Cytotechnology最新文献

{"title":"IRP2 contributes to COPD-associated hypoxic epithelial injury through regulation of Sestrin2-related stress responses and ferroptosis.","authors":"Chunyan Xiong, Min Song, Tianshu He, Yao Ma, Jiang Wang","doi":"10.1007/s10616-026-01066-9","DOIUrl":"10.1007/s10616-026-01066-9","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) is characterized by persistent oxidative stress and airway epithelial injury. However, the molecular mechanisms linking iron metabolism and cellular stress responses in COPD remain unclear. This study aimed to investigate the role of iron regulatory protein 2 (IRP2) in COPD-associated epithelial injury. 16HBE and A549 cells were exposed to cigarette smoke extract (CSE) under a COPD-associated hypoxic microenvironment. IRP2 was silenced using shRNA, and Sestrin2 restoration experiments were performed. Cellular injury was evaluated by cell viability, ROS production, inflammatory cytokines, intracellular Fe²⁺ accumulation, ferroptosis-related proteins, and NRF2 activation. CSE exposure under a COPD-associated hypoxic microenvironment induced epithelial injury, accompanied by increased oxidative stress, inflammation, iron accumulation, and ferroptosis-related changes. IRP2 silencing alleviated these alterations and enhanced NRF2 nuclear activation with increased expression of antioxidant proteins. Restoration of Sestrin2 partially reversed the protective effects induced by IRP2 depletion. Furthermore, pharmacological inhibition of ferroptosis attenuated epithelial injury. IRP2 contributes to COPD-associated epithelial injury by regulating oxidative stress, iron homeostasis, and ferroptosis-related responses, providing new insights into the molecular mechanisms underlying COPD progression.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01066-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"214"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ITGB2 promotes HIF-1α/GLUT1 mediated glucose metabolic reprogramming in renal tubular epithelial cells to aggravate the progression of diabetic kidney disease.","authors":"Jun Peng, Qiaomeng Yuan, Lu Zhou, Wenqi Zhao, Mingrui Zhao","doi":"10.1007/s10616-026-01076-7","DOIUrl":"https://doi.org/10.1007/s10616-026-01076-7","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is characterized by tubular metabolic remodeling, inflammation, and profibrotic injury. However, whether integrin β2 (ITGB2) links high-glucose (HG) stress to hypoxia-inducible factor-1α (HIF-1α)/glucose transporter 1 (GLUT1)-dependent metabolic reprogramming in renal tubular epithelial cells remains unclear. This study investigated the role and underlying mechanism of the ITGB2/HIF-1α/GLUT1 axis in HG-induced tubular injury. ITGB2 expression was first examined in the publicly available human renal transcriptomic dataset GSE30529. HK-2 cells were cultured under normal-glucose, HG, or mannitol osmotic-control conditions. ITGB2 was silenced or overexpressed, and HIF1A or SLC2A1/GLUT1 was knocked down by siRNA. Protein expression, HIF-1α nuclear accumulation, and HIF-1α protein stability were assessed by western blotting, subcellular fractionation, and cycloheximide-chase assays. Metabolic remodeling was evaluated by 2-NBDG uptake, lactate production, extracellular acidification rate (ECAR), oxygen consumption rate (OCR), and ATP content. Tubular injury, inflammatory, and EMT-like/profibrotic phenotypes were assessed by ELISA and RT-qPCR. Dual-luciferase reporter and chromatin immunoprecipitation assays were performed to evaluate HIF-1α-mediated transcriptional regulation of GLUT1. ITGB2 expression was increased in the tubulointerstitial compartment of human diabetic kidneys in GSE30529. In HK-2 cells, HG increased ITGB2, HIF-1α, and GLUT1 expression, accompanied by increased glucose uptake, lactate production, ECAR, and ATP content and reduced OCR, together with enhanced tubular injury, inflammatory, and EMT-like/profibrotic responses. ITGB2 knockdown reduced HIF-1α/GLUT1 expression and nuclear HIF-1α accumulation and accelerated HIF-1α protein decay, suggesting that ITGB2 contributes to HIF-1α protein stability. HIF-1α directly bound to and transcriptionally activated the GLUT1 promoter. ITGB2 overexpression further enhanced metabolic reprogramming and pathological phenotypes, whereas HIF1A or SLC2A1 silencing markedly attenuated these effects. ITGB2 promotes HIF-1α/GLUT1-dependent metabolic reprogramming and contributes to tubular injury, inflammatory, and EMT-like/profibrotic responses in HG-treated HK-2 cells. These findings support a role for the ITGB2/HIF-1α/GLUT1 signaling axis in coordinating metabolic and pathological responses under HG conditions.