Tissue & cell最新文献

{"title":"Modulation of cutaneous wound healing by Losartan: A focus on MCP-1 activity and collagen synthesis","authors":"Mohammad Kazempour ,&nbsp;Mohammad Hashemnia ,&nbsp;Zahra Nikousefat ,&nbsp;Behdad Beheshti Alagha","doi":"10.1016/j.tice.2025.103079","DOIUrl":"10.1016/j.tice.2025.103079","url":null,"abstract":"<div><div>Losartan, a selective angiotensin II type 1 receptor (AT1R) antagonist, has shown anti-inflammatory and anti-fibrotic properties that may accelerate wound healing when applied topically. Impaired wound healing remains a global health concern, leading to chronic wounds, infection, and excessive scarring. This study is the first to evaluate the wound healing potential of topically applied Losartan.</div></div><div><h3>Main methods</h3><div>Full-thickness excisional wounds were created on Sprague-Dawley rats and treated with topical Losartan (5 % or 10 %), base cream, or left untreated. Wound healing was assessed macroscopically and histologically at days 10, 20, and 30 post-injury. In addition to analyzing myeloperoxidase (MPO), monocyte chemotactic protein-1 (MCP-1), glycosaminoglycans (GAGs), and hydroxyproline, further parameters such as wound closure rate, collagen fiber alignment, revascularization, and inflammatory cell infiltration were evaluated.</div></div><div><h3>Key Findings</h3><div>Losartan-treated wounds showed significantly accelerated closure, enhanced cytokeratin 14 (CK14) and improved epithelial regeneration, and reduced inflammatory infiltration. MPO activity was notably decreased, especially in early healing, and MCP-1 modulation followed the macrophage dynamics. Histological results demonstrated enhanced fibroblast maturation, revascularization, and organized collagen deposition. Elevated levels of hydroxyproline and GAGs confirmed improved extracellular matrix formation.</div></div><div><h3>Significance</h3><div>This study is the first to demonstrate the efficacy of topically applied Losartan in promoting wound healing by modulating inflammation, enhancing matrix remodeling, and regulating CK14 expression. These findings support the therapeutic repositioning of Losartan as a novel topical agent and pave the way for its clinical development in the management of chronic wounds, including diabetic and ischemic ulcers.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103079"},"PeriodicalIF":2.5,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842735","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":"Shape and surface modification dependent cellular interactions of gold nanoparticles in a 3D blood-brain-barrier supported neurospheroid model","authors":"Aysel Tomak ,&nbsp;Pelin Saglam-Metiner ,&nbsp;Reyhan Coban ,&nbsp;Ceyda Oksel-Karakus ,&nbsp;Ozlem Yesil-Celiktas","doi":"10.1016/j.tice.2025.103080","DOIUrl":"10.1016/j.tice.2025.103080","url":null,"abstract":"<div><div>Recent investigations have begun to explore the cellular interactions of nanoparticles (NPs) in three-dimensional (3D) neuro-spheroid models of the blood-brain barrier (BBB), offering novel insights into NP transport across the barrier and their potential neurotoxic effects. Building on these findings, we investigated the effects of particle shape and surface modification on the transport dynamics and cellular interactions of gold NPs (AuNPs) using a multicellular 3D spheroid model of the BBB. AuNPs with two different morphologies, spherical and rod-like, were synthesized, modified with polyethylene glycol (PEG) and characterized in detail using Ultraviolet-Visible <strong>(</strong>UV-Vis) Spectroscopy, Scanning Electron Microscopy (SEM), Dynamic Light Scattering (DLS) and Inductively Coupled Plasma Mass Spectrometry (ICP-MS) techniques. A 3D neuro-spheroid model consisting of mouse brain endothelial cells (bEnd.3), motor neuron-like hybrid cells (NSC-34) and glial cells (C6) was employed to evaluate the BBB transport characteristics and cytotoxicity of bare and PEG-coated spherical and rod-shaped AuNPs. Our results indicated that 3D neurospheroid models can serve as orchestral platforms for studying cellular behaviour of NPs. PEGylation of NPs substantially reduced cytotoxic effects compared to bare particles. While spherical AuNPs showed limited translocation through the endothelial barrier, those that entered the spheroid were found to be distributed deeper within the interior. In contrast, rod-shaped particles exhibited a greater capacity to cross the BBB but tended to accumulate near the periphery without deeper penetration. These findings underscore the critical role of shape and surface chemistry in nanoparticle-mediated BBB transport and support the utility of 3D neuro-spheroid models in predicting nanoparticle behavior in brain tissue.