Histology and histopathology, Vol.41, Nº5, (2026)
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- PublicationOpen AccessTargeting thrombin with hirudin alleviates paraquat-induced pulmonary fibrosis via the PAR-1-mediated TGF-β1 pathway(2026) Weijuan Liu; Guowen Zheng; Zhaojun Song; Zike Zhang; Xiao Hu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Paraquat (PQ)-induced pulmonary fibrosis (PF) is a serious disease without specific antidotes. Thrombin is important for promoting fibrosis development. We aimed to explore whether thrombin promotes PQ-induced PF by activating the protease-activated receptor-1 (PAR-1)-mediated transforming growth factor-β1 (TGF-β1) pathway. Methods. Male Sprague Dawley rats received PQ treatment, either alone or with thrombin or hirudin (a thrombin inhibitor) (n=9 in the control, model, thrombin, and hirudin groups). After 7 or 14 days of treatment, oxidative stress (OS) indicators and histopathological damage in the lungs were detected. PF degree was evaluated using Masson staining and hydroxyproline levels in lung tissues and collagen levels in bronchoalveolar lavage fluid. Furthermore, type I collagen (Col-1), TGF-β1, and PAR-1 expression, as well as extracellular signal-regulated kinase 1/2 (ERK1/2) and mothers against decapentaplegic homolog 3 (Smad3) phosphorylation in the lungs, were assessed. To investigate the mechanism of thrombin on PQ induced PF, rats treated with PQ and thrombin further received SCH79797 (a PAR-1 inhibitor) alone or combined with SRI-011381 (a TGF-β agonist) (n=9 in the thrombin+SCH79797 and thrombin+SCH79797+ SRI-011381 groups). In addition to Masson staining and detection of the above-mentioned genes and proteins, alpha-smooth muscle actin (α-SMA), TGFβ receptor type I (TβRI), and type II (TβRII) expression in the lungs were also detected. Results. Both 7 and 14 days of thrombin treatment triggered OS, exacerbated lung histopathological damage, and promoted PF in PQ-stimulated rats. Furthermore, thrombin upregulated Col-1, TGF-β1, and PAR-1 expression as well as ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats. However, hirudin produced the opposite results. Additionally, the role of thrombin in promoting PF, increasing Col-1, TGF-β1, α SMA, PAR-1, TβRI, and TβRII expression and ERK1/2 and Smad3 phosphorylation in PQ-stimulated rats was reversed by SCH79797, while the inhibitory effects of SCH79797 were counteracted by SRI-011381. Conclusions. Thrombin may promote PQ-induced PF by activating PAR-1-mediated TGF-β1, suggesting that PAR-1-mediated TGF-β1 is a potential target for preventing PQ-induced PF.
- PublicationOpen AccessCardioprotective mechanisms of Jiangfu Decoction against myocardial ischemia may involve regulation of the AMPK/PINK1/ Parkin mitochondrial autophagy pathway(2026) Yiwei Hao; Chen Li; Haoying Li; Xue Han; Hefei Wang; Xi Chu; Zhiwei Su; Shijiang Sun; Yawei Zhao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Jiangfu Decoction (JFD) is a classical traditional herbal medicine used to clinically treat ischemic heart disease (IHD). Nonetheless, the influence of JFD on myocardial ischemia (MI), along with its precise underlying mechanism, is still unclear. The objective of this research was to investigate the potential mechanisms by which JFD exerts cardio protective effects on MI induced by isoproterenol (ISO). Methods. An acute MI model was established by subcutaneous injection of ISO (85 mg/kg/d). To evaluate alterations in myocardial structure, electrocardiogram recordings and heart histology examinations were employed. The myocardial ultrastructure was observed by transmission electron microscopy (TEM). Using specific kits, the levels and activities of oxidative stress markers as well as inflammatory cytokines were separately assessed. Western blotting was employed to assess the expression levels of proteins related to adenosine monophosphate activated protein kinase (AMPK), PTEN-induced putative kinase 1 (PINK1), Parkin, Nod-like receptor protein 3 (NLRP3), and Caspase-1. Results. The findings show that JFD treatments markedly diminished heart rate, pathological alterations in cardiac tissue, chondriosome injury, and serum concentrations of creatine kinase, creatine kinasemyocardial band, lactate dehydrogenase, malon dialdehyde, interleukin-1β, and interleukin-18. Concurrently, these treatments augmented the activation of superoxide dismutase, catalase, and glutathione peroxidase in the serum of animals subjected to ISO treatment. Additionally, JFD also reversed the ISO induced changes in the levels of AMPK, PINK1, Parkin, NLRP3, and Caspase-1. Conclusion. JFD exhibits a notable safeguarding influence on MI via a mechanism that involves regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway, inhibition of pyroptosis, and reduction of oxidative stress and inflammation.
