Folia histochemica et cytobiologica最新文献

{"title":"Ginsenoside Rg3 inhibits Ang II-induced cardiac fibrosis via the GLP-1 receptor signaling pathway.","authors":"Jie Zhao, Zheng Yan, Chaokun Guan, Dongsheng Li, Xisheng Yan, Xiao Li, Yanglin Li, Xing Liu, Shifan Tang","doi":"10.5603/fhc.106697","DOIUrl":"10.5603/fhc.106697","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiac fibrosis is a major pathological feature of multiple cardiovascular diseases and an important risk factor for heart failure. Ginsenoside Rg3 (Rg3), a natural triterpenoid saponin extracted from Panax ginseng, has been shown to exert cardioprotective effects. In this study, we assessed the effects of Rg3 on angiotensin II (Ang II)-induced cardiac fibrosis in both cellular and animal models and investigated the underlying mechanisms.</p><p><strong>Material and methods: </strong>For the cellular experiments, primary mouse cardiac fibroblasts (CFs) were treated with Ang II (1 μM) and Rg3 (25, 50, or 100 μM) for 24 h to assess the effects of Rg3 on cardiac fibrosis in vitro. The glucagon-like peptide-1 receptor (GLP-1R) antagonist exendin-3 (9-39) (1 μM) was used to validate the role of GLP-1R signaling in the anti-fibrotic effects of Rg3 in vitro. A CCK-8 assay was performed to assess cell viability. For the animal experiments, male C57BL/6J mice were divided into 4 groups (6 mice per group): Sham, Ang II, Ang II + Rg3 (50 mg/kg), and Ang II + Rg3 (100 mg/kg). Collagen deposition in mouse cardiac tissues was assessed by picrosirius red staining. The expression of fibrosis-related proteins (MMP-2, MMP-9, α-SMA, collagen I, collagen III, and fibronectin), GLP-1R, phosphorylated Smad2/3, total Smad2/3, RhoA, and ROCK2 in CFs and mouse cardiac tissues was examined by RT-qPCR, western blotting, and immunofluorescence staining.</p><p><strong>Results: </strong>Rg3 treatment reversed the Ang II-induced upregulation of MMP-2, MMP-9, α-SMA, collagen I, collagen III, p-Smad2/3, RhoA, and ROCK2 and the downregulation of GLP-1R in CFs. Exendin-3 (9-39) antagonized the effects of Rg3 on the expression of fibrosis-related proteins, GLP-1R, p-Smad2/3, RhoA, and ROCK2 in CFs. Furthermore, Rg3 administration suppressed collagen deposition, reduced the expression of MMP-2, MMP-9, α-SMA, collagen I, collagen III, p-Smad2/3, RhoA, and ROCK2, and increased GLP-1R levels in the cardiac tissues of Ang II-infused mice.</p><p><strong>Conclusions: </strong>Rg3 exerts an anti-fibrotic effect in cardiac fibrosis models by inhibiting activation of the RhoA/ROCK and Smad2/3 pathways through upregulation of GLP-1R.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"60-74"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503452","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":"Exosomal Lnc-DLK1-35 reprograms microglia into a pro-tumorigenic phenotype via a non-canonical cytokine signature to promote glioblastoma progression and chemoresistance.","authors":"Dan Li, Yufeng Li, Zhuo Wang, Xuan Zheng, Yang Wang, Jianxiong Guo, Jingwu Li, Yongliang Liu, Yuhui Li","doi":"10.5603/fhc.109684","DOIUrl":"10.5603/fhc.109684","url":null,"abstract":"<p><strong>Introduction: </strong>Temozolomide (TMZ) resistance in glioblastoma (GBM) involves dynamic crosstalk of cancer cells with tumor-associated microglia, but the role of exosomal long non-coding RNAs (lncRNAs) remains poorly defined.</p><p><strong>Material and methods: </strong>We isolated exosomes from TMZ-sensitive (U251) and TMZ-resistant (U251TR) GBM cells. Lnc-DLK1-35 expression was modulated by overexpression/knockdown and validated by RT-qPCR. Exosome internalization by microglia (HMC3 cells) was tracked via PKH67 labeling. Microglial polarization was assessed by studying morphology, marker expression (CD16/CD32/iNOS/Arg-1/CD206/CD163), and cytokine secretion (ELISA: IL-6, TNF-α, TGF-β, IL-10, CXCL13). Functional impact on GBM cells by indirect co-culture with IL4-activated HMC3 cells was examined using CCK-8 and Transwell assays.