Histology and histopathology, Vol.41, Nº6, (2026)
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- PublicationOpen AccessYolkin tempers inflammatory mediator release and liver pathology in experimental endotoxemia in mice(2026) Jolanta Artym; Maja Kocięba; Ewa Zaczyńska; Kaleta-Kuratewicz; Jan P. Madej; Piotr Kuropka; Aleksandra Zambrowicz; Łukasz Bobak; Michał Zimecki; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaYolkin is an egg yolk-derived protein with immunoregulatory properties. In this work, yolkin was evaluated as a protective agent in endotoxemic BALB/c mice. The mice were pretreated with yolkin either orally in drinking water or intraperitoneally (i.p.) before i.p. injection of E. coli lipopolysaccharide (LPS). Circulating blood leukocyte number, blood cell composition, serum levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and haptoglobin, as well as histological changes in the spleen and the liver, were examined. Yolkin differentially regulated the values of these parameters, depending on the administration protocol; however, the serum levels of TNF-α and IL-6 were generally decreased, and the level of haptoglobin, an acute-phase protein, was elevated. The pretreatment of mice with yolkin led to improved histological architecture in the investigated organs of endotoxemic mice, particularly in the liver, where yolkin diminished an increased level of vascular permeability and reversed a decreased number of Kupffer cells. These changes were independent of the route of yolkin administration. In conclusion, yolkin proved effective in the amelioration of pathogenic consequences of LPS administration and may be considered a potential protective measure for patients at risk of endotoxemia. Histol Histopathol
- PublicationOpen AccessDownregulation of PDCD10 mitigates the malignant biological behavior and increases the sensitivity of esophageal squamous cell carcinoma cells to radiotherapy by inhibiting the PI3K/AKT pathway(2026) Qisong Chen; Qing Gao; Junkai Xu; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaThe intensification of radiotherapy is an effective way to improve the therapeutic efficacy of radiation-sensitive malignancies such as esophageal cancer (EC). Esophageal squamous cell carcinoma (ESCC) accounts for 85% of all EC cases worldwide, with a relatively higher incidence and mortality in East Asia. In this study, we explored the functions and mechanisms of programmed cell death 10 (PDCD10) in the malignancy and radiotherapy sensitivity of ESCC cells. We observed that PDCD10 is highly expressed in ESCC tissues and is correlated with a poor prognosis in patients with ESCC. PDCD10 downregulation suppressed ESCC cell proliferation, migration, and invasion but promoted apoptosis. In addition, it enhanced ionizing radiation (IR)-induced ESCC cell damage, whereas PDCD10 overexpression had the opposite effect. Mechanistically, PDCD10 increased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in ESCC cell lines. The administration of LY294002, a PI3K inhibitor, significantly inhibited the oncogenic functions of PDCD10, leading to an increase in IR-induced cell damage. These findings establish PDCD10 as a critical intrinsic regulator of the sensitivity of ESCC cells to IR through the modulation of the PI3K/AKT pathway.
- PublicationOpen AccessMechanism of lncRNA PLACT1 in regulating the proliferation of pancreatic adenocarcinoma cells through the KLF2/KIAA1522 axis(2026) Xiaoli Hou; Shutao Wu; Wei Sun; Yixia Wang; Yasen Cao; Hong Cheng; Fei Wang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Pancreatic adenocarcinoma (PAAD) is among the most common cancers worldwide. This study aims to investigate the role of long noncoding RNA pancreatic cancer-associated transcript 1 (LncRNA PLACT1) in PAAD cell proliferation. Methods. PAAD and normal cells were cultured. The levels of PLACT1, Krüppel-like factor 2 (KLF2), and KIAA1522 were detected. After PLACT1 expression was interfered with, cell proliferation was detected using the cell counting kit-8, clone formation assay, and 5 ethynyl-2-deoxyuridine (EdU) staining. The binding of PLACT1 to euchromatic histone lysine methyl transferase 2 (EHMT2) was analyzed. The enrichment of EHMT2 and histone H3 lysine 9 dimethylation (H3K9me2) on the KLF2 promoter was analyzed by chromatin immunoprecipitation. KLF2 expression was detected after EHMT2 intervention. The binding of KLF2 to the KIAA1522 promoter was analyzed. The nude mouse xenograft model was constructed to detect the role of PLACT1 in vivo. Results. PLACT1 and KIAA1522 were highly expressed, and KLF2 was poorly expressed in PAAD cells. Silencing PLACT1 decreased cell proliferation, the number of cell clones, and EdU-positive cells. Mechanistically, PLACT1 inhibited KLF2 expression by recruiting EHMT2 to induce H3K9me2 in the KLF2 promoter region, resulting in reduced KLF2 enrichment at the KIAA1522 promoter and increased KIAA1522 expression. KLF2 downregulation or KIAA1522 overexpression alleviated the inhibitory effect of PLACT1 silencing on PAAD cell proliferation. PLACT1 silencing prevented PAAD tumorigenesis by regulating the KLF2/KIAA1522 pathway. Conclusion. PLACT1 silencing inhibited PAAD by inhibiting KLF2 and promoting KIAA1522 expression, suggesting the therapeutic effect of PLACT1 silencing on PAAD.
