Tissue & cell最新文献

{"title":"KPNA2/KPNB1 promotes the malignant progression of gastric cancer induced by M2 macrophage polarization","authors":"Juan Bai ,&nbsp;Ping Chen ,&nbsp;Qingxia Zhou ,&nbsp;Xiaojun Tie ,&nbsp;Xiao Xia ,&nbsp;Yan Wang ,&nbsp;Ling Jin","doi":"10.1016/j.tice.2024.102714","DOIUrl":"10.1016/j.tice.2024.102714","url":null,"abstract":"<div><div>Macrophages in the tumor microenvironment (TME) regulated gastric cancer progression, but the mechanism of macrophage polarization in gastric cancer progression remained unclear. This study mainly explored the molecular mechanism of macrophage polarization in the tumor microenvironment and its impact on the progression of gastric cancer. KPNA2 and KPNB1 expressions in cancer tissues and adjacent non-cancerous tissues were quantified via RT-qPCR and western blot. A correlation analysis was conducted between KPNA2 and KPNB1 expressions, utilizing the GEPIA2 database to link them with macrophage polarization. KPNA2-KPNB1 interaction was investigated on STRING, verified by Co-IP and IF assays. Raw246.7 cells were transfected with KPNA2 overexpression with or without si-KPNB1 plasmids. Then, M1/M2 macrophage markers and the proportion of M2 macrophages were measured by RT-qPCR, western blot, and IF. Co-culturing transfected Raw246.7 with MFC cells showed gastric cancer cell proliferation, apoptosis, migration, and invasion via CCK-8, flow cytometry, and transwell assays. KPNA2 and KPNB1 in gastric cancer tissues were elevated, exhibiting a positive correlation between them. KPNA2 overexpression facilitated the differentiation of macrophages into M2 type. KPNA2 overexpression in macrophages co-cultured with MFC cells stimulated MFC cells proliferation, repressed apoptosis, and enhanced migration/invasion. The interaction between KPNA2 and KPNB1 was confirmed through Co-IP and IF assays. Si-KPNB1 reversed the effects of KPNA2 overexpression on macrophages and gastric cancer cells. KPNA2 promoted the M2 polarization of macrophages by upregulating KPNB1, thereby inducing the proliferation and metastasis of gastric cancer.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102714"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137339","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":"IGF2BPs-regulated TIN2 confers the malignant biological behaviors of gastric cancer cells","authors":"Fang Li,&nbsp;Yadong Zhou,&nbsp;Zhiming Liao,&nbsp;Da Huang,&nbsp;Ziqing Zhang,&nbsp;Guoqun Chen","doi":"10.1016/j.tice.2024.102716","DOIUrl":"10.1016/j.tice.2024.102716","url":null,"abstract":"<div><h3>Background</h3><div>Telomere maintenance is an important feature of tumor cells. Telomeric-repeat binding factor 1 interaction nuclear protein 2 (TIN2), a key member of the shelterin proteins, functions in regulating telomere structure, length and function. Our work sought to investigate the role of TIN2 in controlling gastric cancer (GC) malignant biological behaviors.</div></div><div><h3>Methods</h3><div>The mRNA and protein expressions were examined by qRT-PCR, western blot and immunofluorescence assays. The relative telomerase activity and telomere length were detected using the corresponding kit and qRT-PCR, respectively. The proliferation, migration and invasion abilities were detected by CCK8 and transwell assays, respectively. Cellular oxidative stress level and Fe^2 + content were assessed by DCFH-DA staining and ELISA assays, respectively. The interaction between IGF2BP1/2/3 and TIN2 was analyzed by RIP and RNA pull down assays.</div></div><div><h3>Results</h3><div>TIN2 expression was significantly increased in GC cells compared with it in gastric mucosal epithelial cells. TIN2 knockdown could impair telomerase function and induce DNA injury in GC cells. Moreover, silencing of TIN2 greatly repressed cell proliferation, metastasis, and autophagy in GC cells. Likewise, the antioxidant capacity and Fe²⁺ content were enhanced after TIN2 depletion, leading to the activation of cellular ferroptosis. In terms of mechanism, TIN2 mRNA could be recognized by IGF2BP1/2/3, and its mRNA expression and stability were decreased upon IGF2BP1/2/3 was knocked down.