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01076-7.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"204"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of electrical stimulation on the cardiogenic differentiation of mesenchymal stem cells: A systematic review.","authors":"Alejandra Sandoval Villarreal, Paola Neuta-Arciniegas, John Jairo Cabrera-López, Álvaro José Rojas Arciniegas","doi":"10.1007/s10616-026-01065-w","DOIUrl":"10.1007/s10616-026-01065-w","url":null,"abstract":"<p><p>Electrical stimulation has emerged as a promising strategy for promoting cardiogenic differentiation of mesenchymal stem cells; however, the available evidence remains highly heterogeneous across stimulation parameters, experimental platforms, and outcome measures. This systematic review synthesized the available in vitro evidence regarding the effects of electrical stimulation on MSC cardiogenic differentiation, with particular emphasis on stimulation parameters, experimental platforms and biological outcomes related to early cardiogenic commitment and structural maturation. A systematic search was conducted in seven electronic databases in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. Fifteen preclinical in vitro studies met the eligibility criteria. Human-derived MSCs were the most frequently investigated cell source and carbon-based electrodes were the most commonly reported conductive material. Across the included studies, electrical stimulation was frequently associated with morphological changes and increased expression of markers related to early cardiogenic commitment and structural maturation, although findings were inconsistent for some outcomes. A stimulation frequency of 1 Hz, pulse widths of 5 ms, and stimulation periods of approximately two weeks were the most frequently employed conditions. Nevertheless, substantial heterogeneity in stimulation parameters, experimental platforms and outcome measures precluded direct comparisons among studies and prevented identification of an optimal stimulation protocol. Overall, the available evidence suggests that electrical stimulation may represent a promising strategy for promoting the cardiogenic differentiation of mesenchymal stem cells in vitro; however, greater methodological standardization, standardized outcome assessment and functional characterization are required before definitive conclusions regarding its effectiveness and optimal stimulation protocols can be established.</p><p><strong>Graphical abstract: </strong></p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01065-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"215"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kisspeptin-10 alleviates OGD/R-induced H9c2 cardiomyocyte injury by triggering autophagy via regulating the YY1/TFEB axis.","authors":"Qintong Li, Huayu Liu, Yinying He, Yong Xie, Jingting Mai, Tucheng Huang, Fuwen Huang","doi":"10.1007/s10616-026-01089-2","DOIUrl":"https://doi.org/10.1007/s10616-026-01089-2","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion injury (MIRI) is characterized by exacerbated myocardial damage following the restoration of blood flow after myocardial ischemia, owing to factors such as increased production of reactive oxygen species, calcium overload, and inflammatory responses. Induction of cellular autophagy has been reported to alleviate MIRI. Kisspeptin-10 (Kp-10) is a short peptide produced by hydrolysis of the precursor protein encoded by the KISS1 gene and has shown promising autophagy-inducing properties. Here, the effects of Kp-10 on OGD/R-induced injury were investigated in H9c2 cardiomyocytes using an in vitro model relevant to MIRI. H9c2 cardiomyocytes were treated with OGD/R, followed by incubation with 50 or 100 nM