Tissue & cell最新文献

{"title":"Itga11 promotes osteogenic differentiation, inhibits angiogenesis and proliferation of mesenchymal stem cells under hypoxia","authors":"Jun Zhang ,&nbsp;Na Ren ,&nbsp;Shujuan Chen ,&nbsp;Kun Liu ,&nbsp;Lei Xiong ,&nbsp;Xing Zheng","doi":"10.1016/j.tice.2024.102616","DOIUrl":"10.1016/j.tice.2024.102616","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to explore the role and mechanism of hypoxic environment in rat bone mesenchymal stem cells (rBMSCs) proliferation, osteogenic differentiation and angiogenesis.</div></div><div><h3>Methods</h3><div>Cell proliferation, angiogenesis and osteogenic differentiation were assessed using the CCK-8 assay, tube formation assay and alizarin red staining, respectively. Transcriptomic databases for rBMSCs under hypoxic (1 % O₂) and normoxic (18 % O₂) conditions were constructed to identify differentially expressed genes (DEGs), which were then subjected to gene function annotation and KEGG pathway analysis. To modulate the expression of Itga11, siRNA targeting Itga11 (si-Itga11) and a negative control (si-con), as well as pcDNA-Itga11 and an empty control plasmid (pcDNA), were employed to induce silencing or overexpression of Itga11. The protein levels were evaluated using Western blot analysis.</div></div><div><h3>Results</h3><div>Hypoxia stimulated the proliferation and angiogenesis of rBMSCs but suppressed their osteogenic differentiation. Differential expression analysis identified 541 upregulated and 277 downregulated genes in the hypoxic group compared to the normoxic group. KEGG pathway enrichment analysis suggested that the hypoxic response in rBMSCs is closely associated with the Pi3k /Akt signaling pathway. Itga11 was significantly downregulated in rBMSCs under hypoxic conditions. Overexpression of Itga11 in rBMSCs inhibited their proliferation and angiogenesis and enhanced osteogenic differentiation, while its knockdown had the opposite effect. Itga11 was found to activate the Pi3k /Akt signaling pathway in rBMSCs.</div></div><div><h3>Conclusion</h3><div>Itga11 facilitates osteogenic differentiation and suppresses angiogenesis and proliferation of MSCs under hypoxia by activating the Pi3k /Akt signaling pathway.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102616"},"PeriodicalIF":2.7,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142682258","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":"Organelle-level toxicity of nanometals relevant to titanium implants. Original research and comprehensive literature overview","authors":"Murat Zaimoglu ,&nbsp;Kutsal Devrim Secinti ,&nbsp;Meric A. Altinoz ,&nbsp;Melih Bozkurt ,&nbsp;Umit Eroglu ,&nbsp;Omer Ozpiskin ,&nbsp;Orkhan Mammadkhanli ,&nbsp;Eyup Bayatli ,&nbsp;Yusuf Sukru Caglar ,&nbsp;Ayhan Attar","doi":"10.1016/j.tice.2024.102612","DOIUrl":"10.1016/j.tice.2024.102612","url":null,"abstract":"<div><h3>Objective</h3><div>This study analyzed organelle toxicities of nanometals applied as free formulations or titanium rod-coating materials in rats.</div></div><div><h3>Methods</h3><div>All materials were injected intraperitoneally, including the physiological saline applied to the control group. The first experimental group was implanted with nanosilver-coated titanium rods, and the second, third, and fourth groups received free nanosilver at rising levels. The fifth group was implanted with nanosilver, nanocopper, and nanozinc-coated titanium rods, and the sixth group received the same nanometals as free formulations. Light and electron microscopy and ICP-Mass Spectrometry were utilized to determine the neural, hepatic, and renal toxicities and tissue metal levels.</div></div><div><h3>Results</h3><div>In brains, neuropil, myelin, and cellular damages occurred, especially in groups receiving high-dose nanosilver or nanometal combinations. Histiocyte accumulation and dark mitochondria within hepatocytes were discernible in the liver. Kidneys were the organs that were most severely affected by nanometal toxicity. The nephrotoxicity was apparent with the perturbations of the membrane infoldings and mitochondrial damage in the proximal and distal convoluted epithelia. Large angular peroxisomes developed inside the mesangial cells, and Golgi bodies increased in epithelial cells. Systemic metal levels increased on the thirtieth and prominently dropped on the sixtieth day.