- PublicationOpen AccessMorphological evidence of telocytes in DHEA-induced polycystic ovary syndrome model(2026) Mehmet Yüncü; Yurdun Kuyucu; Esma İşçel; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaPolycystic Ovary Syndrome (PCOS) is a condition causing histopathological alterations in the ovarian stroma. Telocytes (TCs) are specialized interstitial/stromal cells present in the connective tissue of various organs. In this study, we investigated the presence and spatial organization of TCs in the ovaries of a rat model of PCOS induced by dehydro epiandrosterone (DHEA). The ovarian tissues from both PCOS and control groups were stained using hematoxylin-eosin (H&E), Bielschowsky's silver stain, methylene blue, and toluidine blue for light microscopy analysis, and scanned digitally. Ovaries were marked with double-labeled immunofluorescence with CD34/estrogen receptor-α (ER-α) and vimentin/ progesterone receptor-A (PR-A) and evaluated with a confocal microscope. The ultrastructure and telopodes (TPs) of TCs were also examined by transmission electron microscopy. TCs were identified in both groups, localized within follicular walls, adjacent to follicles, in stromal regions distant from the follicles, and perivascular areas. CD34/ER-α and vimentin/PR-A cells were significantly increased in PCOS. In conclusion, TCs were preserved in the DHEA-induced PCOS model, and according to our quantitative analysis, their ultrastructural features were unaffected by the PCOS microenvironment. Our findings suggest a potential association between TCs and the pathophysiology of PCOS. Further studies are necessary to elucidate the functional relationship of TCs in the development and progression of PCOS.
- PublicationOpen AccessRole of connexin 43 in odontogenesis and odontogenic tumors(2026) Ronell Bologna Molina; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaConnexin 43 (Cx43) is a transmembrane protein forming gap junctions essential for intercellular communication, regulating ion and molecule exchange, and coordinating key developmental and pathological processes. In odontogenesis, Cx43 expression in ameloblasts and odontoblasts orchestrates differentiation, mineralization, and tissue repair. Its dynamic regulation influences enamel and dentin formation, while altered expression is linked to defective tooth development. Beyond dental tissues, Cx43 participates in craniofacial morphogenesis and bone remodeling. In odontogenic tumors, Cx43 shows heterogeneous expression patterns, reflecting its role in tumor architecture, differentiation, and aggressiveness. High mesenchymal expression is seen in ameloblastic fibromas and fibro-odontomas, whereas follicular ameloblastomas and odontogenic keratocysts exhibit downregulation, particularly in basal cells, correlating with increased proliferation, anti apoptosis, and autophagy markers. These variations in odontogenic tumors suggest that Cx43 may act as a tumor suppressor by maintaining epithelial organization and regulating cell polarity. Molecularly, Cx43 interacts with MAPK/ERK, PI3K/AKT, and Wnt/β-catenin pathways, influencing cell cycle control, apoptosis, and epithelial-mesenchymal interactions. Loss of Cx43 disrupts gap junctional intercellular communication, potentially enhancing tumor progression. Therapeutically, modulating Cx43 could inhibit tumor angiogenesis, restore normal growth control, and promote differentiation toward less aggressive phenotypes. However, given its dual role in tumor suppression and tissue repair, targeted interventions must be context specific. Cx43 emerges as a promising diagnostic, prognostic, and therapeutic biomarker in different neoplasias, warranting further investigation to optimize clinical applications. The objective of this work is to review current information on the role of CX43 in normal tissue and odontogenic tumors to evaluate its possible usefulness as a future therapeutic target.
