Tissue & cell最新文献

{"title":"Spermatogenesis and ultrastructure of the spermatozoa at three ploidy levels in the bivalve species, Corbicula fluminea","authors":"Jie Pi ,&nbsp;Yangxin Tang ,&nbsp;Ying Fu ,&nbsp;Xu Wang ,&nbsp;Linwei Liu ,&nbsp;Xinhua Liu ,&nbsp;Jianguo Xiang ,&nbsp;Deliang Li","doi":"10.1016/j.tice.2025.102797","DOIUrl":"10.1016/j.tice.2025.102797","url":null,"abstract":"<div><div>A histological and ultrastructural examination of spermatogenesis and spermatozoa in diploid, triploid and tetraploid <em>Corbicula fluminea</em> was conducted. In the Yangtze River estuary, the spermatozoa of <em>C. flumiena</em> exhibited a primitive uniflagellate structure, whereas a modified biflagellate morphology was observed in inland freshwater habitats. This study presents the initial observation of sperm morula in spermatogenesis in <em>C. fluminea</em>. The mature spermatozoa were released as single cells and as spermatozeugmata. It was observed that uniflagellate spermatozoa undergo two meiotic divisions during it formation, whereas biflagellate spermatozoa undergo only one. The uniflagellate and biflagellate spermatozoa were observed to comprise of three distinct parts: the head, middle piece and tail. The longest and shortest spermatozoa (69.24 μm ± 1.70 <em>vs</em> 54.11 μm ± 1.26) were both biflagellate spermatozoa, originating from tetraploid and diploid individuals, respectively. The number of mitochondria was observed to increase in accordance with ploidy. In the uniflagellate spermatozoa, the two centrioles were observed to be oriented perpendicular to each other. In contrast, the two centrioles were oriented in parallel with each other in biflagellate spermatozoa, with each centriole attaching a flagellum. The undulating membrane of the tail contains a substantial number of glycogen granules. The differences in spermiogenesis, sperm morphology and structure between <em>C. flumiena</em> from estuarine (amphogenesis and in vitro development) and inland freshwater habitats (androgenesis and brooding larvae in the inner demibranch) result in better adaptations to the respective reproduction modes.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102797"},"PeriodicalIF":2.7,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin reduced vandetanib induced myocardial injury by regulating redox balance and NLRP3 inflammasome pathway","authors":"Fen Wang ,&nbsp;Jianwei Li ,&nbsp;Zhixuan Zhang ,&nbsp;Guangyi Huang ,&nbsp;Xiaodong Zhang ,&nbsp;Qian Liu ,&nbsp;Wang Xiao ,&nbsp;Fengqi Liu ,&nbsp;Jialong Sun ,&nbsp;Yankui Liu ,&nbsp;Yiyi Ma ,&nbsp;Ruijuan Zhuang ,&nbsp;Yingqiang Du ,&nbsp;Xiaoyan Wang ,&nbsp;Changzheng Gao ,&nbsp;Xin Gu","doi":"10.1016/j.tice.2025.102795","DOIUrl":"10.1016/j.tice.2025.102795","url":null,"abstract":"<div><div>Baicalin has garnered attention for its potential therapeutic effects on various cardiovascular conditions, including drug-induced cardiac injury. In this study, we utilized a murine model to explore the protective role of baicalin against cardiac dysfunction induced by vandetanib. Our findings indicate that baicalin administration effectively ameliorated vandetanib-induced cardiac injury. Echocardiographic assessments revealed significant improvements in the myocardial contraction in mice treated with baicalin compared with those receiving vandetanib alone. Histological analysis revealed reduced myocardial inflammation and fibrosis in baicalin-treated mice. Specifically, baicalin suppressed proinflammatory factors such as IL-6, IL-1β, and TNF-α, thereby attenuating the inflammatory response triggered by vandetanib. Moreover, baicalin inhibited myocardial apoptosis, as evidenced by decreased levels of Caspase-3, Bax, and p53, while concurrently elevated expression of the antiapoptotic protein Bcl-2. Mechanistically, baicalin-mediated inhibition of the NLRP3 inflammasome pathway has emerged as a crucial aspect of its cardioprotective action