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103080"},"PeriodicalIF":2.5,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842738","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":"Human recombinant leptin-induced nitric oxide release from endothelium depends on the membrane localization pattern of endothelial nitric oxide synthase","authors":"Reji Manjunathan ,&nbsp;Swaraj Sinha ,&nbsp;Akila Swaminathan ,&nbsp;Dharanibalan Kasiviswanathan ,&nbsp;Malathi Ragunathan ,&nbsp;Suvro Chatterjee","doi":"10.1016/j.tice.2025.103083","DOIUrl":"10.1016/j.tice.2025.103083","url":null,"abstract":"<div><div>The form of nitric oxide (NO) released from endothelial nitric oxide synthase (eNOS) can influence various aspects of the angiogenic process. The endogenous hormone leptin can induce different physiological processes, such as angiogenesis, at low concentrations. Several studies suggest that leptin's ability to induce endothelium-dependent vascular relaxation is mediated by stimulating NO through distinct signalling pathways. Therefore, an attempt has been made to understand the optimal concentration and incubation time of human recombinant leptin for the enzymatic release of NO from eNOS. Changes in the localisation and phosphorylation pattern of eNOS in cultured endothelium under different concentrations and incubation times are examined. Five nanomolar concentration of human recombinant leptin, within 6 min of incubation, can induce a significant level of NO from activated eNOS in cultured endothelium through plasma membrane localisation and phosphorylation of eNOS. Our findings suggest that human recombinant leptin can modulate NO-dependent pathways, opening new therapeutic avenues for angiogenesis-related disorders, such as wound healing, when used at appropriate concentrations and incubation times. This capacity of human recombinant leptin supports its potential therapeutic application in pathological conditions like ischaemic heart diseases and wound healing processes, where angiogenesis requires early intervention.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103083"},"PeriodicalIF":2.5,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144827367","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":"Ganoderic acid A alleviate psoriasis by inhibiting GSDMD-mediated pyroptosis","authors":"Chenggen Xiao ,&nbsp;Junchen Chen ,&nbsp;Xingchen Zhou ,&nbsp;Hong Liu","doi":"10.1016/j.tice.2025.103078","DOIUrl":"10.1016/j.tice.2025.103078","url":null,"abstract":"<div><h3>Objective</h3><div>Psoriasis is a chronic inflammatory dermatological condition characterized by the infiltration of inflammatory cells into the dermal layer. This study aimed to elucidate the anti-inflammatory properties and underlying molecular mechanisms of Ganoderic acid A in the treatment of psoriasis.</div></div><div><h3>Methods</h3><div>A psoriasis model was induced in mice using IMQ to evaluate the effects of Ganoderic acid A in vivo. The Psoriasis Area and Severity Index (PASI) was employed to assess the severity of skin inflammation in the lesions. Techniques such as hematoxylin-eosin staining, RNA sequencing and immunofluorescence assays were utilized to evaluate the efficacy. Both in vivo and exvivo experiments were conducted to confirm the clinical relevance and explore the regulatory mechanisms involved.</div></div><div><h3>Results</h3><div>The findings demonstrated that both intraperitoneal and topical applications of Ganoderic acid A alleviate psoriasis effectively. Specifically, Ganoderic acid A resulted in a reduction in skin thickness, erythema, scaling and the expression of inflammatory cytokines. Mechanistically, Ganoderic acid A was shown to reduce the secretion of skin inflammatory factors by inhibiting pyroptosis through the GSDMD pathway.</div></div><div><h3>Conclusion</h3><div>Ganoderic acid A exhibits potential as a therapeutic agent for psoriasis and may be considered for inclusion in dietary recommendations for patients.