- PublicationOpen AccessHistologic evaluation of the effect of grape seed oil and ferric sulfate in pulpotomy applied to molar teeth of rats: An in vivo study(2026) Günay Yapici Yavuz; Ebru Elibol Annaç; Aydın Keskinrüzgar; Muhammed Baybatmaz; İlknur Öz; Mesut Tozar; Osman Küçükkelepçe; Kamile Nur Tozar; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. The objective of this study was to examine the healing potential of Grape Seed Oil (GSO) on the pulp tissue that remains following pulpotomy treatment. Materials and Methods. The upper first molars of 18 two-month-old male Wistar albino rats were divided into two groups according to the material used in pulpotomy treatment. In the pulpotomy treatment group, GSO was used, while ferric sulfate (FS) was used in the control group. The rats were euthanized at 24 hours, 15 days, and 30 days following treatment. Histopathological evaluation of the samples was conducted using the hematoxylin-eosin staining method. The evaluation was conducted to ascertain alterations in connective tissue, vascular changes (i.e., angiopathic findings), inflammation, and hemorrhagic findings in the pulp. The data obtained in this study were analyzed with the IBM SPSS Statistics Version 21 software program. Results. In the present study, it was observed that the inflammatory response in the GSO group was higher than that in the FS group at 24 hours. The investigation revealed that the vascular response exhibited a higher magnitude in the GSO group compared to the FS group at 24 hours and at day 15. However, this response exhibited a decline at day 30. Despite an increase in hemorrhaging on the 15th day in the GSO group, this phenomenon decreased over time. Conclusions. It has been observed that GSO is a biocompatible material that can be used as an alternative to FS in pulpotomy treatment.
- PublicationOpen AccessCrumbs3: Expression and biological significance in normal and neoplastic tissues(2026) Akane Kitta-Kunihiro; Chiemi Ikude; Eisaku Kondo; Hidekazu Iioka; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaCellular polarity plays a fundamental role in tissue organization and homeostasis, and its disruption is closely linked to tumorigenesis. Crumbs3 (CRB3), a conserved polarity protein, is essential for epithelial morphogenesis, tight-junction formation, and barrier function. This review summarizes current knowledge regarding CRB3 expression in normal and malignant human tissues and its dual roles in cancer progression. Systematic immunohistochemical analyses revealed strong CRB3 expression in non-neoplastic glandular epithelia of the gastrointestinal, hepato-pancreato-biliary, renal, and respiratory tracts, as well as in fetal tissues, suggesting its importance in organ development and maintenance. In neoplastic tissues, represented by colorectal adenocarcinoma and oral squamous cell carcinoma, CRB3 expression is preserved or even enhanced compared with normal tissues, which promotes tumor cell migration, triggering invasion/ metastasis as well as cellular proliferation through signaling pathways involving FGFR and RhoA activation. Conversely, previous studies reported that CRB3 functions as a tumor suppressor, based on findings that CRB3 expression induces loss of epithelial mesenchymal transition, whereas loss of CRB3 expression attenuates the integrity of tight junctions, resulting in significantly poorer prognosis in certain cancers. Current data thus suggest that the biological role of CRB3 in tumors is complex. Whether CRB3 acts as a tumor accelerator or suppressor may depend on the individual-specific, unique characteristics of tumor cells. Understanding these dual functions may contribute to the development of novel polarity-targeted therapeutic strategies for cancers of differing origin.