and promotes redox balance in myocardial cells under vandetanib-induced oxidative stress. It upregulated the expression of the antioxidant enzymes SOD1 and SOD2, thereby mitigating intracellular ROS accumulation and preserving cardiomyocyte viability. In conclusion, our study highlights baicalin as a promising therapeutic agent for mitigating vandetanib-induced cardiac injury through multiple mechanisms, including anti-inflammatory, antiapoptotic, antioxidant, and NLRP3 inflammasome inhibitory actions. Our findings will be further validated in clinical trials and explore the translational potential of baicalin in treating drug-induced cardiotoxicity in humans.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102795"},"PeriodicalIF":2.7,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dihydroartemisinin attenuates acetic acid-induced ulcerative colitis in rats: Suppression of inflammation and modulation of NFκβ/TNF-α/RIPK1-mediated necroptosis and apoptosis","authors":"Mamdouh Eldesoqui ,&nbsp;Lashin S. Ali ,&nbsp;Omnia S. Erfan ,&nbsp;Amal F. Dawood ,&nbsp;Abdelnaser A. Badawy ,&nbsp;Sahar K. Ali ,&nbsp;Zeinab A. Mohammed ,&nbsp;Alia Mohamed Mahmoud ,&nbsp;Eman M. Embaby ,&nbsp;Eman Mohamad El Nashar ,&nbsp;Majed Aldehri ,&nbsp;Hind Zafrah ,&nbsp;Norah Saeed Al-Zahrani ,&nbsp;Rania Hassan Mohamed Soliman","doi":"10.1016/j.tice.2025.102791","DOIUrl":"10.1016/j.tice.2025.102791","url":null,"abstract":"<div><h3>Background</h3><div>Ulcerative colitis (UC) is an inflammatory bowel disease characterized by the overproduction of reactive oxygen species (ROS) and the release of inflammatory mediators. Dihydroartemisinin (DHA) is a semi-synthetic active metabolite of artemisinin that has anti-inflammatory, antioxidant, and anti-fibrotic properties.</div></div><div><h3>Objective</h3><div>This study aimed to assess the therapeutic benefits of DHA on acetic acid(AA) -induced UC in rats, with particular emphasis on its anti-inflammatory effects and its influence on NFκB/TNF-α/RIPK1 necroptotic pathways.</div></div><div><h3>Methods</h3><div>Eighteen rats were allocated into control, acetic acid-induced colitis (AA), and DHA-treated (AA+DHA) groups. Colitis was caused by rectal instillation of 5 % acetic acid. DHA was supplied via intraperitoneal injection. Histological, biochemical studies of oxidative stress, inflammatory and anti-inflammatory mediators, Western blotting for TNF-α, RIPK1, and caspase 3, and immunohistochemical assessment of NFκB, TNF-α, and RIPK1, were conducted.</div></div><div><h3>Results</h3><div>DHA treatment markedly diminished macroscopic damage, disease activity index, histopathology scores, and malondialdehyde (MDA) levels, enhancing glutathione (GSH) levels. Additionally, DHA decreased serum TNF-α and IL-6 and increased IL-10. Western blotting and immunohistochemistry investigations validated the reduced expression of TNF-α, RIPK1, and caspase 3 in DHA-treated rats.</div></div><div><h3>Conclusion</h3><div>DHA demonstrates protective properties against acetic acid-induced UC by decreasing oxidative stress and inflammation, modifying TNF-α activity to regulate apoptotic and necroptotic pathways. So, DHA may be a favorable therapeutic alternative for the management of ulcerative colitis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102791"},"PeriodicalIF":2.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of ossification of the entheses in spondyloarthritis physiopathogenic aspects and possible therapeutic implication","authors":"Barile Raffaele,&nbsp;Maruotti Nicola,&nbsp;Rotondo Cinzia,&nbsp;Rella Valeria,&nbsp;Cantatore Francesco Paolo,&nbsp;Corrado Addolorata","doi":"10.1016/j.tice.2025.102803","DOIUrl":"10.1016/j.tice.2025.102803","url":null,"abstract":"<div><div>This review examines the molecular mechanisms driving structural damage in Spondyloarthritis (SpA), a chronic inflammatory condition characterized by new bone formation that can lead to