1.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71378","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the Dysregulated Pathways and Candidate Therapeutic Compounds for Primary Ovarian Cancer Using Whole Transcriptomics Data and Next Generation Knowledge Discovery Strategies","authors":"Peter Natesan Pushparaj,&nbsp;Kalamegam Gauthaman,&nbsp;Alaa G. Alahmadi,&nbsp;Reem Nabil Hassan,&nbsp;Hind A. Alkhatabi,&nbsp;Ammar AL-Farga","doi":"10.1111/jcmm.71356","DOIUrl":"10.1111/jcmm.71356","url":null,"abstract":"<p>Ovarian cancer (OC) is a type of gynaecological cancer with a higher mortality rate due to diagnosis at an advanced stage and limited treatment options. This study aimed to leverage transcriptomic data to identify cellular and molecular pathways and potential anti-cancer compounds that specifically target primary invasive epithelial ovarian cancer (EOC). By employing next-generation knowledge discovery (NGKD) methodologies, we sought to unravel the intricate molecular landscape of primary invasive EOC using RNA sequencing (RNA-seq) data and decipher potential therapeutics for this debilitating disease. We performed NGKD analysis of the Gene Expression Omnibus (GEO) dataset GSE1295399 obtained from whole RNA-seq experiments. Using the raw counts and filtered metadata from GEO, we identified 2123 differentially expressed genes (DEGs) based on a Log₂ fold change (≤ ±0.6) and a <i>p</i>-value cutoff of &lt; 0.05, between primary invasive EOC and benign EOC using the ExpressAnalyst platform. The DEGs were further analysed using both ExpressAnalyst and WebGestalt tools for differentially regulated cellular and molecular pathways and gene ontology (GOs), including biological process (GO-BP), molecular function (GO-MF) and cellular components (GO-CC). Both L1000 Fire Works Display (L1000FWD) and L1000 Characteristic Direction Signature Search Engine (L1000CDS2) tools were used to decipher synthetic or natural chemical compounds with the potential to reverse OC-associated gene signatures. DEGs implicated in key cellular and molecular pathways, such as oxidative phosphorylation, cell cycle, proteasome, programmed cell death protein-1 (PD-1) signalling, nuclear factor kappa B (NF-kB) signalling, cytokine and chemokine signalling, natural killer cell-mediated cytotoxicity and microRNAs in cancer, were positively enriched. The ribosome, translation, translational initiation and elongation and transforming growth factor-beta (TGF-β) signalling were negatively enriched in primary invasive EOC. Based on NGKD analysis, we identified approximately 50 synthetic or natural compounds, including naproxol, palbociclib, etoposide, wortmannin, PP-110, AZD-8055, amsacrine and BRD-K6595526. The results of this study could aid in the development of personalized treatment plans based on the unique profile of each tumour type, thus facilitating the development of personalized or precision treatment plans and improving diagnostic and prognostic capabilities in the clinic. In conclusion, the combination of RNA-seq and cutting-edge NGKD methodologies holds significant promise for identifying key cellular and molecular pathways and OC therapeutics.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vitro Effects of Anaesthetic Compounds on a Panel of Solid Tumour Cell Lines—An Exploratory Study","authors":"Olga Grajdieru,&nbsp;Alexandru Cristian Sabo,&nbsp;Adrian Bogdan Tigu,&nbsp;Andrei Ivancuta,&nbsp;Cristian Silviu Moldovan,&nbsp;Andrada Uhl,&nbsp;Miruna Cristina Ungurenasu,&nbsp;Andrada-Ioana Balmez,&nbsp;Ada Moisescu,&nbsp;Simina Pîrv,&nbsp;Madalina Nistor,&nbsp;Ximena-Maria Muresan,&nbsp;Diana Cenariu,&nbsp;Ciprian Tomuleasa,&nbsp;Catalin Constantinescu","doi":"10.1111/jcmm.71307","DOIUrl":"10.1111/jcmm.71307","url":null,"abstract":"<p>Anaesthetic agents are essential for surgical procedures, yet their potential role on tumour cell biology remains incompletely