</p><p><strong>Results: </strong>Lnc-DLK1-35 was enriched in U251TR cells and their exosomes. GBM exosomes delivered Lnc-DLK1-35 to microglia, inducing a unique GBM-educated phenotype: amoeboid morphology, elevated type 1 macrophage (M1) markers (CD16, iNOS) but suppressed immunoregulatory factors (IL-10, CXCL13). This reprogramming required exosomal transfer. In addition, indirect co-culture with IL4-activated HMC3 cells enhanced GBM malignancy, reduced TMZ sensitivity and promoted migration and invasion.</p><p><strong>Conclusions: </strong>Exosomal Lnc-DLK1-35 reprograms cultured microglia cells into a pro-tumorigenic state via a non-canonical cytokine signature, driving TMZ resistance and invasion. Targeting this axis disrupts microglia-GBM communication, revealing a novel therapeutic strategy.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"48-59"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431732","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":"Expression of BDNF-TrkB-AKT1 pathway components and apoptosis-related factors across yak brain regions at low and high altitudes.","authors":"Qian Zhang, Yan Cui, Junfeng He, Yangyang Pan, Meng Wang, Hongliang Jin","doi":"10.5603/fhc.110409","DOIUrl":"10.5603/fhc.110409","url":null,"abstract":"<p><strong>Introduction: </strong>This study investigated the expression of brain-derived neurotrophic factor (BDNF) signaling components (BDNF-TrkB-AKT1) and apoptosis-related factors (Bcl-2 and Bax) in yak brain regions at different altitudes.</p><p><strong>Material and methods: </strong>The cerebral cortex, cerebellum, hippocampus, thalamus, and medulla oblongata were collected from 3-year-old yaks living at low and high altitudes. The relative mRNA expression of BDNF, TrkB, AKT1, Bcl-2, and Bax was assessed by qRT-PCR. Protein abundance and cellular localization of BDNF, TrkB, AKT1, Bcl-2, and Bax were evaluated by Western blotting and immunohistochemistry, with immunoreactivity quantified by optical density analysis.</p><p><strong>Results: </strong>Within each altitude group, BDNF, TrkB, AKT1, and Bcl-2 mRNA expression and the corresponding protein levels (BDNF, TrkB, AKT1, and Bcl-2) were significantly higher in the cerebral cortex and hippocampus than in the cerebellum, thalamus, and medulla oblongata (P < 0.05). In contrast, Bax mRNA and Bax protein levels did not differ significantly among the five regions. Compared with low-altitude yaks, high-altitude yaks showed significantly higher BDNF, TrkB, AKT1, and Bcl-2 mRNA expression and higher BDNF, TrkB, AKT1, and Bcl-2 protein levels in brain tissues (P < 0.05), whereas Bax protein expression did not differ between altitude groups. Immunohistochemistry revealed immunoreactivity for BDNF, TrkB, AKT1, Bcl-2, and Bax in both altitude groups, with prominent labeling in cortical pyramidal neurons and across the pyramidal cell layer in the hippocampal CA region. Immunoreactivity was also detected in large neurons of the thalamus and medulla oblongata. In the cerebellum, labeling was strongest in Purkinje cells, with weaker signals in the granule cell layer and molecular layer.</p><p><strong>Conclusions: </strong>BDNF-TrkB-AKT1 pathway components and Bcl-2 showed relatively higher expression in the cerebral cortex and hippocampus within each altitude group, whereas Bax expression did not vary across regions. These patterns are consistent with an association between BDNF-TrkB-AKT1 signaling and increased Bcl-2 expression without a corresponding increase in Bax, which may support neuronal adaptation in the cerebral cortex and hippocampus. Elevated expression of BDNF, TrkB, AKT1, and Bcl-2 at high altitude suggests enhanced adaptation to hypoxia in high-altitude yaks; the underlying mechanisms require further investigation.