</div></div><div><h3>Conclusion</h3><div>These results provide insights into the extent of injury and organelle targets of nanometals and will guide optimizing the nanomaterials and implants used in the surgical practice.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102612"},"PeriodicalIF":2.7,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639964","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":"Evaluation of resveratrol's protective effect on hydrocortisone-induced growth inhibition in the peripubertal rat epiphyseal plate","authors":"Serkan Kemer ,&nbsp;Sefa Metin ,&nbsp;Ertugrul Celik ,&nbsp;Soner Mamuk ,&nbsp;Hakan Ergun","doi":"10.1016/j.tice.2024.102607","DOIUrl":"10.1016/j.tice.2024.102607","url":null,"abstract":"<div><h3>Objective</h3><div>Chronic use of glucocorticoids during childhood can lead to a decrease in hormone release, including ACTH, GH, TSH, and LH, as well as reduced IGF-1 activity. This can result in osteoporotic changes and hinder growth in height. Resveratrol, an antioxidant with phytoestrogen properties, may improve bone health by increasing bone mineral density in postmenopausal women. It has been shown that resveratrol promotes osteoblastic bone formation and reduces osteoclastic resorption. We aimed to investigate the protective effects of resveratrol on the growth inhibition of the epiphyseal plate induced by hydrocortisone in peripubertal Wistar Albino rats.</div></div><div><h3>Methods</h3><div>Rats were randomized into 6 groups and treated with hydrocortisone (10 mg/kg/day) and resveratrol (10–50–100 mg/kg/day) for 10 days after a standard AP tibia radiograph was taken. Blood and tibia bones were collected and evaluated for bone biomarkers (osteopontin, sclerostin), histopathological measures, and apoptosis markers.</div></div><div><h3>Results</h3><div>Subcutaneous administration of hydrocortisone for 10 days significantly reduced tibia linear growth, as evaluated by radiography (23.4 % vs. 15.1 %, p&lt;0.001). In the group that received 50 mg/kg/day of resveratrol and 10 mg/kg/day of hydrocortisone together, the tibia growth inhibition disappeared both radiographically and histologically. High-dose resveratrol (100 mg/kg/day) significantly reduced plasma sclerostin (p&lt;0.001) and increased osteopontin blood levels (p&lt;0.05) compared to the control group.</div></div><div><h3>Conclusion</h3><div>The inhibitory effect of 10 mg/kg/day hydrocortisone on tibia bone was reversed with 50 mg/kg/day oral resveratrol. Resveratrol's phytoestrogen property is thought to accelerate chondrocyte cellular senescence, counteracting hydrocortisone's inhibitory effect on gonadotropin secretion and senescence.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102607"},"PeriodicalIF":2.7,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681853","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":"Application of exosomes for the regeneration of skin wounds: Principles, recent applications and limitations","authors":"Ali Esmaeili ,&nbsp;Ghasem Noorkhajavi ,&nbsp;Masoud Soleimani ,&nbsp;Hana Farsinezhad ,&nbsp;Saeid Bagheri-Mohammadi ,&nbsp;Saeed Heidari Keshel","doi":"10.1016/j.tice.2024.102611","DOIUrl":"10.1016/j.tice.2024.102611","url":null,"abstract":"<div><div>In the medical field, wound healing poses significant challenges due to its complexity and time-consuming nature. Cell-free wound repair, notably the utilization of exosomes (EXOs), has made significant progress in recent years. Urine, saliva, umbilical cord, blood, mesenchymal stem cells and breast milk cells can be used to extract and purify EXOs, which are Nano-sized lipid bilayer vesicles. Besides their relatively little toxicity, non-specific immunogenicity and excellent biocompatibility, EXOs also contain bioactive molecules such as proteins, lipids, microRNAs (miRNAs), and messenger RNAs (mRNAs). Their bioactive compounds have anti-inflammatory properties and can speed up wound healing. Various medicinal agents can also be contained within the EXOs. This review briefly provides new information on the different aspects of EXOs and evaluate the application of EXOs as a promising therapy in the regeneration of skin wounds in recent pre-clinical and clinical studies.