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103078"},"PeriodicalIF":2.5,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842736","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 pyroptosis in vitiligo","authors":"Yingying Geng,&nbsp;Pengfei Huang,&nbsp;Tingting Cui","doi":"10.1016/j.tice.2025.103081","DOIUrl":"10.1016/j.tice.2025.103081","url":null,"abstract":"<div><div>Vitiligo is a common depigmentation disorder characterized by the loss of skin pigmentation, resulting in white patches on the skin. The pathogenesis of vitiligo involves complex interactions between genetic, immunological and environmental factors. Recent studies have implicated pyroptosis, a form of programmed cell death, in the development and progression of vitiligo. Pyroptosis is characterized by the activation of inflammatory caspases, such as caspase-1, leading to cell lysis and the release of inflammatory cytokines. This process has been linked to the melanocytes and other cells within local microenvironment, as well as immune response observed in vitiligo, This review explores the mechanisms underlying pyroptosis and its implications for the physiological alterations in melanocytes and keratinocytes during vitiligo pathogenesis. Furthermore, we also summaries the crosstalk between pyroptosis and other pathogenic mechanisms in vitiligo. These findings not only enhance our understanding of melanocyte death but also suggest novel therapeutic targets for vitiligo.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103081"},"PeriodicalIF":2.5,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144867116","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":"Bee venom alleviates isoproterenol-induced cardiac hypertrophy via JAK2/NF-κB signaling cascade","authors":"Peiying Shi ,&nbsp;Shuo Han ,&nbsp;Yang Sun,&nbsp;Mengmeng Li,&nbsp;Xueling Xu","doi":"10.1016/j.tice.2025.103077","DOIUrl":"10.1016/j.tice.2025.103077","url":null,"abstract":"<div><div>Pathological cardiac hypertrophy (CH) often progresses towards heart failure, which presents a serious threat to global public health security. Fortunately, peptides from animal venoms have emerged as potential drugs for the therapeutic care of cardiovascular diseases. This paper aims to investigate the therapeutic potentials and mechanism of bee venom (BV) using isoproterenol (ISO)-induced CH models <em>in vivo</em> and <em>in vitro</em>. Melittin was identified as the dominant component in air-dried BV using UPLC-Q/TOF-MS, and subsequently it confirmed that BV prevented electrocardiogram and echocardiography abnormalities, and attenuated morphological and histopathological alterations of hypertrophic hearts in mice. Mechanistically, through network pharmacology exploration, angiotensin-converting enzyme (ACE) and renin (REN) were predicted as the key targets of melittin against CH. This was further confirmed by the <em>in vitro</em> experimental results that BV significantly downregulated the protein or mRNA expression levels of CH markers (β-MHC, ANP, BNP), ACE, and IL-1β in ISO-induced hypertrophic cardiomyocytes. Furthermore, it was ascertained that BV inhibited JAK2/NF-κB signaling cascade via decreasing the protein expression ratio of p-JAK2/JAK2 and the protein expression level of NF-κB. This study showed that BV alleviated ISO-induced CH <em>in vivo</em> and <em>in vitro</em> via JAK2/NF-κB signaling cascade, providing a basis for treating CH with BV or melittin.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103077"},"PeriodicalIF":2.5,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144828228","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":"LARS1 knockdown suppresses the biological activities of thyroid cancer cells by stimulating autophagy","authors":"Congwen Jin,&nbsp;Chuanhong Li,&nbsp;Linlin Chen,&nbsp;Hao Liu,&nbsp;Yousheng Yu,&nbsp;Benxin Chen","doi":"10.1016/j.tice.2025.103075","DOIUrl":"10.1016/j.tice.2025.103075","url":null,"abstract":"<div><h3>Background</h3><div>Given the elevated prevalence of thyroid cancer in China and its status as the leading malignant endocrine tumor, identifying molecular targets for intervention is critical. This study sought to define the functional significance of LARS1 in thyroid cancer pathogenesis and delineate the mechanistic pathways involved.