</div></div><div><h3>Conclusion</h3><div>Knockdown of TIN2 could restrained telomerase function and the malignant abilities of proliferation, metastasis and autophagy but induced ferroptosis of GC cells, which suggested that targeting TIN2 might be a therapeutic strategy for GC</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102716"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137582","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":"Immunohistochemical identification of ACE-2 (SARS-COV II entry mechanism) in the gastrointestinal tract, kidney and lung of rhesus monkeys (Macaca mulatta) and squirrel monkeys (Saimiri sciureus)","authors":"Larissa dos Santos Sebould Marinho ,&nbsp;Márcia Cristina Ribeiro Andrade ,&nbsp;Cláudia Andréa de Araújo Lopes ,&nbsp;Kassia Valéria Gomes Coelho da Silva ,&nbsp;Kauet de Matos Gama e Souza ,&nbsp;Clarice Machado-Santos","doi":"10.1016/j.tice.2024.102711","DOIUrl":"10.1016/j.tice.2024.102711","url":null,"abstract":"<div><div>SARS-Cov-2 is a corona virus that causes COVID-19 disease, a viral infection responsible for the pandemic decreed by the World Health Organization in March 2020. Angiotensin-converting enzyme 2 (ACE-2) functions as the main receptor for SARS-Cov-2. The study aimed to detect the expression of ACE-2 in the gastrointestinal tract, kidney, and lung in the rhesus monkeys and squirrel monkeys. The sections from 18 rhesus monkey and 17 squirrel monkeys were incubated with rabbit polyclonal antibody to ACE2 (ab65863). In the lung of the rhesus monkeys, the presence of ACE-2 was noted in the bronchial mucosa of the respiratory epithelium. In the kidney, there was irregular in the proximal convoluted tubules. In the pyloric stomach, duodenum and in the large intestine it was observed on the surface of the lining epithelium. In the lung of the squirrel monkeys, this marking was present in both the ciliated cylindrical and goblet cell sof the bronchi. In the kidney light marking was observed along the surfasse of the cubic epithelium of the proximal convoluted tubules and in the renal glomerulus. No markings were observed throughout the stomach and intense staining was observed along the surfasse of the intestinal epithelium of the duodenum, jejunum and ileum, as well as in the intestinal glands. In our study, we can observe not able differences in the distribution of ACE2 between the two species of primates analysed. These differences must be considered in experimental studies on this disease, which continues to be a topic of notable importance for Public Health.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102711"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955691","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":"Targeting Siglec-15 mediates mitochondrial retrograde regulation of cervical cancer development","authors":"Jing Wang ,&nbsp;Zenghui Li ,&nbsp;Yifan He ,&nbsp;Yongli Chu","doi":"10.1016/j.tice.2024.102713","DOIUrl":"10.1016/j.tice.2024.102713","url":null,"abstract":"<div><div>Cervical cancer (CCA) is the predominant cause of fatalities from gynecologic malignancies, with metastasis responsible for 80 % of cancer-related mortalities. This study preliminarily examined the involvement of Sialic Acid Binding Ig Like Lectin 15 (Siglec-15) in the development of CCA and its probable mechanisms. We assessed the capacity of Siglec-15 to modulate CCA progression by establishing knockdown and overexpression Siglec-15 cell lines, supplemented with animal models, using both in vivo and in vitro dual investigations. Our findings indicate that Siglec-15 is significantly expressed in CCA cell lines and is intimately associated with the proliferation, migration, and invasion capabilities of CCA cells, as well as mitochondrial ROS homeostasis. The suppression of Siglec-15 expression markedly reduced tumor growth in mice, potentially due to Siglec-15’s role in regulating the Mitogen-Activated Protein Kinase (MAPK) signaling pathway, which mediates the retrograde regulation of mitochondrial ROS homeostasis. Siglec-15 may emerge as a novel therapeutic target and prognostic marker for patients with CCA.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102713"},"PeriodicalIF":2.7,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932694","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":"The potential of bone marrow derived mesenchymal stem cells in treating cisplatin induced sensorineural hearing loss in a guinea pig animal model","authors":"Mohamed Hassan Ali Elsayed Abdelwahed ,&nbsp;Mohamed Hussien Badreldin ,&nbsp;Ibrahim Hassan Ibrahim ,&nbsp;Reham Farouk Zittoon ,&nbsp;Rania A. Galhom ,&nbsp;Sally S. Mohammed ,&nbsp;Yehia Mohamed Ashry","doi":"10.1016/j.tice.2024.102703","DOIUrl":"10.1016/j.tice.2024.102703","url":null,"abstract":"<div><h3>Background</h3><div>Sensorineural hearing loss (SNHL) is the most common sensory deficit worldwide. Current solutions for SNHL, including hearing aids, cochlear implants, and hearing assistive devices, do not provide consistent results and fail to address the underlying pathology of hair cell and ganglion cell damage. Stem cell therapy is a cornerstone in regenerative medicine. It provides new hope to treat SNHL by replacing/regenerating damaged hair cells and ganglion cells. Mesenchymal stem cells are an interesting choice in stem cell therapy.