partial or complete spinal ankylosis. We explore the complex interplay between inflammation, mechanical stress, and bone metabolism in SpA, focusing on key signaling pathways and cytokines that contribute to disease progression. The review analyzes both structural and inflammatory aspects, particularly the role of enthesis biology and the impact of mechanical factors. Additionally, we assess how current therapeutic approaches, including biologic treatments targeting specific inflammatory pathways such as tumor necrosis factor inhibitors, affect disease progression. While these treatments can reduce inflammation and manage clinical symptoms, their limited ability to completely prevent new bone formation highlights the complexity of the underlying pathological processes. We also evaluate emerging therapeutic strategies targeting specific molecular pathways involved in bone formation. Understanding these intricate molecular mechanisms and their interactions is crucial for developing more effective targeted therapies that could potentially not only manage symptoms but also prevent or reverse structural damage in SpA patients.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102803"},"PeriodicalIF":2.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143446064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing ribosome biogenesis regulator 1 homolog (RRS1) inhibits angiogenesis and cisplatin resistance of lung cancer cells by activating ferroptosis mediated by p53 pathway","authors":"Ling Lin ,&nbsp;Ying Zou ,&nbsp;Di Zhang","doi":"10.1016/j.tice.2025.102796","DOIUrl":"10.1016/j.tice.2025.102796","url":null,"abstract":"<div><h3>Background</h3><div>Human RRS1 gene is abnormally expressed in many cancers, and RRS1 can inhibit the level of p53. Ferroptosis mediated by p53 pathway may be a potential therapeutic strategy for cancer. However, the specific role of RRS1 in lung cancer is not clear.</div></div><div><h3>Methods</h3><div>The correlation between the expression level of RRS1 and the overall survival of lung cancer patients was explored through UALCAN and Kaplan-Meier plotter. A549 cells and drug-resistant A549/DDP cells were used in vitro. Wound healing, Transwell and tubule formation experiment were used to detect the abilities of cell invasion, migration and tube formation. Detecting the level of lipid ROS by BODIPY(581/591) C11 staining, the expression level of total iron and ferroptosis-related proteins were detected, so as to judge the ferroptosis in cells. Detecting the apoptosis by flow cytometry and the expression of apoptosis-related proteins by western blot, so as to observe the effect of interfering with RRS1 on cisplatin resistance of cells.</div></div><div><h3>Results</h3><div>The expression of RRS1 was up-regulated, and its level was negatively correlated with the overall survival time of lung cancer patients. In vitro experiments showed that RRS1 interference reduced the invasion and migration of lung cancer cells, inhibited the expressions of MMP2 and MMP9 proteins and decreased the tube-forming ability of cells. After interfering with RRS1, the level of p53, lipid ROS and the total iron content in cells increased, the expression of SLC7A11 and GPX4 decreased while the expression of ACSL4 increased, which indicated that ferroptosis was enhanced. Interference with RRS1 increased the apoptosis of drug-resistant cells, decreased the expression of Bcl2 while increased the expression of Bax and caspase3(cleaved), which decreased the cisplatin resistance of lung cancer cell A549. However, after silencing p53, these effects were reversed.</div></div><div><h3>Conclusion</h3><div>RRS1 inhibits angiogenesis and cisplatin resistance of lung cancer cells by activating ferroptosis mediated by p53 pathway.