understood. Emerging evidence suggests that these compounds can act both as protumor and antitumor agents, influencing cellular processes such as proliferation, migration and cell death mechanisms. Eight commonly used anaesthetic compounds were tested on five tumour cell lines—A549Luc2, HCT116Luc2, HUH7, MDAMB231Luc2 and SKMEL28Luc2. Cytotoxicity was assessed by MTT assay, while morphological changes were analysed using confocal fluorescence microscopy. Functional assays were used for wound healing, colony formation, flow cytometry for cell death and cell cycle and gene expression profiling was assessed by RT-qPCR. Morphological evaluation revealed profound compound-specific alterations, including mitochondrial fragmentation, nuclear condensation, osmotic swelling and cell structure alterations. Lidocaine and ropivacaine induced stress fibre formation and swelling, while tunnelling nanotubes were observed as signs of cellular stress. The structural changes are correlated with impaired migration, reduced colony formation and necrosis-dominated cell death. Gene expression analysis showed heterogeneous changes of apoptotic and cell cycle regulators, with caspase upregulation and NF-kB activation in specific cases. Anaesthetic agents exert pleiotropic, cell-line-dependent effects, primarily inhibiting tumour growth and motility in our cell models through structural destabilization and stress signalling. These findings underscore the need for advanced models to clarify clinical relevance and to confirm the best choice of anaesthesia technique tailored to the patient's specific cancer type.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the KIFC1-SRSF3-PKM Axis Suppresses Cervical Cancer Glycolysis and Enhances Radiosensitivity","authors":"Junxia Liu,&nbsp;Jiahao Li,&nbsp;Haiting Zhou,&nbsp;Wentao Ha,&nbsp;Xinyu Wu,&nbsp;Xiangdong Liu,&nbsp;Yizhi Jiang,&nbsp;Chen Gong,&nbsp;Yi Cheng,&nbsp;Qingxu Liu,&nbsp;Tengfei Chao,&nbsp;Huihua Xiong","doi":"10.1111/jcmm.71373","DOIUrl":"10.1111/jcmm.71373","url":null,"abstract":"<p>Metabolic reprogramming towards enhanced glycolysis contributes to cervical cancer progression and radioresistance, but its upstream regulatory mechanisms remain poorly understood. Here, we investigated the role and underlying mechanisms of kinesin family member C1 (KIFC1) in glycolytic reprogramming and radiosensitivity in cervical cancer. KIFC1 expression and clinical relevance were analysed using public datasets and cervical cancer tissue microarrays. In vitro and in vivo assays were performed to evaluate the effects of KIFC1 on tumour growth, glycolysis and radiosensitivity. Transcriptomic and molecular interaction analyses were performed to define the KIFC1-SRSF3-PKM regulatory axis. KIFC1 was upregulated in cervical cancer tissues and associated with poor clinical outcomes. KIFC1 depletion inhibited tumour growth, reduced glycolytic activity and enhanced radiosensitivity both in vitro and in vivo. Mechanistically, KIFC1 may facilitate the nuclear localization of the splicing factor SRSF3, thereby influencing PKM alternative splicing. Loss of KIFC1 resulted in cytoplasmic retention of SRSF3 and a switch from the pro-glycolytic PKM2 isoform to PKM1, leading to impaired glycolysis. This splicing-mediated metabolic reprogramming was a key determinant of radiosensitization and could be partially reversed by pharmacological activation of PKM2. These findings identify the KIFC1-SRSF3-PKM axis as a novel splicing–metabolic checkpoint governing radiosensitivity in cervical cancer and highlight KIFC1 as a promising therapeutic target for improving radiotherapy efficacy in cervical cancer.