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"39-47"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431735","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":"MOTS-c primes adrenal cortex metabolism without directly driving steroidogenesis.","authors":"Malgorzata Blatkiewicz, Kacper Kaminski, Marta Sobalska-Kwapis, Marta Szyszka, Anna Olechnowicz, Karol Jopek, Marcin Rucinski","doi":"10.5603/fhc.110668","DOIUrl":"10.5603/fhc.110668","url":null,"abstract":"<p><strong>Introduction: </strong>Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c), a 16-amino acid mitochondrial-derived peptide, regulates cellular metabolism through AMPK and mTOR signaling and exerts protective effects across multiple endocrine tissues. However, its role in adrenal physiology remains unexplored. We hypothesized that MOTS-c establishes \"steroidogenic readiness\" by priming metabolic pathways rather than directly activating hormone synthesis.</p><p><strong>Material and methods: </strong>Adult male Wistar rats (n = 16) received continuous MOTS-c (0.1 μmol/24 h) or saline via subcutaneous micro-osmotic pumps for 24 hours. Adrenal tissues were analyzed using qRT-PCR, immunohistochemistry, ELISA, and RNA-sequencing.</p><p><strong>Results: </strong>MOTS-c showed significantly higher expression in ZF/ZR vs. ZG. MOTS-c treatment did not alter classical steroidogenic genes or circulating corticosterone and aldosterone levels. RNA-seq identified 39 differentially expressed genes, notably upregulation of purinergic receptor P2ry4 (4.3-fold, P < 0.05) - a novel MOTS-C target enhancing calcium signaling. Additional changes included upregulation of Apoc4 and downregulation of stress markers Bag3 and Smurf2, mitochondrial carrier Slc25a30, and peroxisomal factor Pex11a. Gene Set Enrichment Analysis revealed inhibition of cAMP response, mitophagy, and histone deacetylation pathways, alongside activation of cell proliferation, indicating metabolic reprogramming without steroidogenic activation.</p><p><strong>Conclusions: </strong>MOTS-c functions as a metabolic conductor that primes adrenocortical cells for enhanced steroidogenic responsiveness without stimulating basal hormone synthesis. By upregulating calcium signaling, modulating lipid metabolism, downregulating stress-response proteins, and inhibiting mitophagy, MOTS-c establishes a preparatory metabolic state optimized for subsequent ACTH or stress stimulation. These findings reveal a novel preparatory mechanism in adrenal physiology and identify MOTS-c as a potential therapeutic target for HPA axis disorders requiring enhanced adrenal reserve capacity without basal hypercortisolemia.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"26-38"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431749","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":"CRISPR-mediated MLH1 disruption suppresses endometrial cancer growth via genomic instability induction and Wnt/β-catenin pathway inhibition.","authors":"Baoling Xing, Xiaoying Zhang, Li Shen, Xinpeng Zhang","doi":"10.5603/fhc.111186","DOIUrl":"10.5603/fhc.111186","url":null,"abstract":"<p><strong>Introduction: </strong>MutL homolog 1 (MLH1) loss is a defining molecular feature of endometrial cancer (EC) and a principal driver of microsatellite instability (MSI). Ishikawa cells harbor intrinsic MLH1 promoter hypermethylation, resulting in reduced but not abolished MLH1 expression and placing these cells in a vulnerable, partially compromised mismatch repair state. This study explores the effects of MLH1 knockdown (MLH1-KD) on MSI, cellular functions, signaling pathways, and tumor growth in Ishikawa EC cells.</p><p><strong>Material and methods: </strong>Using CRISPR/Cas9, we created an MLH1-KD Ishikawa EC cell line, validated through Sanger sequencing, qRT-PCR, western blotting, comet assays, and γ-H2AX analysis. Functional assays assessed proliferation, migration, and cell cycle progression and apoptosis. RNA sequencing identified global transcriptomic changes, and Wnt/β-catenin pathway activity was measured by a dual-luciferase reporter assay. A xenograft model evaluated tumor growth in vivo.