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102796"},"PeriodicalIF":2.7,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of pterostilbene on inducing apoptosis in normal bladder and bladder cancer cells","authors":"Chen-Hsun Ho ,&nbsp;Chia-Kwung Fan ,&nbsp;Yi-Chen Chu ,&nbsp;Shih-Ping Liu ,&nbsp;Po-Ching Cheng","doi":"10.1016/j.tice.2025.102794","DOIUrl":"10.1016/j.tice.2025.102794","url":null,"abstract":"<div><div>Bladder cancer is the most common type of urinary tumor. Current research has focused on alternative therapies that protect the bladder. Some studies suggested that cancer can be treated by inducing apoptosis. Therefore, finding new drugs for related or adjuvant treatments has become important. PT is a natural derivative of resveratrol. The antioxidant effects of PT include the scavenging of extracellular ROS and the induction of apoptosis. PT has been shown to induce several types of tumor cell death; however, the detailed mechanism of action remains unclear. The present examined PT's cytotoxicity and apoptosis-inducing abilities as an anti-bladder cancer drug in normal bladder epithelial and bladder cancer cells. Under PT treatment, bladder cancer HTB-9 cells showed a significant apoptotic effect compared to normal bladder epithelial SV-HUC-1 cells in a dose- and time-dependent manner. Fluorescence microscopy, flow cytometry, and western blotting showed a positive correlation with the expression of apoptotic proteins, especially caspase-3. PT promoted the apoptosis of bladder cancer cells in a time- and dose-dependent manner and had no significant effect on normal bladder epithelial cells involved in internal and external apoptotic pathways, especially the internal ones. The results demonstrate the potential of PT to promote apoptotic death in bladder cancer cells, suggesting its possible use as a drug to treat bladder cancer.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102794"},"PeriodicalIF":2.7,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436428","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":"Pumpkin seeds oil rescues colchicine-induced neurotoxicity in rats via modifying oxidative stress, DNA damage, and immunoexpression of BDNF and GFAP","authors":"Dina Y. Hegab ,&nbsp;Nabela I. El-Sharkawy ,&nbsp;Gihan G. Moustafa ,&nbsp;Yasmina M. Abd-Elhakim ,&nbsp;Enas N. Said ,&nbsp;Mohamed M.M. Metwally ,&nbsp;Taghred M. Saber","doi":"10.1016/j.tice.2025.102792","DOIUrl":"10.1016/j.tice.2025.102792","url":null,"abstract":"<div><div>Colchicine (CHC), a poisonous plant alkaloid, has been widely utilized for decades in the treatment of gout, but has a rather low therapeutic index, which causes oxidative stress leading to cognitive impairment, brain damage, apoptosis, and hitopathological alterations in humans and experimental animals. The present investigation evaluated the potential palliative effect of the pumpkin seeds oil (PSO) at a dose of 4 ml/kg b.wt against CHC (0.6 mg/kg b.wt) -induced neurotoxic and neurobehavioral effects in rats. Forty male rats weighing 245–260 g were assigned to four groups. The results displayed that CHC exposure induced neurobehavioral disorders and a remarkable decline in the serotonin and dopamine levels and the immunoexpression of BDNF and GFAP in the brain. Besides, CHC treatment evoked brain oxidative stress, as manifested by depleted antioxidant enzyme activities and elevated malondialdehyde (MDA) and protein carbonyl (PC) levels. Also, CHC triggered brain DNA damage, as indicated by a marked increment in the brain 8-Hydroxyguanosine (8-OHdG) level. However, concurrent treatment with the PSO effectively attenuated the CHC-induced toxic effects as evidenced by a noticeable increase in the serotonin (33 ± 3.05) and dopamine (2.48 ± 0.40) concentrations, and the BDNF and GFAP immunoexpression in the brain. Moreover, PSO mitigated CHC-induced brain oxidative stress and DNA damage as shown by elevated antioxidant enzyme activities (164 ± 3.46 SOD and 7.55 ± 0.43 CAT) and reduced MDA (1.62 ± 0.23), PC (1.35 ± 0.23), and 8-OHdG (3.02 ± 0.33) levels. These results