- PublicationOpen AccessUnraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach(2026) Shihui Liu; Hejing Ruan; Yuzhe Cheng; Yan Qiao; Jiawei Wang; Xiaojun Liu; Chuanmiao Liu; Wen Zhao; Siyuan Wang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. This study aimed to identify key molecules that potentially mediate the mechanisms by which YAP deletion or inhibition attenuates liver fibrosis. Materials and Methods. C57BL/6 mice were divided into four groups: control, carbon tetrachloride (CCl4), CCl4-YAP-HKO, and CCl4-verteporfin (VP). RNA sequencing (RNA-seq) and proteomic analysis were conducted. Immunohistochemistry and western blotting were also performed to verify the differentially expressed genes (DEGs) identified through the multi omics approach. Human subjects were enrolled to further assess the identified DEGs. Results. In comparison with the CCl4 group, both the CCl4-YAP-HKO and CCl4-VP groups exhibited liver fibrosis regression. RNA-seq and proteomic analyses identified 12 commonly differentially expressed molecules. Immunohistochemistry and western blotting validated that heat shock protein 27 (HSP27), heat shock protein 70 (HSP70), and p62 expression were significantly reduced, and milk fat globule-epidermal growth factor 8 (MFGE8) expression was elevated in both the CCl4-YAP-HKO and CCl4-VP groups compared with the CCl4 group. Furthermore, plasma p62, HSP27, and HSP70 levels were increased with the occurrence of chronic hepatitis B and HBV-related cirrhosis, whereas MFGE8 levels were decreased. Spearman’s correlation analysis further illustrated a significant association between these biomarkers and YAP levels. Conclusions. This study identified HSP27, HSP70, p62, and MFGE8 as crucial YAP-related molecules involved in liver fibrosis.
- PublicationOpen AccessA clinicopathological study of eight cases presenting a biphasic structure: A distinct variant of pulmonary carcinoma(2026) Qiuyao Li; Jiwei Ma; Kun Yang; Xiaoyan Lin; Huifeng Jiang; Yali Xu; Lin Song; Yu Zhang; Xiaoqian Liu; Zheng Mou; Wenjing Su; Hongyu Wang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBiphasic structures, which are composed of outer basal cells and inner glandular cells, are frequently indicative of salivary gland-type tumors or benign lesions, such as bronchial adenoma, within the lung. However, the occurrence of a biphasic structure in lung cancer is rarely reported and can lead to significant challenges and confusion in diagnosis, particularly in biopsy specimens. In our study, we collected eight lung epithelial tumors that presented with a distinct biphasic structure component and examined their clinicopathological characteristics. Histological examination revealed that the biphasic structure component, often intermingled with conventional squamous cell carcinoma or adeno carcinoma, was defined by basal cells encircling the glandular epithelium. Immunohistochemical analysis demonstrated a distinctive peripheral p40 staining pattern in the biphasic structure component. Genetic analysis identified driver mutations in seven out of eight patients, which are typically associated with conventional pulmonary adenocarcinomas, including EGFR L858R, EGFR 19-del, EGFR 20-ins, and KRAS mutations. The presence of biphasic structure components in these cases confirms a genuine form of lung cancer, likely representing a variant of lung adenocarcinoma. This study's findings enhance the understanding of lung cancer's morphological diversity and caution against prematurely dismissing the malignancy potential of pulmonary epithelial lesions based solely on the presence of basal cells, especially with biopsy specimens.