</div></div><div><h3>Aim of the work</h3><div>Evaluation of bone marrow derived mesenchymal stem cell (BM-MSC) transplantation to improve SNHL management.</div></div><div><h3>Methods</h3><div>An experimental study was conducted using 40 recipient guinea pigs, randomly divided into four groups, along with 4 donor guinea pigs for bone marrow harvesting to isolate BM-MSC. Group I (12 animals) served as the control, receiving neither ototoxic drugs nor stem cell treatment. Group II (12 animals) received intraperitoneal cisplatin (1.5 mg/kg/day for 8 days) to induce sensorineural hearing loss, but no stem cell treatment. Group III (12 animals) received IP cisplatin to induce SNHL, followed by BM-MSC transplantation via round window injection one week later. Groups I, II, and III were euthanized 5 weeks after the last cisplatin injection, and their cochleae were examined using light microscopy, scanning electron microscopy, and fluorescent light microscopy to assess the effect of stem cell transplantation on the recovery of neurosensory tissue in the cochlea after cisplatin treatment. Group IV (4 animals) received IP cisplatin to induce SNHL, followed by transplantation of fluorescein-labeled BM-MSC (FLBM-MSC) via round window injection one week later and were euthanized after one week to study stem cell migration and homing.</div></div><div><h3>Results</h3><div>Light Microscopy: Group I exhibited a normal structure in the organ of Corti, spiral ganglion, and stria vascularis. In contrast, Group II demonstrated degeneration in these areas. Group III showed a preserved structure in the organ of Corti, spiral ganglion, and stria vascularis, with statistically significant differences compared to Group II (p &lt; .05). Scanning Electron Microscopy: Group I displayed normal ultrastructure of the organ of Corti, while Group II showed a loss of outer hair cells. Group III demonstrated preserved ultrastructure of the organ of Corti. Fluorescent Light Microscopy: In Group IV, transplanted cells were observed to home into the cochlear lateral wall, organ of Corti, and spiral ganglion.</div></div><div><h3>Conclusion</h3><div>The study showed that BM-MSCs, delivered via round window injection, can migrate to cochlear regions and protect key structures after cisplatin-induced SNHL in guinea pigs, suggesting their potential as a treatment for SNHL.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102703"},"PeriodicalIF":2.7,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932698","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":"Characterizing thyroid follicles histogenesis in the human fetuses: A morphological approach","authors":"Chacchu Bhattarai ,&nbsp;Phanindra Prasad Poudel ,&nbsp;Mahendra Raj Pandey ,&nbsp;Chandni Gupta ,&nbsp;Sneha Guruprasad Kalthur","doi":"10.1016/j.tice.2024.102710","DOIUrl":"10.1016/j.tice.2024.102710","url":null,"abstract":"<div><div>Thyroid gland which is responsible for the maintenance of metabolism and growth is derived from thyroglossal duct, an outpocketing of foregut. The microscopic study of thyroid gland during development in first, second and third trimesters has utmost significance to understand the several developmental thyroid disorders metabolically and structurally. This study is descriptive observational study carried in tissue sections taken from thyroid gland of still birth and spontaneously aborted human fetuses of first, second and third trimester. The processed thyroid gland tissues were sectioned and conventional haematoxylin and eosin stain was used to study the detail histomorphology of this gland during these trimesters. Multiple shapes (round, oval and irregular) of thyroid follicles with variation in vascularity and fibrous capsule were observed in human fetuses during their development. Dimensions of epithelial cells (height and weight), outer and inner boundaries of thyroid follicles and number of parafollicular cells were increased as age progresses from first to third trimester whereas diameters, radius, perimeter, area and colloid volume of follicles were decreased as age progresses from first to third trimester. But the area of cytoplasm with nuclei (A_nc), cytoplasmic area (A_c) and nuclear-to-cytoplasmic (N/C) ratio were increased from first to second trimester thereafter decreased in third trimester. This study can act as baseline study to understand histomorphological differences in developing human fetal thyroid gland and to understand associated thyroid gland related disorders during its development.