concluded that PSO could serve as a therapeutic strategy to ameliorate the neurotoxic and neurobehavioral impacts of CHC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102792"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective effects of selenium against lithium-induced cerebellar toxicity in rats: The role of apoptosis, gliosis, and aging markers","authors":"Nora Elshehawy Helal ,&nbsp;Lashin Saad Ali ,&nbsp;Wael M. Elsaed ,&nbsp;Mohamed Berika ,&nbsp;Yasir Hassan Elhassan ,&nbsp;Khaled S. El-Bayoumi ,&nbsp;Abdelnaser A. Badawy ,&nbsp;Mosaab Salah El-din El-Agawy ,&nbsp;Amal Fahmy Dawood ,&nbsp;Mamdouh Eldesoqui","doi":"10.1016/j.tice.2025.102779","DOIUrl":"10.1016/j.tice.2025.102779","url":null,"abstract":"<div><h3>Background</h3><div>Prolonged lithium therapy in psychiatric disorders may be complicated by multi-organ dysfunction, particularly in the nervous system. Toxicity to the cerebellum is one of these, which, while uncommon, inevitably emerges negatively and permanently. Selenium is a trace element regarded as one of the critical antioxidants. Numerous investigations have validated selenium's neuroprotective properties against various neurotoxic medications. The degree of affliction of the nerve cells is assessed using GFAP, a marker of astrocytosis; Caspase-3, a marker of apoptosis; and klotho, a marker of anti-aging.</div></div><div><h3>Aim of the study</h3><div>This study is designed to investigate the cerebellar structural and functional changes in lithium-treated rats and the postulated neuroprotective role of selenium.</div></div><div><h3>Methodology</h3><div>A total of 24 adult male albino rats were divided into 4 groups: control, selenium (1 mg/kg in water solution by gavage daily), lithium (by intraperitoneal injection of 25 mg/kg lithium carbonate dissolved in 0.9 % NaCL twice daily for 4 weeks), and lithium-selenium group. Motor coordination was evaluated using the rotarod test. Cerebellar malonaldehyde (MDA) and reduced glutathione (GSH) were measured, and histopathological examination and immunohistochemical expression of Klotho, GFAP, and Caspase 3 were evaluated.</div></div><div><h3>Results</h3><div>The lithium-treated group exhibited reduced latency on the rotarod test, elevated oxidative stress indicators, and an altered cerebellar structure in HE and cresyl violet-stained sections. Moreover, there was a diminished Klotho expression and increased levels of both caspase-3 and GFAP expression. Selenium administration reduced latency time, diminished oxidative stress markers, mitigated lithium-induced cerebellar alterations, increased Klotho expression, and lowered the expression of caspase-3 and GFAP.</div></div><div><h3>Conclusion</h3><div>Lithium exposure causes alterations in the cerebellar cortical structure in albino rats. Selenium protected the cerebellar cortex from such changes by enhancing Klotho expression, diminishing oxidative stress, and reducing apoptosis.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102779"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autonomic nervous system imbalance in diabetic mouse choroids","authors":"Yuan-jun Qin ,&nbsp;Yong-Chao Zhang ,&nbsp;Yunru Lin ,&nbsp;Yiyi Hong ,&nbsp;Xufang Sun ,&nbsp;Fan Xu ,&nbsp;Changzheng Chen","doi":"10.1016/j.tice.2025.102798","DOIUrl":"10.1016/j.tice.2025.102798","url":null,"abstract":"<div><h3>Purpose</h3><div>We investigated neurohomeostasis and its possible underlying mechanisms in the choroids of diabetic mice.</div></div><div><h3>Methods</h3><div>Streptozotocin-induced diabetic mice were used in this study. Choroidal nerve fiber alterations were observed via transmission electron microscopy (TEM). The levels of epinephrine and acetylcholine in the choroid were determined via ultra-high-performance liquid chromatography–tandem mass spectrometry. Tyrosine hydroxylase (TH), choline acetyl transferase (ChAT), and neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), and calcitonin gene-related peptide (CGRP) levels were evaluated by western blot or quantitative real-time polymerase chain reaction. In addition, immunofluorescence staining were used to analyze the changes in key enzymes (TH, dopamine beta-hydroxylase (DβH), and CGRP) in the superior cervical sympathetic ganglia (SCG) and trigeminal ganglia (TG).