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102611"},"PeriodicalIF":2.7,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648813","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":"Protective effect of beta-carotene on hepato-nephrotoxicity of gentamicin in male Wistar rats","authors":"Susan Sabbagh ,&nbsp;Parisa Rayatpishe ,&nbsp;Mehdi Goudarzi ,&nbsp;Mohammad Mehdi Behvandi ,&nbsp;Reza Norouzirad","doi":"10.1016/j.tice.2024.102613","DOIUrl":"10.1016/j.tice.2024.102613","url":null,"abstract":"<div><h3>Background</h3><div>Despite causing significant tissue damage at the molecular and cellular levels, partly due to its induction of oxidative stress, it remains of interest in medical applications. Beta-carotene, found in fruits and vegetables, is being studied for its antioxidant properties. This study aimed to explore beta-carotene's protective effects against gentamicin-induced hepatorenal toxicity.</div></div><div><h3>Method</h3><div>Thirty male Wistar-rats were divided into five groups. Control group received normal-saline, while the canola group received canola oil (beta-carotene solvent). Gentamicin group received 100 mg/kg gentamicin injections for seven days. Beta-carotene groups were treated with beta-carotene at doses of 10 and 20 mg/kg for 10 days, along with gentamicin from the fourth day for 7 days. Serum and tissue hepatorenal function tests were performed at the end of the study.</div></div><div><h3>Results</h3><div>Gentamicin resulted in hepatorenal damage. Beta-carotene alongside gentamicin significantly decreased serum SGOT (152.3 ± 12.7 vs. 264.8 ± 9.3 IU/L), SGPT (65.7 ± 2.5 vs. 98.0 ± 4.8 IU/L), creatinine (0.74 ± 0.0 vs. 1.5 ± 0.1 mg/dL), and urea (78.1 ± 10.7 vs. 207.4 ± 23.6 mg/dL) in comparison to gentamicin alone (p &lt; 0.05). Beta-carotene caused a significant decrease in vacuolar degeneration, interstitial nephritis and infiltration of lymphocytes in kidney, and cell necrosis, vacuolar degeneration and infiltration of leukocytes compared to the gentamicin group; additionally, beta-carotene prevented increase in oxidative stress in gentamicin group.</div></div><div><h3>Conclusion</h3><div>Administration of gentamicin alone resulted in hepatorenal toxicity, whereas beta-carotene could prevent gentamicin-induced oxidative stress imbalance and tissue damage. Therefore, beta-carotene could serve as an adjunctive therapy to mitigate hepatorenal toxicity in patients undergoing gentamicin treatment.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102613"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628815","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":"Assessment of the protective effect of vitamin E supplementation on oxidative damage of diabetic rat spleen induced by streptozotocin","authors":"Mst. Maya Khatun ,&nbsp;Md. Farhad Sarker ,&nbsp;Md. Hemayet Hossain ,&nbsp;Md. Tariqul Islam ,&nbsp;Barun Kanti Saha ,&nbsp;Safaet Alam ,&nbsp;A.S.M. Golam Kibria ,&nbsp;Khurram Murad ,&nbsp;Md. Javid Hasan ,&nbsp;Nusrat Jahan Mouri ,&nbsp;Afzal Hossain ,&nbsp;Rasheda Akter","doi":"10.1016/j.tice.2024.102605","DOIUrl":"10.1016/j.tice.2024.102605","url":null,"abstract":"<div><h3>Aims</h3><div>Increased oxidative stress in diabetes mellitus may lead to splenic damage, contributing to decreased immunity. This study aims to evaluate the potential of vitamin E supplements as a protective agent against spleen injury by examining physiological, hematological, biochemical, and histological changes in diabetic rat model.