Kp-10. Markedly reduced cell viability, an increased apoptotic rate and MDA levels, and diminished SOD and CAT activities were observed in OGD/R-stimulated H9c2 cardiomyocytes. These changes were accompanied by downregulated LC3-II/I, ATG5, and Beclin1, decreased nuclear levels of YY1 and TFEB, and reduced transcriptional activities of YY1 and TFEB, all of which were remarkably reversed by Kp-10. Moreover, the effects of Kp-10 on cell viability, oxidative stress, and the expression of autophagy-related proteins were substantially abolished by silencing YY1 or TFEB. Collectively, Kp-10 attenuated OGD/R-induced H9c2 cardiomyocyte injury in vitro, possibly by enhancing autophagy through the YY1/TFEB axis. These findings provide a cellular basis for further investigation of Kp-10 in MIRI, although validation in animal models is required before its clinical relevance can be assessed.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01089-2.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"212"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The neuroprotective mechanism of baicalein related to mitophagy mediated by MAPK1/RSK1 in a murine model of Parkinson's disease.","authors":"Hanzi Zhao, Tao Xu, Sheng Gao, Zhiyao Huang, Chengyou Cai, Xiaoli Hou, Hong Cheng","doi":"10.1007/s10616-026-01081-w","DOIUrl":"https://doi.org/10.1007/s10616-026-01081-w","url":null,"abstract":"<p><p>This study aims to investigate the neuroprotective effects and underlying molecular mechanisms of baicalein (Bai) in a mouse model of Parkinson's disease (PD) induced by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Using an MPTP-induced PD mouse model, the effects of Bai intraperitoneal injection on motor function and dopaminergic neuronal injury were assessed. Adeno-associated virus serotype 9 (AAV9)-mediated mitogen-activated protein kinase 1 overexpression (oe-MAPK1) was employed for gain-of-function experiments. Western blot technique was adopted to measure the levels of MAPK1, ribosomal protein S6 kinase 1 (RSK1), phosphorylated RSK1, PTEN-induced putative kinase 1 (PINK1), Parkin, microtubule-associated protein 1 light chain 3 (LC3)-II/I, and p62. Additionally, mitochondrial membrane potential and mitochondrial ultrastructure were observed to assess mitochondrial function. The binding between Bai and MAPK1 was examined using molecular docking and cellular thermal shift assay. Bai intraperitoneal injection markedly alleviated motor deficits, mitigated dopaminergic neuronal loss, raised mitochondrial membrane potential, and reduced ultrastructural mitochondrial damage post MPTP-induced PD in mice. Meanwhile, Bai upregulated PINK1, Parkin, and the LC3-II/I ratio while downregulating p62, indicating enhanced mitophagy. With a binding energy of -7.8 kcal/mol, Bai could directly bind to MAPK1, which destabilized MAPK1 thermostability and suppressed MAPK1 expression as well as subsequent RSK1 phosphorylation. Notably, MAPK1 overexpression repressed mitophagy, aggravated motor dysfunction and neuronal damage, and partially abrogated the neuroprotective efficacy of Bai. Bai binds directly to MAPK1, suppresses the MAPK1/RSK1 signaling cascade, triggers mitophagy, and ultimately ameliorates motor impairment and neuronal degeneration, conferring neuroprotection against PD in mice.</p><p><strong>Graphical abstract: </strong>Baicalein inhibits the MAPK1 and p-RSK1 signaling pathway in a Parkinson's disease mouse model treated with MPTP. This inhibition activates mitophagy, increases levels of PINK1, Parkin, and the LC3-II/I ratio, while decreasing p62.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"208"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Achyranthoside D attenuates chondrocyte pyroptosis and inflammation in osteoarthritis via NLRP3.","authors":"Haiyan Zhou, Shengyong Wang, Junshan Lu, Jing Gao, Shuai Tao","doi":"10.1007/s10616-026-01077-6","DOIUrl":"https://doi.org/10.1007/s10616-026-01077-6","url":null,"abstract":"<p><p>Osteoarthritis (OA) is an age-associated chronic degenerative joint disorder characterized by inflammation and cartilage degeneration. The NLRP3 inflammasome has been implicated in various inflammatory and age-related diseases. Achyranthes bidentata Blume (A. bidentata) is an herbal medicine commonly used for OA treatment. Achyranthoside D (AD) is a glucuronide saponin isolated from Achyranthes bidentata. However, the regulatory mechanism of AD in OA requires further elucidation. This study aimed to verify the therapeutic effect of AD on OA and identify the underlying mechanism for retarding OA progression. Anterior cruciate ligament transection (ACLT) was performed to construct an OA model. Chondrocytes induced with 5 µg/mL LPS were used for the in vitro study. Histomorphological differences were assessed using Safranin O-fast green staining. Cell viability/pyroptosis and inflammatory factor levels were analyzed using the MTT assay, flow cytometry, and ELISA. Western blotting was used to detect NLRP3-related inflammation and pyroptosis markers in chondrocytes or rat cartilage tissues. AD protected against cartilage destruction, chondrocyte pyroptosis, and inflammation in OA rats. Moreover, LPS-induced NLRP3-related inflammation and pyroptosis markers in chondrocytes were blocked by an NLRP3 inhibitor (MCC950) or AD in a dose-dependent manner. MCC950 or AD also attenuated the inflammatory response and increased cell viability in LPS-induced chondrocytes. AD attenuated OA by decreasing cartilage degradation and suppressing the inflammatory response and chondrocyte pyroptosis through inhibition of NLRP3 inflammasome activation, which may represent a promising therapeutic option for OA.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01077-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"205"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-cancer effect of vitexin onto the CFPAC-1 and MIAPaCa-2 pancreatic cancer cells.","authors":"Kevser Yaşar, Ahmet Ata Özçimen, Hatice Oruç Demirbağ","doi":"10.1007/s10616-026-01079-4","DOIUrl":"https://doi.org/10.1007/s10616-026-01079-4","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is an important type of cancer due to its rapid spread, late diagnosis and limited treatment options. Anti-tumoral properties of vitexin, a natural flavonoid found in the green parts of plants, have taken their place in in-vitro cancer studies. In this study, the effect of vitexin on the potential of cytotoxic, apoptotic, migratory and metastatic states in CFPAC-1 and MIAPaCa-2 cells was studied. MTT test was used to determine the proliferative effect and IC₅₀ dose. Metastatic Zeb-1, apoptotic caspase-3, -8, and - 9 gene expression analysis was performed by Real Time PCR techniques to investigate anti-migratory/metastatic and apoptotic effects. A wound-healing experiment was performed to observe anti-migratory/metastatic effects. As a result of the MTT experiment, the proliferative effect was measured as IC₅₀ concentration. The IC₅₀ concentration of CFPAC-1 cells was found to be 312 µM. The IC₅₀ concentration of MIAPaCa - 2 cells was approximately found to be 500 µM. As a result of apoptotic experiments, the high expression of caspase-3 and - 9 genes was observed in vitexin-treated MiaPaCa-2 cells. To result of the migration assay, a low rate of closure and complete closure were observed in CFPAC-1 and MIAPaCa-2 cells, respectively. On the other hand, the decreased expression of the Zeb-1 gene was observed in CFPAC-1 cells.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"207"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105447","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Androgen-mediated DKK1 upregulation in bronchial epithelial cells suppresses Th2 response and ameliorates asthma.","authors":"Yongsheng Shang, Qing Ren, Bin Wu, Danhong Li, Jieru Xu, Yu Wang, Mengjie Wang, Tingting Pan, Lihong Li, Hangjiong Qu","doi":"10.1007/s10616-026-01067-8","DOIUrl":"10.1007/s10616-026-01067-8","url":null,"abstract":"<p><p>Asthma is a chronic airway disease where androgens play a regulatory role. Dickkopf-1 (DKK1), a secreted glycoprotein, is positively correlated with androgens. This study aims to explore whether androgens upregulate DKK1 to inhibit Th2 response, potentially alleviating asthma. First, an asthma model was established using immunodeficient male mice. These mice were then divided into five groups and administered dihydrotestosterone (DHT) and/or the DKK-1 inhibitor