- PublicationOpen AccessElectroacupuncture ameliorates learning and memory impairment by inhibiting inflammation and promoting synaptic plasticity via inhibition of the NF-KB/NLRP3 signaling pathway in cerebral ischemic rats(2026) Guoyuan Pan; Dan Lu1; Mingjin Zhu; Guifen Yang; Chenyi Huang; Yisu Shou; Xiong Jiangnan; Fang Luo; Sun Di; Chuchu Huang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaObjective. Electroacupuncture (EA) has a protective effect on cerebral ischemic injury. However, the specific mechanism of action of EA has not been studied. In this study, we investigated whether EA was involved in the treatment of learning and memory impairment in rats with cerebral ischemia‒reperfusion injury (CIRI) through the NF-KB/NLRP3 signaling pathway. Methods. Ninety-five male Sprague–Dawley (SD) rats were randomly divided into five groups, each consisting of 19 rats. A rat model of cerebral ischemia was established using transient middle cerebral artery occlusion (tMCAO) combined with cerebral blood flow monitoring. Intervention treatments consisted of electroacupuncture and lipopolysaccharide (an NF-κB agonist) injection. The behavior, spatial learning, and memory ability of the rats were evaluated with the Morris water maze method. The degree of brain injury in the rats was observed via triphenyl tetrazolium chloride (TTC), hematoxylin-eosin (H&E), and Fluoro-Jade B (FJB) staining. The expression levels of proteins related to the inflammatory response, pyroptosis, and synaptic plasticity were determined via western blotting and immunofluorescence staining. Changes in dendrites and spines were observed via Golgi-Cox staining. Results. Compared with those of the tMCAO group, the neural function scores and escape latency of the EA+tMCAO group were reduced. The cerebral infarct volume and the number of denatured neurons decreased. NF-κB, caspase-1, NLRP3, and IL-18 expression levels were significantly decreased. PSD95, SYP, and BDNF expression levels were significantly increased. The total number of dendrite junctions and the total length of dendrites increased. Compared with the EA+tMCAO and NS+EA+tMCAO groups, the escape latency in the lipopolysaccharide (LPS)+EA+tMCAO group was significantly increased. NF-κB, IL-18, and cleaved caspase-1 expression levels were elevated. Conclusion. EA may inhibit NF-κB/NLRP3 pathway proteins; regulate the neuroinflammatory response; promote the expression of PSD-95, SYN, and BDNF; improve the structure of dendrites and dendritic spines; and alleviate cognitive impairment in rats with CIRI.
- PublicationOpen AccessUCHL1 enhances TSC1 transcription by stabilizing FOXO1 through deubiquitination in knee osteoarthritis(2026) Jiawei Lu; Chonghao Gu; Zikang Xie; Zhongyu Xia; Bingqing Guo; Tao Jiang; Yu Wang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaFerroptosis has been shown to play a significant role in the pathophysiological progression of knee osteoarthritis (KOA). In this study, we sought to investigate the biological role of Ubiquitin C-terminal hydrolase 1 (UCHL1) in KOA and elucidate its underlying molecular mechanisms. An in vitro KOA cell model was established by stimulating C28/I2 chondrocytes with IL-1β, and UCHL1 expression was decreased in IL-1β-treated chondrocytes. Notably, overexpression of UCHL1 significantly alleviated IL-1β induced ferroptosis and extracellular matrix (ECM) degradation. Mechanistically, UCHL1 facilitated the deubiquitination and stabilization of FOXO1. Knockdown of FOXO1 partially reversed the inhibitory effects of UCHL1 on ferroptosis and ECM degradation. Furthermore, FOXO1 was found to bind to the Tuberous Sclerosis Complex 1 (TSC1) promoter, enhancing TSC1 transcription. Intriguingly, knockdown of FOXO1 counteracted the inhibitory effects of UCHL1 overexpression on ferroptosis and ECM degradation, while these effects were rescued by TSC1 overe xpression. In vivo experiments demonstrated that UCHL1 alleviated cartilage damage in KOA rats by inhibiting ferroptosis and ECM degradation through the FOXO1/TSC1 axis. These findings demonstrate the pivotal role of UCHL1 in regulating ferroptosis and maintaining ECM homeostasis, offering novel insights into the molecular mechanisms driving KOA progression.