</div></div><div><h3>Methods</h3><div>Diabetes was induced in male wistar albino rats through an intraperitoneal injection of 50 mg/kg Streptozotocin, and the rats were randomly divided into five groups. The rats were then administered varying doses of vitamin E for 14 consecutive days. Assessments included renal function tests, blood glucose levels, complete blood counts, lipid profiles, tissue oxidative stress and spleen histology. An acute toxicity study was also conducted on normal rats.</div></div><div><h3>Results</h3><div>Vitamin E supplementation did not result in any mortality up to 5000 mg/kg body weight. The treated diabetic group showed improved metabolic characteristics, such as normal body weight, food and water intake and a reduced spleen index compared to the untreated diabetic group. Significant improvements were observed in hematological parameters like packed cell volume (PCV), hemoglobin concentration, RBC (red blood cells) and WBC (white blood cells) counts. HCA (Hierarchical Cluster Analysis) of these parameters indicated that doses of 100 mg/kg and 150 mg/kg were most similar to normal condition. Catalase and MDA (Malondialdehyde) assays showed a substantial reduction in oxidative stress in spleen tissue and histopathological examination revealed significant regenerative effects.</div></div><div><h3>Conclusion</h3><div>This study demonstrated that vitamin E supplementation significantly enhanced various metabolic, hematological, biochemical, and histological parameters in the diabetic group compared to those who did not receive the treatment. Among the doses tested, 100 mg/kg and 150 mg/kg body weight were found to yield the most favorable outcomes.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102605"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628766","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":"Evaluation of decellularized sheep kidney scaffolds for renal tissue engineering: Biocompatibility and stem cell differentiation potential","authors":"Maryam Jahanvar ,&nbsp;Saber Zahri ,&nbsp;Arash Abdolmaleki ,&nbsp;Asadollah Asadi","doi":"10.1016/j.tice.2024.102594","DOIUrl":"10.1016/j.tice.2024.102594","url":null,"abstract":"<div><div>Tissue engineering (TE) combines scaffolds, cells, and bioactive chemicals in order to create tissues. The objective is to restore or sustain tissue functionality and expedite the recovery of damaged tissues or organs in a controlled laboratory environment. This study aimed to evaluate the properties and biocompatibility of decellularized sheep kidney scaffolds (DKS) and to explore the differentiation potential of adipose-derived mesenchymal stem cells (ADSCs) into renal cells. After decellularizing sheep kidneys using freeze-drying and detergent techniques, we conducted histological studies, DNA quantification, and ultrastructural evaluations using scanning electron microscopy (SEM). Furthermore, to assay the feasibility and attachment of stem cells to the decellularized scaffolds, ADSCs were cultured on the scaffolds and subjected to the MTT assay. The expression of the <em>pax2</em> gene was analyzed using real-time PCR to determine the differentiation of MSCs into kidney cells. DNA quantitation revealed a significant reduction in the quantity of DNA present in the scaffold tissue compared to the control kidney tissue. Ultrastructural examination confirmed the preservation of the decellularized scaffold's ultrastructure. Histological analysis demonstrated the complete removal of nuclear material from the scaffold. Additionally, Pax2 gene expression was significantly increased in ADSC cells cultured on the scaffold compared to the control group. The results demonstrate that the produced scaffolds are well-suited for regenerative medicine, exhibiting excellent biocompatibility and providing a conducive environment for the differentiation of ADSCs.