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations","authors":"Sanyin Chen,&nbsp;Yi Yang,&nbsp;Xiaohua Pan,&nbsp;Yu Pan,&nbsp;Sa Cai","doi":"10.1111/jcmm.71357","DOIUrl":"10.1111/jcmm.71357","url":null,"abstract":"<p>Aging is a complex, pervasive biological process that causes irreversible declines in function across organ systems. The skin, the body's largest organ, interfaces directly with the external environment and undergoes aging driven by intrinsic (chronological) and extrinsic (environmental) factors, which result in functional deterioration and greater susceptibility to related disorders. Although numerous anti-aging strategies have been investigated, relatively few specifically target the skin. This review delineates the principal phenotypes and underlying mechanisms of skin aging. Phenotypic hallmarks include reduced regenerative capacity, chronic inflammation and impaired barrier function, whereas key mechanisms comprise oxidative stress, DNA damage, paracrine induction of cellular senescence and epigenetic alterations. The review evaluates recent research advances and associated clinical challenges in mitigating skin aging, with particular emphasis on pharmacological interventions and stem cell therapy. Finally, it briefly reviews delivery systems for natural anti-aging compounds and explores the potential of artificial intelligence (AI) to accelerate novel drug discovery.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prmt6 Deficiency Drives Osteoblast Senescence Promoting Age-Related Osteoporosis via Epigenetic Remodelling of the H3R2me2a/Sting/Ifitm3 Pathway","authors":"Yuxue Wang,&nbsp;Xiaoyong Ge,&nbsp;Shengjie Chang,&nbsp;Diankai Wang,&nbsp;Ke Xu,&nbsp;Haowei Xu,&nbsp;Xiaowei Liu,&nbsp;Shanjin Wang","doi":"10.1111/jcmm.71308","DOIUrl":"10.1111/jcmm.71308","url":null,"abstract":"<p>Protein arginine methyltransferase 6 (Prmt6), an epigenetic regulator, plays an unclear role in bone homeostasis and osteoblast senescence. In this study, we employed Western blot, qPCR, immunofluorescence, SA-β-Gal staining, and RNA-seq to systematically investigate the regulatory mechanism of the Prmt6/H3R2me2a/Sting/Ifitm3 axis in osteoblast senescence, and further validated the association of relevant molecules with osteoporosis at the animal level using immunohistochemistry and micro-CT. Our results showed that Prmt6 deficiency led to bone loss and induced osteoblast senescence in mice. Mechanistically, Prmt6 ablation was accompanied by reduced H3R2me2a modification and increased chromatin accessibility at the Sting promoter, suggesting that this histone mark may restrict local chromatin opening, thereby triggering sustained activation of the Sting pathway and marked upregulation of its classical downstream target gene Ifitm3. Functional experiments confirmed that inhibiting Sting or knocking down Ifitm3 effectively alleviated the senescent phenotype of osteoblasts. Consistently, in aged bone tissues, Prmt6 and H3R2me2a expression were decreased, while Sting and Ifitm3 levels were elevated. Collectively, this study reveals a previously unreported Prmt6/H3R2me2a/Sting/Ifitm3 signalling axis that maintains osteoblast homeostasis by constraining excessive activation of the Sting/Ifitm3 axis via epigenetic repressive modifications, offering a novel target for epigenetic intervention in osteoporosis.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71308","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artemotil Attenuates Fibrosis-Associated Chondrocyte Remodelling in Osteoarthritis in Association With STC1-Related TGF-β/SMAD2/3 Signalling","authors":"Guang Zhu,&nbsp;Yang Yang,&nbsp;Ye Ma,&nbsp;Gang Wu,&nbsp;Kuanmin Tian,&nbsp;Xiaoxin He,&nbsp;Rui Wang,&nbsp;Penggang Ma,&nbsp;Zhiqun Tang,&nbsp;Qunhua Jin","doi":"10.1111/jcmm.71374","DOIUrl":"10.1111/jcmm.71374","url":null,"abstract":"<p>Cartilage fibrosis contributes to extracellular matrix remodelling and structural deterioration during osteoarthritis (OA) progression; however, the molecular regulators involved in this process remain incompletely understood. Stanniocalcin-1 (STC1) has been implicated in tissue remodelling and fibrosis-associated