- PublicationOpen AccessIntermittent fasting-induced autophagy normalization confers hepatic protection in metabolic dysfunction-associated fatty liver disease: Mechanistic insights and implications(2026) Gehan El-Akabawy; MoezAlIslam E. Faris; Manoj B. Menon; Mohamed Abdel Wahab; Farida Hussan; Mohd Hazim Bin Zulkaflee; Nabil Eid; Payal Bhatnagar; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaMetabolic dysfunction-associated fatty liver disease (MAFLD) is a chronic liver condition that can progress to steatohepatitis, cirrhosis, and even liver cancer. Macroautophagy (hereinafter referred to as autophagy) is a pro-survival mechanism that facilitates the lysosomal clearance of damaged organelles, abnormal proteins, and excess lipids. A growing body of evidence indicates that autophagy dysfunction and reduced autophagic flux play critical roles in the pathogenesis of MAFLD. Therefore, restoring autophagy in MAFLD may help reduce steatosis and prevent disease progression. Intermittent fasting (IF), involving periods of restricted to no food intake alternating with periods of regulated/free eating, has been demonstrated to have beneficial effects on body composition, glucose regulation, lipid profiles, and liver function in studies involving both animal models of MAFLD and human subjects. Studies involving individuals with obesity and MAFLD have shown that Ramadan intermittent fasting (RIF), an Islamic religious practice that involves abstaining from food and water intake from sunrise to sunset over approximately 30 consecutive days, significantly reduces body weight, BMI, fat mass, and inflammatory markers while improving liver function and steatosis. The hepatoprotective effects of RIF are associated with the enhanced expression of autophagy-related genes and the restoration of autophagic flux. This upregulation of autophagy as a result of RIF makes it a potentially promising therapeutic strategy for MAFLD. This review summarizes various forms of IF, the mechanisms of autophagy, and evidence of autophagy dysfunction in MAFLD. It also explores how IF, specifically RIF, may normalize autophagy, reduce hepatic steatosis, and improve liver function in human subjects.
- PublicationOpen AccessOcular adnexal lymphomas: A comprehensive review with emphasis on histopathologic and magnetic resonance imaging appearance(2026) Carlotta Scavone; Renato Farina; Corrado Inì; Francesco Tiralongo; Davide Castiglione; Federica Cosentino; Maria Chiara Lo Greco; Stefano Palmucci; Corrado Spatola; Emanuele David; Giuseppe Broggi; Serena Salzano; Rosario Caltabiano; Gabriele Caputo; Salvatore Ascanio; Andrea Russo; Matteo Fallico; Antonio Longo; Antonio Basile; Pietro Valerio Foti; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaOcular adnexal lymphomas (OALs) are a heterogeneous group of malignant lymphoproliferative tumors originating from clonal proliferations of lymphocytes, with a multifactorial etiopathogenesis. They can be distinguished in primary, involving ocular adnexa, and secondary, affecting also an additional site. Pathologically OALs encompass four histological subtypes with different biological behaviour and prognosis. The diagnosis relies on clinical manifestations, imaging and histopathological examinations. Clinical symptoms are classified in ophthalmologic, often nonspecific, and constitutional, indicating a systemic involvement. As regards cross-sectional imaging, computed tomography (CT) and magnetic resonance imaging (MRI) play a complementary role, nevertheless MRI outperforms other imaging methods due to the possibility to perform functional techniques such as diffusion-weighted imaging (DWI) and perfusion weighted imaging (PWI). At conventional MRI, OALs demonstrate iso- or hypointensity on T1-weighted and T2-weighted sequences relative to cerebral cortex; enhancement is usually homogeneous. PWI and particularly DWI can be useful in discriminating OALs from benign orbital lymphoproliferative disorders (OLPDs) and from other malignant intraorbital tumors, since OALs, due to their high cellularity, demonstrate diffusion restriction with considerably low apparent diffusion coefficient value. Biopsy is needed for final diagnosis and accurate subtyping and grading. Differential diagnosis of OALs, in addition to benign OLPDs, includes granulomatous diseases, metabolic diseases, epithelial neoplasms and metastases. Structured report can be useful to make reporting of imaging findings more accurate and to improve communication between ophthalmologist and radiologist; moreover, it can represent a valuable decision supporting tool to assist the multidisciplinary management of the disease. Treatment options include systemic chemotherapy, radiotherapy, immunotherapy and surgical excision.