WAY-262,611. Airway inflammation and lung tissue damage were assessed in each group. Furthermore, bronchoalveolar lavage fluid (BALF) inflammatory markers, the helper T cell 1/helper T cell 2 (Th1/Th2) ratio, and relevant parameters in serum and lung tissue were evaluated. Next, we established an asthma cell model using airway epithelial cells (BECs) and dust mites (HDM) stimulation. After treating with negative control (si-NC) and DKK1-targeted small interfering RNA (si-DKK1), five cell groups were established, with DHT treatment included. We assessed DHT's impact on DKK1 expression in BECs, then co-cultured these five cell groups with CD4⁺ T cells to verify links to Th1/Th2-related factors. Firstly, the in vivo experiments showed that DHT attenuated asthma-induced lung damage and inflammation, reduced Th2's proportion, and normalized Th1/Th2 balance. Co-treatment with WAY-262,611 reversed DHT's protection impact. Subsequently, in vitro cell experiments confirmed that DHT suppressed Th2 response; siRNA-mediated DKK1 knockdown abrogated this suppression. Androgens promote the expression of DKK1 in BECs, thereby inhibiting Th2 response and ultimately improving asthma.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01067-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"209"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149135133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: HOXD9 affecting glioma proliferation and invasion.","authors":"Zixuan Jing, Chenglong Li, Zefu Li","doi":"10.1007/s10616-026-01083-8","DOIUrl":"https://doi.org/10.1007/s10616-026-01083-8","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-026-00964-2.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"210"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650228/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GJA1-mediated mitochondrial transfer from adipose-derived stem cells underpins the enhanced therapeutic efficacy of tetramethylpyrazine on wound healing.","authors":"Jinghe Zhou, Jinsheng Li, Huifang Xu","doi":"10.1007/s10616-026-01078-5","DOIUrl":"https://doi.org/10.1007/s10616-026-01078-5","url":null,"abstract":"<p><p>Tetramethylpyrazine (TMP), a natural active compound with known wound-healing and pro-angiogenic properties, was investigated in this study to elucidate the molecular mechanisms underlying its synergistic effects with adipose-derived stem cells (ADSCs) in skin injury repair, focusing on mitochondrial transfer. A full-thickness skin wound model in rats was established to assess therapeutic outcomes. Histological evaluation using hematoxylin-eosin and Masson staining revealed that TMP augmented the beneficial effects of ADSCs, improving skin thickness and collagen deposition in wound tissues. Transmission electron microscopy and immunofluorescence analysis demonstrated that the combined treatment restored mitochondrial ultrastructure within the wound microenvironment and enhanced mitochondrial content in endothelial cells. To further explore the underlying mechanisms, an in vitro inflammatory human umbilical vein endothelial cell (HUVEC) model was established and co-cultured with ADSCs in the presence of TMP. The results indicated that TMP treatment increased mitochondrial homeostasis and mitochondrial transfer from ADSCs to HUVECs, while enhancing expression of angiogenic factors and reducing inflammatory cytokines levels. To determine the role of connexin 43 (GJA1) in this process, lentiviral-mediated shRNA knockdown was performed in ADSCs. GJA1 deficiency abolished the pro-angiogenic effects of TMP and impaired mitochondrial transfer to HUVECs, confirming the critical role of GJA1 in mediating these processes. Collectively, these findings demonstrate that TMP enhances the therapeutic efficacy of ADSCs in wound healing by facilitating GJA1-dependent mitochondrial transfer, thereby improving endothelial cell function and promoting angiogenesis.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at https://doi.org/10.1007/s10616-026-01078-5.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 6","pages":"206"},"PeriodicalIF":2.2,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149105436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}