</div></div><div><h3>Materials and methods</h3><div>We measured LARS1 protein expression in adjacent normal and cancer tissues using immunohistochemistry. First, we knocked down LARS1 in CAL-62 and 8305 C cell lines using si-LARS1 and then inhibited autophagy using an mTOR agonist. Second, we measured cell proliferation, apoptosis rate, invasion, migration and ultrastructure using CCK-8 assay, EdU assay, flow cytometry, TUNEL staining, Transwell assay, wound healing assay and transmission electron microscopy, LC3B protein levels were evaluated by IF staining. <em>ATG7, beclin1, P62</em> and <em>TIM23</em> gene expression levels were measured by RT-qPCR; and LC3, ATG7, beclin1, P62 and TIM23 protein expression levels were assessed by western blot.</div></div><div><h3>Results</h3><div>Elevated LARS1 protein expression was consistently observed in tumor specimens relative to normal counterparts (P &lt; 0.001). Depletion of LARS1 expression resulted in a pronounced attenuation of cellular proliferation concurrent with a substantial elevation in apoptotic rates. Furthermore, the capacities of cancer cells for invasion and migration were markedly impaired following LARS1 knockdown (P &lt; 0.001). This manipulation also led to significant enhancements in the expression levels of both the protein and mRNA encoding ATG7 and beclin1, while diminishing the levels of TIM23 and P62. A concomitant increase in the LC3-II to LC3-I ratio was also documented. Notably, the tumor-suppressive outcomes elicited by si-LARS1 were counteracted upon administration of an mTOR agonist.</div></div><div><h3>Conclusion</h3><div>LARS1 knockdown suppressed thyroid cancer cell abilities by regulating autophagy activation through mTOR inhibition <em>in vitro</em>.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103075"},"PeriodicalIF":2.5,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144827370","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 White Pekin Duck's (Anas platyrhynchos) Liver: New perspectives on its anatomical gross, casting, and histological features","authors":"Zeinab K. Aboghanima ,&nbsp;Ashraf El Sharaby ,&nbsp;Asmaa Aboelnour ,&nbsp;Mohamed M.A. Abumandour ,&nbsp;Ahmed G. Nomir","doi":"10.1016/j.tice.2025.103073","DOIUrl":"10.1016/j.tice.2025.103073","url":null,"abstract":"<div><div>The study aimed to analyze the anatomical gross and casting, correlation analysis of the liver dimensions, and histological features of the white Pekin duck’s liver. The casting technique is the first to accurately describe the hepatic veins, portal hepatic veins, and intrahepatic arteries. The liver had two triangular lobes, with the right being larger and featuring a dorsal process on the left lobe, cranio-dorsal and caudo-dorsal processes on the right lobe, and the porta hepatis on the visceral surface. Blood is collected from the body’s caudal part through the caudal vena cava and passes through the cranio-dorsal part of the right lobe. The venous drainage of the hepatic parenchyma is through the right, left, and middle hepatic veins. The hepatic portal venous system was composed of two hepatic portal veins (left and right); the larger right one entered through the right portal fissure, passing through the intrahepatic parenchyma, while the left one entered through the left portal fissure. Hepatic arteries enter through two right and three small left hepatic arteries. The dorsal right hepatic artery originated from the right branch of the celiac artery, while the ventral one originated from the pancreaticoduodenal artery. The left hepatic arteries originate from the ventral gastric artery. Liver parenchyma was enclosed by a thin CT capsule with poorly defined lobules, consisting of hepatocytes in uneven plates. Hepatocyte plates contained a single layer of thick cells, with large Kupffer cells in the irregular parenchyma. All hepatic apparatus had a positive PAS reaction and moderately reacted to Masson’s trichrome stains, especially at the portal region and hepatic capsule, and the reticular fibers appeared mainly around the portal triad by Gomori stain.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103073"},"PeriodicalIF":2.