</div></div><div><h3>Results</h3><div>TEM revealed a loose myelin sheath around nerve fibers, axon atrophy, and cytoplasmic vacuoles in Schwann cells in diabetic choroids. Lower epinephrine levels were observed in diabetic mice. Although no difference was found in acetylcholine level, the epinephrine-to-acetylcholine ratio was greatly decreased. Decreased TH and increased ChAT, nNOS, VIP, NPY, and CGRP were found in diabetic choroids. Fewer TH-positive and DβH-positive neuronal cells were found in the SCGs of diabetic mice. More CGRP-positive and fewer TH-positive neuronal cells were observed in the TG of diabetic mice.</div></div><div><h3>Conclusions</h3><div>Altered markers of the sympathetic, parasympathetic and sensory systems were present in diabetic mouse choroids. An imbalanced choroidal nervous system might explain the initiation of choroidal neovascularization in diabetic patients.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102798"},"PeriodicalIF":2.7,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GIT2 negatively regulates the NF-κB pathway directly or indirectly by regulating TRAF3 expression to promote osteogenic differentiation of BMSCs","authors":"Yanna Wang ,&nbsp;Changyuan Wang ,&nbsp;Ying Gong ,&nbsp;Qingchen Li ,&nbsp;Mozhen Liu ,&nbsp;Huijun Sun","doi":"10.1016/j.tice.2025.102790","DOIUrl":"10.1016/j.tice.2025.102790","url":null,"abstract":"<div><h3>Background aims</h3><div>Osteoporosis (OP) is a common disease of aging, which is closely related to the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). DNA damage, as a senescence-associated secretory phenotype (SASP), plays an important role in aging diseases including OP. GIT2 has been identified as a DNA repair gene and alleviates aging-related phenotypes. However, the relationship between GIT2 and osteogenic differentiation of BMSCs remains unclear.</div></div><div><h3>Methods</h3><div>Here, we used bioinformatics analysis to identify the gene GIT2, which is closely related to aging, OP and DNA damage, and its downstream targets. Then, H₂O₂ -induced BMSCs senescence model and ovariectomy-induced mice OP model was established in vitro and in vivo, respectively. Micro-CT, H&amp;E staining, toluidine blue staining, and calcein double labeling were used to analyze bone mass, osteogenic differentiation phenotype, and bone formation rate. Comet assay, Elisa and immunofluorescence were used to analyze senescence-related phenotypes. Western blotting was used to detect the protein levels of GIT2/TRAF3/NF-κB axis and osteogenesis-related markers.</div></div><div><h3>Results</h3><div>Our results showed that GTI2 and TRAF3 were positively correlated with OP-related markers. On the one hand, GIT2 could inhibit the activation of both canonical and non-canonical NF-κB signaling pathways by positively regulating TRAF3. On the other hand, GIT2 could directly bind to P65, a component of the classical NF-κB signaling pathway, and P52, a component of the non-classical NF-κB signaling pathway, to inhibit their activation, improve DNA damage repair, alleviate cell senescence, and further promote osteogenic differentiation of BMSCs.</div></div><div><h3>Conclusions</h3><div>In summary, the present study demonstrates that GIT2 plays a crucial regulatory role in promoting osteogenic differentiation of BMSCs, which provides new ideas for the prevention and treatment of OP and other aging-related diseases.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"94 ","pages":"Article 102790"},"PeriodicalIF":2.7,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}