signalling, but its role in chondrocyte fibrotic phenotype transition remains unclear. In this study, primary mouse chondrocytes stimulated with interleukin-1β (IL-1β), a destabilization of the medial meniscus (DMM) mouse model, and human OA cartilage samples were used to investigate the involvement of STC1 in OA-associated fibrotic remodelling. Quantitative proteomic profiling identified STC1 as a differentially regulated candidate associated with inflammatory and fibrotic responses. STC1 expression was elevated under OA-related conditions and was accompanied by increased SMAD2/3 phosphorylation. In SW1353 chondrosarcoma-derived chondrocytic cells, STC1 overexpression enhanced fibrosis-associated phenotypic changes, including increased COL1A1, ADAMTS5, and MMP-3 expression, reduced COL2A1 expression, and increased SMAD2/3 phosphorylation. Pharmacological modulation experiments further supported an association between STC1 and TGF-β/SMAD2/3 signalling activity. Artemotil attenuated fibrotic and catabolic responses in IL-1β-stimulated chondrocytes, reduced cartilage degeneration in DMM-induced OA, and was associated with reduced STC1 expression and reduced SMAD2/3 phosphorylation. Restoration of STC1 expression partially attenuated the effects of Artemotil on fibrosis-related markers and signalling alterations. These findings support a functional association between STC1, TGF-β-responsive SMAD2/3 signalling, and fibrosis-associated chondrocyte remodelling in OA and identify this signalling relationship as responsive to Artemotil intervention.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation","authors":"Qingqing He,&nbsp;Junlin Liu","doi":"10.1111/jcmm.71367","DOIUrl":"10.1111/jcmm.71367","url":null,"abstract":"<p>Psoriasis is a chronic inflammatory skin disorder driven by immune dysregulation and keratinocyte hyperproliferation. Calcitriol, the active form of vitamin D, shows therapeutic potential, but its molecular mechanisms remain incompletely understood. <i>CHI3L2</i> (chitinase-3-like protein 2) is a member of the chitinase-like protein family implicated in inflammatory and tissue-remodelling processes, yet its role in psoriasis has not been explored. Here, we investigated whether <i>CHI3L2</i> mediates the anti-psoriatic effects of calcitriol. Topical application of calcitriol alleviated imiquimod (IMQ)-induced psoriasiform lesions in both unilateral and bilateral mouse ear models, as evidenced by reduced clinical scores, epidermal thickening and pro-inflammatory cytokine expression (IL-1α, IL-6, IL-17A, IL-23A). In M5-stimulated HaCaT cells, calcitriol reversed aberrant proliferation, migration and inflammatory responses, and restored keratin expression (KRT1/KRT6). RNA-seq identified <i>CHI3L2</i> as the most significantly downregulated gene following calcitriol treatment. <i>CHI3L2</i> knockdown phenocopied the protective effects of calcitriol, suppressing cell proliferation, migration and inflammation. Mechanistically, calcitriol downregulated <i>CHI3L2</i> via inhibition of STAT3 phosphorylation at Tyr705. Collectively, these findings demonstrate that calcitriol ameliorates psoriatic inflammation and keratinocyte hyperproliferation through <i>CHI3L2</i> downregulation mediated by the STAT3 pathway, highlighting <i>CHI3L2</i> as a potential therapeutic target for psoriasis.