- PublicationOpen AccessPIP5K3 upregulation correlates with unfavorable prognosis in patients with nasopharyngeal carcinoma(2026) Hung-Chang Wu; Ching-Chieh Yang; Yun-Tzu Lin; Chien-Feng Li; Shih-Lun Chang; Yu-Hsuan Kuo; Szu-Chi Yao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Nasopharyngeal carcinoma (NPC) is prevalent in East and Southeast Asia, with metastasis and recurrence leading to poor prognosis. Identifying prognostic biomarkers is essential. Methods. We analyzed differentially expressed genes involved in the phosphatidylinositol metabolic process (GO: 0046488) and tumorigenesis (GSE12452) in NPC. Associations between PIP5K3 expression and clinicopathological features were assessed using chi square tests and Cox proportional hazards models. Results. PIP5K3 was significantly upregulated in NPC tissues, correlating with advanced stage (p=0.001) and nodal metastasis (p<0.001). High PIP5K3 expression was associated with worse disease-specific survival (DSS), distant metastasis-free survival (DMeFS), and local recurrence-free survival (LRFS). Multivariate analysis confirmed its association with poor prognosis (DSS: HR=4.321, DMeFS: HR=2.883, LRFS: HR=2.249; all p<0.001). Conclusions. PIP5K3 upregulation is associated with unfavorable clinical outcomes in NPC and may serve as a novel prognostic biomarker and potential therapeutic target.
- PublicationOpen AccessElp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion(2026) Hao Shang; Xiali Shi; Hanmei Jiang; Ji Di; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Gastric cancer (GC) seriously affects the life and health of patients, and the role of Elp3 in GC is still unclear; therefore, the aim of this study was to investigate the role and mechanism of Elp3 overexpression in GC. Methods. Elp3-overexpressing HGC27 cells were constructed with an overexpression plasmid, and Elp3 overexpressing GC nude mice were prepared, which were intervened by histone acetylation inhibitor (SAHA) or JNK pathway inhibitor (SP600125). The protein interactions between Elp3 and JNK1 were verified by Co-immunoprecipitation (Co-IP) assay. Cell prolifera tion, migration, invasion, JNK/MAPK pathway, and histopathological changes were evaluated with CCK-8, clone formation assay, scratch assay, Transwell, qRT PCR, western blot, and HE staining. Results. Elp3 interacted with JNK1 protein, and Elp3 overexpression promoted GC proliferation, invasion, migration, elevated HAT activity, and activation of the JNK/MAPK pathway. A histone acetylation inhibitor attenuated the promotional effect of Elp3 overexpression on GC and activation of the JNK/MAPK pathway. Further, inhibition of the JNK/MAPK pathway also suppressed the promotion of GC by Elp3 overexpression. Conclusion. Elp3 may be involved in GC progression by activating the JNK/MAPK pathway through histone acetylation.
- PublicationOpen AccessNovoMem® vs CorMatrix®: Decellularisation efficiency and extracellular matrix integrity for future vascular grafting(2026) Jun Wei Heng; Shalini Rajan; Nur Sabrina Zainal Abidin; Ng Min Hwei1; Nadiah Sulaiman; Ahmad Hafiz Murtadha; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaNovoMem®, a collagen membrane derived from supercritical carbon dioxide (scCO2) decellularised porcine pericardium, is currently used as a barrier in dental bone grafts. In line with sustainable development goals, repurposing NovoMem® for vascular grafts presents a strategic opportunity. This study aims to evaluate NovoMem®'s decellularisation efficiency and extracellular matrix (ECM) preservation to assess its potential for vascular tissue engineering. The decellularisation efficiency was assessed using haematoxylin and eosin (H&E) staining and DNA quantification to confirm cellular removal and fulfilment of the proposed minimal criteria of decellularisation. ECM integrity was evaluated through collagen staining (Picrosirius red), elastin staining (Elastin van Gieson), and an insoluble collagen assay to measure total collagen. NovoMem® showed significantly reduced cellular content while preserving ECM architecture. The decellularised tissue had minimal residual DNA and retained its collagen framework. Compared with CorMatrix®, a commercially available chemically decellularised cardiac patch from porcine small intestinal submucosa (SIS) that has been repurposed for vascular grafts, NovoMem® exhibited superior decellularisation efficiency with comparable ECM preservation. NovoMem® also possesses biocompatibility, supporting mesenchymal stem cell growth. In conclusion, NovoMem® has minimal cellular content with preserved structural integrity, thus suggesting it as an effective vascular graft that could integrate with host tissues with minimal risk of alloreactivity, potentially improving graft efficacy and long-term patency.