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102594"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628773","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":"Combating oxidative stress and inflammation in gentamicin-induced nephrotoxicity using hydrogen-rich water","authors":"Mustafa Oguz Cumaoglu ,&nbsp;Mustafa Makav ,&nbsp;Serpil Dag ,&nbsp;Ayfer Yildiz Uysal ,&nbsp;Lale Baser ,&nbsp;Tyler W. LeBaron ,&nbsp;Duried Alwazeer","doi":"10.1016/j.tice.2024.102604","DOIUrl":"10.1016/j.tice.2024.102604","url":null,"abstract":"<div><div>Gentamicin-induced nephrotoxicity primarily results from renal inflammatory cascades and increased oxidative stress. This study aims to examine the effects of hydrogen-rich water (HRW) on gentamicin-induced renal damage in rats. Thirty-two rats were equally divided into four groups, including control (no treatment), hydrogen, gentamicin, and gentamicin+hydrogen. At the end of one week, all animals were euthanized following ethical rules, and blood and tissue samples were analyzed for examining Malondialdehyde (MDA), glutathione (GSH), Tumor Necrosis Factor-Alfa (TNF-α), Tumor Necrosis Factor-Beta (TNF-β), Interleukin 6 (IL-6), endoglin, endocan, urea, creatinine, Na⁺, and K⁺ parameters. Levels of 8-Hydroxyguanosine (8-OHdG), MDA, and Bax were immunohistochemically analyzed. Data showed that while MDA (control <em>P</em>&lt;0.0001, H₂ <em>P</em>&lt;0.0001<em>, ‎</em>Genta+H₂ <em>P</em>&lt;0.0007), TNF-α (control <em>P</em>&lt;0.0002, H₂ <em>P</em>&lt;0.0040, <em>‎</em>Genta+H₂ <em>P</em>&lt;0.0381), IL-6 (control <em>P</em>&lt;0.0044<em>,</em> H₂ <em>P&lt;</em>0.0070<em>, ‎</em>Genta+H₂ <em>P</em>&lt;0.0109), endocan (control <em>P</em>&lt;0.0460<em>,</em> H₂ <em>P</em>&lt;0.0286, <em>‎</em>Genta+H₂ <em>P</em>&lt;0.0452), and endoglin (control <em>P</em>&lt;0.0131<em>,</em> H₂ <em>P</em>&lt;0.0164, <em>‎</em>Genta+H₂ <em>P</em>&lt;0.0397), urea (control <em>P</em>&lt;0.0024<em>,</em> H₂ <em>P</em>&lt;0.0001<em>, ‎</em>Genta+H₂ <em>P</em>&lt;0.0180), and creatinine parameters (control <em>P</em>&lt;0.0017<em>,</em> H₂ <em>P</em>&lt;0.0178, <em>‎</em>Genta+H₂ <em>P</em>&lt;0.0011<em>)</em> increased in the gentamicin group compared to the other groups<em>,</em> a decrease in these parameters was observed in the gentamicin+hydrogen group compared to the gentamicin group<em>.</em> The Genta group had greater levels of TNF-β than the control (<em>P</em>&lt;0.0042) and H2 groups (<em>P</em>&lt;0.0268). GSH content was higher in the hydrogen group compared to the gentamicin group. Immunohistochemically, 8-OHdG, MDA, and Bax expressions increased in the gentamicin group compared to the control group, whereas they decreased in the gentamicin+hydrogen group compared to the gentamicin group. Hydrogen may be an alternative treatment for oxidative stress-induced nephrotoxicity.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102604"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628769","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":"Platelet-rich plasma ameliorates dexamethasone-induced myopathy by suppressing autophagy and enhancing myogenic potential through modulation of Myo-D, Pax-7, and myogenin expression","authors":"Sally M. Safwat ,&nbsp;Dalia M. Abdel Ghaffar ,&nbsp;Mamdouh Eldesoqui ,&nbsp;Sally Abdallah Mostafa ,&nbsp;Eman A.E. Farrag ,&nbsp;Fardous El-Senduny ,&nbsp;Basma Osman ,&nbsp;Eman Mohamad El Nashar ,&nbsp;Shaker Hassan Alshehri ,&nbsp;A. Alhefzi ,&nbsp;Mohammed Saeed Alasmry ,&nbsp;Omar Aboubakr Elnashar ,&nbsp;Zienab Helmy Eldken","doi":"10.1016/j.tice.2024.102602","DOIUrl":"10.1016/j.tice.2024.102602","url":null,"abstract":"<div><h3>Background</h3><div>Muscle tissue is essential for overall well-being that declines with age and different illnesses. Glucocorticoids, despite being efficient in treating inflammation, can induce muscle weakness (known as glucocorticoid-induced myopathy) by affecting protein breakdown and synthesis. Glucocorticoids have a negative impact on satellite cells, which play a role in muscle regeneration. Platelet rich plasma (PRP), containing concentrated growth factors, has a potential role in enhancing tissue repair and could be used to ameliorates combat muscle wasting caused by glucocorticoids.