</p><p><strong>Results: </strong>MLH1-KD cells showed MSI-H characteristics, increased DNA damage, and downregulation of key EC-related genes. Functionally, MLH1-KD led to significant reductions in cell proliferation and migration, which was accompanied by cell cycle arrest and a marked increase in apoptosis. RNA sequencing revealed profound alterations in the Wnt signaling pathway. Crucially, this was confirmed by a dual-luciferase reporter assay, which showed a significant inhibition of Wnt/β-catenin signaling activity. In vivo, MLH1-KD significantly decreased tumor weight and size in nude mice.</p><p><strong>Conclusions: </strong>In EC cells with pre-existing MLH1 promoter methylation, MLH1-KD leads to MSI-H, enhances genomic instability, disrupts Wnt signaling, impairs cellular functions, and inhibits tumor growth, highlighting Wnt signaling and MSI-H as potential therapeutic targets in EC.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"75-87"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607562","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":"Latent transforming growth factor beta binding protein 1 (LTBP1): roles as a multifunctional extracellular matrix regulator in human disease - from molecular mechanisms to clinical translation prospects.","authors":"Yi Liu, Minming Yi, Huan Wei, Xuewei Gu, Wenyan Liao","doi":"10.5603/fhc.110761","DOIUrl":"10.5603/fhc.110761","url":null,"abstract":"<p><p>Latent transforming growth factor beta binding protein 1 (LTBP1) is a key regulator of the extracellular matrix (ECM). However, its role as a molecular hub that integrates biochemical signals within the mechanical microenvironment across diverse human diseases has not been systematically elucidated. To address this, this review provides an in-depth analysis of the current evidence chain for LTBP1, from basic biology to disease mechanisms. The analysis indicates that through its isoforms, post-translational modifications (PTMs), and dynamic conformation, LTBP1 not only precisely modulates the spatiotemporal activity of TGF-β but also independently orchestrates ECM assembly and mediates direct cell signaling. In disease, LTBP1's function exhibits strong context-dependency: it acts as a \"double-edged sword\" in cancer (driving progression or suppressing growth); it serves as a key pathological mediator in fibrosis, and contributes to structural defects in cardiovascular, neurological, and developmental disorders. These mechanisms lay a solid foundation for its clinical translation: LTBP1 is established as a multidimensional biomarker and constitutes a novel target for a range of intervention strategies, from targeted therapies and cell therapies to functionalized biomaterials. In summary, establishing LTBP1 as a key pathological integrator in systematic studies, provides a new framework and direction for understanding common mechanisms of complex diseases and developing precision medicine strategies.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"1-25"},"PeriodicalIF":2.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431675","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":"Inhibition of STAT1 alleviates oxidative damage in retinal pigment epithelial cells and exhibits neuroprotective effects in autoimmune optic neuritis by upregulating IFI30 lysosomal thiol reductase.","authors":"Siqi Ma, Jiajia Yuan","doi":"10.5603/fhc.104300","DOIUrl":"10.5603/fhc.104300","url":null,"abstract":"<p><strong>Introduction: </strong>Oxidative damage-induced retinal pigment epithelial (RPE) cell apoptosis and optic nerve inflammation and demyelination are closely related to the pathogenesis of optic neuritis (ON). STAT1 has been found to be activated in the retina and optic nerve of ON rats. This study aimed to determine whether STAT1 depletion exerts neuroprotective effects against ON in both cellular and animal models.