- PublicationOpen Access1,25-Dihydroxyvitamin D3 mitigates high glucose-induced oxidative stress, inflammation, and extracellular matrix accumulation in glomerular mesangial cells via the ROS/TXNIP/NLRP3 pathway(2026) Bo Chen; Chunjiang Zhang; Lin Jia; Xingyu Yao; Gang Liu; Qingyue Meng; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologiaackground. 1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) is a physiologically active form of vitamin D. Our study investigated the renoprotective functions of 1,25(OH)2D3 in diabetic nephropathy (DN) progression and its underlying mechanism targeting the ROS/TXNIP/NLRP3 inflammasome pathway. Methods. DN was induced in Wistar rats via high-fat diet (4 weeks) and streptozotocin injection (30 mg/kg, i.p.); hyperglycemic rats were randomized into DN and DN + 1,25(OH)2D3 (16 μg/kg, 12 weeks) groups. Rat mesangial HBZY-1 cells were maintained under normal glucose (5.5 mM), high glucose (25 mM), high glucose plus 1,25(OH)2D3 (1-50 nM), or high glucose plus N acetylcysteine (NAC, 10 mM). Cell viability was assessed by the CCK-8 assay. Oxidative stress parameters (ROS via DCFH-DA fluorescence, MDA content, SOD activity) and pyroptosis markers (LDH release, PI/Hoechst 33342 nuclear staining) were quantified. Renal histopathology was performed using PAS and Masson trichrome staining. Biochemical analyses included serum creatinine, urea nitrogen, and 24h urinary protein quantification. Molecular profiling encompassed ELISA (IL-1β, IL-6, TNF-α, IL-18, fibronectin, collagen IV), RT-qPCR (NOX2, NOX4, NLRP3, ASC), western blotting (TXNIP, NLRP3, ASC, caspase-1, IL-1β, IL-18, collagen IV, fibronectin, laminin), and TXNIP immunofluorescence. Results. 1,25(OH)2D3 significantly attenuated high glucose-induced pathological alterations in HBZY-1 cells, including ROS overproduction, TXNIP upregulation, NLRP3 inflammasome activation, oxidative stress, inflammation, extracellular matrix (ECM) deposition, and pyroptotic cell death. Consistently, 1,25(OH)2D3 suppressed ROS/TXNIP/ NLRP3/caspase-1 signaling, ameliorated renal dysfunction, and mitigated histopathological damage in DN rats. Conclusion. 1,25(OH)2D3 confers renoprotection in DN by inhibiting the ROS/TXNIP/NLRP3 inflamma some axis, thereby suppressing oxidative stress, inflammatory cytokine production, ECM accumulation, and pyroptotic cell death in glomerular mesangial cells and renal tissues.
- PublicationOpen AccessMPO-Mediated oxidative stress regulates lung tissue damage in T-COPD through activation of the NLRP3 inflammasome(2026) Kaican Zong; E Jiang; Chunyan Luo; Hengyi Chen; Wen Li; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e Histiologiaurpose. This study aimed to investigate the role of MPO in regulating the NLRP3 signaling pathway and its impact on lung injury in a Mycobacterium tuberculosis-induced chronic obstructive pulmonary disease (T-COPD) model. Methods. T-COPD was induced in mice by stimulating with M. tuberculosis, and lung tissues were collected for histological analysis. ELISA, qPCR, and western blot assays were performed to assess the expression of pro-inflammatory cytokines and markers of lung injury, including Myeloperoxidase (MPO) and NOD-like receptor protein 3 (NLRP3). MPO-IN-5, an MPO inhibitor, was used to treat T-COPD mice, and its effects on inflammation and lung damage were evaluated. In vitro, murine lung epithelial MLE-12 cells were treated with LPS, CSE, and M. tuberculosis with or without MPO treatment, followed by assessments of cell viability, apoptosis, ROS levels, and NLRP3 pathway activity. Results. Histological analysis of the M. tuberculosis/ COPD group revealed significant pulmonary edema, inflammatory cell infiltration, and granuloma formation in the liver and spleen, compared with the COPD group. Pro-inflammatory cytokines TNF-α, IL-18, and IL-6 were elevated in the blood of the M. tuberculosis/COPD group. In the lungs, MPO expression and NLRP3 pathway activation were significantly increased. Treatment with MPO-IN-5 reduced the levels of LDH, CRP, and PCT, and reversed the morphological and inflammatory changes in lung tissue. Furthermore, MPO-IN-5 treatment also significantly decreased ROS production and the expression of inflammatory cytokines. In vitro, MPO treatment exacerbated NLRP3 activation in murine lung epithelial MLE-12 cells, while MPO inhibition (with MPO-IN-5) or NLRP3 knockdown mitigated these effects, enhancing cell proliferation and reducing apoptosis. Conclusion. Our results suggest that MPO plays a critical role in regulating the NLRP3 signaling pathway, contributing to lung injury in the T-COPD model. Inhibition of MPO with MPO-IN-5 effectively alleviates inflammation, reduces oxidative stress, and suppresses NLRP3 pathway activation, highlighting its potential as a therapeutic target for T-COPD.
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