</div></div><div><h3>Aim</h3><div>The purpose of this study was to identify how PRP can affect dexamethasone-induced myopathy in a rat model.</div></div><div><h3>Methods</h3><div>Twenty-four male rats were divided into four equal groups: control, PRP, steroid (dexamethasone) treated for induction of myopathy, and steroid then treated with PRP for three weeks. Skeletal muscle contractile properties, protein content of the muscle, oxidative stress markers, histological structure, myogenin gene expression and immunohistochemical expression of Myo-D, Pax-7 and LC3 were assessed.</div></div><div><h3>Results</h3><div>dexamethasone caused significant muscle weakness, decreased protein content, increased oxidative stress, decreased expression of myogenic genes and upregulated LC3 expression. PRP administration significantly improved muscle function, increased protein content, reduced oxidative stress, and upregulated myogenic genes. Histological results confirmed these findings. Additionally, PRP decreased autophagy marker LC3 expression and increased muscle stem cell markers MyoD and Pax7.</div></div><div><h3>Conclusion</h3><div>These results suggested that PRP could effectively prevent and reverse dexamethasone-induced muscle atrophy by promoting muscle protein synthesis, reducing oxidative stress, decreasing autophagy, and enhancing muscle stem cell activity. This study supports the potential role of PRP as a therapeutic strategy for muscle wasting disorders.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102602"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628798","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":"Calreticulin-driven autophagy enhances cell proliferation in laryngeal squamous cell carcinoma","authors":"Shufeng Gao,&nbsp;Xintao Wang,&nbsp;Yun Huang,&nbsp;Longgui You","doi":"10.1016/j.tice.2024.102603","DOIUrl":"10.1016/j.tice.2024.102603","url":null,"abstract":"<div><h3>Background</h3><div>Calreticulin (CALR) is a multifunctional calcium-binding protein. Recent studies have revealed that CALR contributes to tumor development and promotes cancer cell proliferation. However, how CALR affects the development of laryngeal squamous cell carcinoma (LSCC) remains mysterious. Thus, this study aimed to explore the effect of CALR on LSCC development and uncover its underlying mechanisms.</div></div><div><h3>Methods</h3><div>CALR expression in LSCC cell lines and tissues was examined by qRT-PCR and western blot analysis and its functional role was detected via <em>in vivo</em> and <em>in vitro</em> assays. Cell proliferation was discriminated with CCK-8 and colony formation assays, while apoptosis was analyzed using flow cytometry. Autophagy levels were measured via LC3 immunofluorescence, and western blot assay was conducted to assess apoptosis- and autophagy-related proteins. Additionally, a mouse xenograft model was employed to determine the impact of CALR knockdown on tumor growth.</div></div><div><h3>Results</h3><div>We found that CALR knockdown reduced LSCC cell viability and proliferation while enhancing apoptosis, whereas CALR overexpression showed opposite effects. <em>In vivo</em> experiments verified that CALR knockdown suppressed tumor growth. In addition, elevated CALR expression induced autophagy in LSCC cells, while autophagy inhibitor 3-MA (2.5 mM) reversed the anti-apoptosis effects of CALR overexpression.</div></div><div><h3>Conclusion</h3><div>Our study identifies CALR as an oncogene in LSCC, where it promotes tumor progression by inducing autophagy and inhibiting apoptosis. Targeting CALR or modulating autophagy may represent novel therapeutic strategies for LSCC.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102603"},"PeriodicalIF":2.7,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648836","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}