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102710"},"PeriodicalIF":2.7,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142955690","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":"The role of HM13 expression and its relationship to PI3K/Akt and p53 signaling pathways in colorectal cancer","authors":"Xiao Jin,&nbsp;Hao Wang,&nbsp;Yong Wang","doi":"10.1016/j.tice.2024.102702","DOIUrl":"10.1016/j.tice.2024.102702","url":null,"abstract":"<div><div>Histocompatibility minor 13 (HM13) is a signal sequence stubbed intramembrane cleavage catalytic protein. Increasing evidence supports the association among HM13 expression, tumor-infiltrating immune cells (TIICs), and cancer. However, its role on formation and progression of colorectal cancer (CRC) has not been explored. In this study, we aim to identify the role and function of HM13 on the progression of CRC and explore the possible mechanism. The findings of our study indicate that HM13 is significantly upregulated in colorectal cancer (CRC) compared to normal colorectal tissues (<em>P&lt;</em> 0.001). Moreover, the elevated expression of HM13 is associated with unfavorable prognosis in CRC patients. Furthermore, our results demonstrate that the overexpression of HM13 contributes to enhanced proliferation and migration, as well as suppressed apoptosis, in SM480 and HCT116 cell lines (<em>P&lt;</em>0.001). Conversely, the downregulation of HM13 (shHM13) yields opposite effects. Additionally, the administration of LY294003 and nutlin-3 effectively inhibits proliferation and migration, while promoting apoptosis in HCT116 cells (<em>P&lt;</em>0.001). However, the presence of HM13 counteracts these changes. In an in vivo study, the knockdown of HM13 (shHM13) significantly reduces tumor growth and the proportion of Ki-67 positive cells, while increasing the percentage of tunel-positive cells (<em>P&lt;</em>0.001). Also, shHM13 decreased the level of p-PI3K/PI3K and p-AKT/AKT, upregulated p53 and p21 activities. It can thus be concluded that HM13 might be a novel oncogene in CRC and regulates proliferation, migration and apoptosis by modulating the PI3K/Akt and p53 signaling pathways.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102702"},"PeriodicalIF":2.7,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928428","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":"CNPY2 modulates senescence-associated secretory phenotype in tendon stem/progenitor cells","authors":"Gang Xu ,&nbsp;Youhua Wang","doi":"10.1016/j.tice.2024.102706","DOIUrl":"10.1016/j.tice.2024.102706","url":null,"abstract":"<div><div>Age-related diseases are often linked to chronic inflammation. Senescent cells secrete inflammatory cytokines, chemokines and matrix metalloproteinases, collectively referred to as the senescence-associated secretory phenotype (SASP). The current study discovered that aging leads to the accumulation of senescent tendon stem/progenitor cells (TSPCs) in tendon tissue, resulting in the development of a SASP. Conditioned medium from aged TSPCs induced cellular inflammation in young TSPCs. In addition, we found that Canopy homolog 2 (CNPY2) expression is reduced during tendon aging. CNPY2 deficiency causes TSPCs senescence and SASP. Our findings showed that the NF-κB signaling pathway is activated in CNPY2 knockdown TSPCs, pharmacological inhibition of NF-κB signaling pathway with BMS-345541 attenuated SASP of senescent TSPCs, which indicated that CNPY2 regulates TSPCs SASP might through NF-κB signaling pathway. Our findings suggested that CNPY2 plays an important role in TSPCs senescence and SASP, CNPY2 could be a promising target for age-related tendon disorders.