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenotyping of Human Pulp Cells After Cryopreservation","authors":"Camila Maura Morais Lima dos Santos,&nbsp;Washington Henrique Themoteo da Silva,&nbsp;Fernanda Rodrigues Guedes,&nbsp;Milla Christian de Paula,&nbsp;Leslie Morse,&nbsp;Ricardo Battaglino,&nbsp;Marcelo José Barbosa Silva,&nbsp;Ana Paula Turrioni","doi":"10.1111/jcmm.71362","DOIUrl":"10.1111/jcmm.71362","url":null,"abstract":"<p>This study aimed to compare cell viability, morphology, cell yield, and stem cell-associated marker expression of cryopreserved human dental pulp cells (HDPCs) across different passages following thawing and serial in vitro expansion. HDPCs were isolated from three healthy donors, cryopreserved at −80°C for 3 months, and subsequently evaluated at different passages. Non-cryopreserved passage 0 (P0) cells were used as the baseline control. Cell viability was assessed using the MTT assay, cell morphology and complementary cell counting by scanning electron microscopy (SEM), and phenotypic marker expression (CD44, CD146, STRO-1, and CD45) by flow cytometry. P6 and P10 showed significantly higher cell viability than P0 and P12 (<i>p</i> &lt; 0.05), whereas SEM-based cell counting showed a higher number of cells at P6 than at P0, P3, and P12 (<i>p</i> &lt; 0.05). The percentage of CD146-positive cells decreased from 32.1% and 32.3% at P0 and P3, respectively, to 4.9% and 5.2% at P10 and P12 (<i>p</i> &lt; 0.05). A similar passage-dependent reduction was observed for STRO-1 expression. Overall, HDPCs exhibited passage-dependent changes following cryopreservation, thawing, and serial expansion. Intermediate passages, particularly P6, showed favourable cell viability and yield, whereas earlier passages better preserved progenitor-associated phenotypic markers. These findings highlight the importance of passage selection when cryopreserved HDPCs are expanded for subsequent experimental applications.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71362","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ABCG2 and ABCC2 Expression Levels and Their Relationship With Disease Severity in Acute Pancreatitis","authors":"Süleyman Baş,&nbsp;Esra Güzel Tanoğlu,&nbsp;Alpaslan Tanoğlu,&nbsp;Hafize Tuğba Karahan,&nbsp;Muhammed Said Gökçe,&nbsp;Murat Yeniçeri,&nbsp;Mustafa Can Şenoymak,&nbsp;Kadem Arslan","doi":"10.1111/jcmm.71368","DOIUrl":"10.1111/jcmm.71368","url":null,"abstract":"<p>The aim of this study was to evaluate the expression levels of <i>ABCG2</i> and <i>ABCC2</i>, members of the ATP-binding cassette (ABC) transporter gene family, in patients with acute pancreatitis and to investigate their potential associations with disease presence as well as clinical and radiological disease severity. This prospective study included 80 patients diagnosed with acute pancreatitis and 96 healthy controls. Disease severity in acute pancreatitis was assessed using the Ranson score and computed tomography (CT) findings. <i>ABCG2</i> and <i>ABCC2</i> gene expression levels were measured in peripheral blood samples using quantitative real-time polymerase chain reaction (qRT-PCR). Statistical analyses, including between-group comparisons and evaluations of associations between gene expression and disease severity, were performed using SPSS version 25.0. <i>ABCG2</i> gene expression levels were significantly lower in patients with acute pancreatitis than in healthy controls (<i>p</i> = 0.025). However, <i>ABCG2</i> expression was significantly higher in moderate and severe acute pancreatitis cases based on CT findings compared with mild cases (<i>p</i> = 0.038). <i>ABCC2</i> gene expression showed no significant association with either the presence of acute pancreatitis or disease severity. In ROC analysis, the area under the curve (AUC) for <i>ABCG2</i> gene expression was statistically significant (AUC = 0.598, <i>p</i> = 0.025). This study suggests that <i>ABCG2</i> gene expression may be associated with the presence of acute pancreatitis and radiological disease severity. <i>ABCG2</i> may represent a dynamically regulated candidate biomarker related to inflammatory and cellular stress processes in acute pancreatitis. Further studies including larger patient cohorts and preferably multicenter designs are needed to validate these findings.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 18","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71368","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}