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144827369","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":"Effect of dietary L-arginine supplementation on the expression of vascular endothelial growth factor A, its receptors, and nitric oxide system components in the pancreas of streptozotocin-induced diabetic rats","authors":"Duygu Yaman Gram ,&nbsp;Meryem Şentürk ,&nbsp;Gonca Kamacı Özocak ,&nbsp;Nesrin Delibaşı Doğan ,&nbsp;Görkem Ekebaş ,&nbsp;Ayhan Atasever ,&nbsp;Meryem Eren","doi":"10.1016/j.tice.2025.103072","DOIUrl":"10.1016/j.tice.2025.103072","url":null,"abstract":"<div><div>T1DM is characterized by elevated blood glucose levels, insulin insufficiency, and alterations in vessel formation. Therefore, the expression of insulin, active caspase-3, inflammatory factors such as TNF-α and NF-κB, and components of the NO and VEGFA systems were investigated in the pancreas of STZ-induced diabetic rats. Blood glucose levels and body weight were also measured. Additionally, the effects of L-arginine supplementation on the same parameters were evaluated. The body weight of the STZ and STZ + L-arginine groups was lower than that of the control and L-arginine groups. L-arginine supplementation reduced blood glucose levels and increased insulin levels in diabetic rats. Degenerative changes in β-cells were observed in the pancreas of the diabetic group. Insulin expression was low in the STZ-group, while it was higher in the STZ + L-arginine group. VEGFA was localized in the islets, epithelial cells of glands, tubules, and endothelial cells in both the control and L-arginine groups. A similar localization pattern was observed for VEGFA in the STZ and STZ + L-arginine groups. Expression of eNOS and VEGFR2/FLK1/KDR was detected in the islets of the control and L-arginine groups. Their expression was low in the STZ and STZ + L-arginine groups. However, VEGFR2/FLK1/KDR signal intensity was stronger in STZ + L-arginine group than in the STZ group. The expression levels of iNOS, active caspase-3, TNF-α, and NF-κB were significantly higher in STZ group than in the control group.</div><div>In conclusion, although L-arginine treatment reversed STZ-induced hyperglycemia and insulin deficiency, it did not exert a significant effect on the expression levels of iNOS, active caspase-3, TNF-α, or NF-κB. Additionally, L-arginine appears essential for islet vessel maintenance by increasing VEGFR2/FLK1/KDR expression.</div></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"97 ","pages":"Article 103072"},"PeriodicalIF":2.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144861008","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":"Altered lung inflammation and expression of endoplasmic reticulum stress markers in male mice aged-asthma model.","authors":"Farshad Armin, Hamdollah Panahpour, Ramin Salimnejad, Hakimeh Saadati, Ali Abedi, Mohammad Reza Aslani","doi":"10.1016/j.tice.2025.102938","DOIUrl":"https://doi.org/10.1016/j.tice.2025.102938","url":null,"abstract":"<p><p>Although there is a strong correlation between aging and asthma pathophysiology, the underlying mechanism has not been fully elucidated. The endoplasmic reticulum (ER) has been demonstrated to be a crucial intracellular organelle involved in the pathogenesis of numerous diseases. The aim of the current study was to investigate ER stress markers in the lung tissue of aged ovalbumin (OVA)-sensitized mice. Male BALB/C mice were randomly divided into the following four groups (10 in each): 1) control, 2) OVA-sensitized (OVA), 3) D-galactose-induced aging (D-gal), and 4) OVA-sensitized associated with D-galactose-induced aging (OVA+D-gal). Total WBCs and differential cells were counted using the bronchoalveolar lavage (BAL) fluid. Lung tissue was analyzed for ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) through Real Time-PCR technique as well as histopathological assessment. The data indicated a significant increase in both total WBCs and differential cells within the OVA, D-gal, and OVA+D-gal groups when compared to the control group, particularly evident in the OVA+D-gal group. Also, the results showed that the increased expression of ER stress markers (ATF4, ATF6, GRP78, CHOP, and XBP1) was significantly higher in the OVA, D-gal, and OVA+D-gal groups than in the control group. Interestingly, the increased expression of CHOP, ATF4, and XBP1 was observed in the OVA+D-gal group more than in other groups. In aged OVA-sensitized mice, the findings revealed a maladaptive ER stress response in their lung tissue, characterized by elevated levels of CHOP, ATF4, and XBP1 expression.</p>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"95 ","pages":"102938"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050074","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}