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102706"},"PeriodicalIF":2.7,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928342","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":"Structural isomers of carene persuade apoptotic cell death by inhibiting cell cycle in breast cancer cells: An in silico and in vitro approach","authors":"Haribalan Perumalsamy ,&nbsp;Johan Sukweenadhi ,&nbsp;Anuj Ranjan ,&nbsp;Akhilesh Dubey ,&nbsp;Manohar Mahadev ,&nbsp;Mohamed Farouk Elsadek ,&nbsp;Saeedah Musaed Almutairi ,&nbsp;Daewon Sohn ,&nbsp;Sri Renukadevi Balusamy","doi":"10.1016/j.tice.2024.102701","DOIUrl":"10.1016/j.tice.2024.102701","url":null,"abstract":"<div><div>For the first time, our study provides a comprehensive examination of the anti-cancer effects of structural isomers of carene in breast cancer cells, specifically focusing on cell cycle inhibition and the induction of apoptosis. We utilized the hydro-distillation method to extract <em>Piper nigrum</em> seed essential oil (PNS-EO) and identified its bioactive components through gas chromatography-mass spectrometry (GC-MS) analysis. A total of 46 bioactive compounds were isolated via hydro-distillation, identified through GC-MS analysis, and validated by co-injection using GC analysis. The major constituent, 3-carene displayed the most substantial anti-proliferative effect on the breast cancer cell line MCF-7, with an IC₅₀ value of 11.19 µg/mL. Further, docking studies were conducted to evaluate the putative role of 3-carene in inhibiting the cell cycle proteins (CDKN2A, CCND1, CDK4), as well as proteins in the apoptosis pathway (BCL-XL, BAX, BAK, Caspase 3). Additionally, we employed fluorescence-activated cell sorting (FACS) and clonogenic assays to evaluate cell cycle inhibition and time-dependent initiation of apoptosis. Moreover, fluorescence techniques including Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), Hoechst staining, and Propidium iodide (PI) staining were performed to assess cell death and apoptosis. Furthermore, molecular techniques such as quantitative real-time PCR (qPCR) and western blotting were utilized to investigate the mechanism of cell death was elucidated through the inhibition of <em>Bcl-2</em>, <em>MMP2</em>, <em>MMP9</em>, and <em>Akt</em> expression, alongside the activation of <em>Bax</em>, <em>cytochrome C</em>, and <em>Caspases 3</em> and <em>9</em>. Our findings indicate that 3-carene, isolated through hydro-distillation, effectively hinders the cell cycle and promotes apoptosis in MCF-7 cells. Consequently, it shows promise for incorporation into combinational anti-cancer therapies, warranting further research.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102701"},"PeriodicalIF":2.7,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137340","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":"Development of a rat airway organoids model for studying chronic obstructive pulmonary disease","authors":"Chuanlai Yang ,&nbsp;Hongwei Yang ,&nbsp;Yangling Xian ,&nbsp;Nanyi Liu ,&nbsp;Haoyin Tan ,&nbsp;Zirui Ren ,&nbsp;Yanzhen Lin ,&nbsp;Huan Zhao ,&nbsp;Changjian Fang ,&nbsp;Kang Yu ,&nbsp;Dequan Pan ,&nbsp;Yali Zhang ,&nbsp;Xiumin Huang ,&nbsp;Ningshao Xia ,&nbsp;Wei Wang ,&nbsp;Tong Cheng","doi":"10.1016/j.tice.2024.102692","DOIUrl":"10.1016/j.tice.2024.102692","url":null,"abstract":"<div><div>Chronic obstructive pulmonary disease (COPD) poses global health challenges owing to limited treatment options and high rates of morbidity and mortality. Airway organoids have recently become a valuable resource for the investigation of respiratory diseases. However, limited access to clinical tissue samples hinders the use of airway organoids to study COPD. Therefore, alternative models that can mimic human airway pathology without relying on human tissues are needed. In this study, airway organoids were developed from tracheal epithelial cells obtained from 8-week-old Sprague-Dawley rats and exposed to lipopolysaccharide (LPS) to induce COPD-like characteristics. Exposure to LPS leads to structural changes in organoids, including an increase in goblet cells, a decrease in ciliated cells, increased mucin production, and elevated levels of pro-inflammatory cytokines. The COPD drugs erdosteine and R-HP210 effectively reduced mucin secretion, although none was able to restore the function of ciliated cells. Inflammatory markers responded differently, with ensifentrine and erdosteine significantly reducing cytokine levels. These results demonstrate that rat airway organoids replicate important aspects of human COPD pathology, thus providing an accessible, ethical, and clinically relevant alternative to human tissues and traditional animal models to enhance our understanding of COPD pathogenesis and evaluate potential treatments.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"93 ","pages":"Article 102692"},"PeriodicalIF":2.7,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142915650","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}