</p><p><strong>Material and methods: </strong>ARPE-19 cells were stimulated by H₂O₂ to induce oxidative stress, followed by STAT1 and IFI30 silencing. CCK-8 and flow cytometry assays assessed ARPE-19 cell viability and apoptosis. RT-qPCR, Western blotting, DCFH-DA staining, and commercial kits detected the levels of STAT1, IFI30, apoptosis markers, and antioxidant/oxidative markers. CHIP and luciferase reporter assays validated the binding between STAT1 and IFI30 promoter. Female C57BL/6 mice were immunised with myelin oligodendrocyte glycoprotein (MOG) peptide (MOG35-55) to induce experimental autoimmune encephalomyelitis, an animal model of ON. Optic nerve inflammation, demyelination, axonal loss, and retinal ganglion cell (RGC) apoptosis in encephalomyelitis (EAE) mice after STAT1 knockdown were evaluated via haematoxylin and eosin, luxol fast blue, immunofluorescence, and Brn3a-TUNEL double staining.</p><p><strong>Results: </strong>STAT1 silencing reversed the H₂O₂-induced increase of cell apoptosis and oxidative stress and the decrease in cell viability in ARPE-19 cells. STAT1 bound with the IFI30 promoter region and negatively regulated its expression. IFI30 knockdown antagonised the protection of STAT1 silencing against H₂O₂-induced oxidative stress and apoptosis in ARPE-19 cells. STAT1 depletion alleviated optic nerve inflammation, demyelination, axonal loss, and RGC apoptosis in EAE mice.</p><p><strong>Conclusions: </strong>STAT1 silencing exhibits neuroprotective effects against ON by upregulating IFI30.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"11-27"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729647","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":"Expression of O-GlcNAcylation in pulp tissue and dental pulp stem cells of healthy dental organs.","authors":"María Cristina Franco-Arellanes, Perla Xóchitl Toledo-Valdes, Cynthia Díaz-Hernández, Risk Díaz-Castillejos, Eunice Daysi García-Reyes, Saira Karina Ramírez-Thomé, Beatriz Xóchitl Ávila-Curiel, María Cristina Castañeda-Patlán, Edgar Zenteno, Carlos Josué Solórzano-Mata","doi":"10.5603/fhc.103756","DOIUrl":"10.5603/fhc.103756","url":null,"abstract":"<p><strong>Introduction: </strong>O-GlcNAcylation is a post-translational modification in which a single N-Acetyl-D-Glucosamine (GlcNAc) molecule is added to Ser or Thr residues of proteins. The O-N-acetylglucosaminyl transferase (OGT) enzyme is responsible for adding GlcNAc to the target proteins and N-acetyl-β-D-glucosaminidase (OGA) that removes the GlcNAc residue. O-GlcNAcylation has been described in the pathophysiology of several diseases; however, little has been studied in dental tissue. The aim of the present work is to characterise the product of O-GlcNAcylation and its enzymes at the tissue level in the dental pulp, as well as its expression in dental pulp stem cells (DPSCs) both in situ and in vitro. This enables the recognition of the behaviour of O-GlcNAcylation in pulp tissue without pathology.</p><p><strong>Material and methods: </strong>Pulp tissue was obtained from 10 healthy donors, and the expression of O-GlcNAc, OGT, and OGA was analysed using immunofluorescence with specific antibodies in different regions of the dental pulp. DPSCs were isolated, cultured, and identified with anti-STRO1 (antibody specific for human CD34+ cells, useful for DPSC identification). The expression of O-GlcNAc in DPSCs was confirmed in vitro through Western blot.</p><p><strong>Results: </strong>Different regions of the dental pulp and DPSCs express O-GlcNAc and the enzymes OGT and OGA. O-GlcNAc and OGT expression was more prominent in the odontoblastic layer, cell-rich zone, and in the central core. OGA was distributed throughout the pulp tissue with lower immunoreactivity compared to OGT.</p><p><strong>Conclusions: </strong>Our results suggest that O-GlcNAcylation may play a relevant role in human dental pulp homeostasis and in physiology of DPSCs.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"1-10"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729645","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":"Molecular landscape of the mouse adrenal gland and adjacent adipose tissue by spatial transcriptomics.","authors":"Malgorzata Blatkiewicz, Szymon Hryhorowicz, Marta Szyszka, Joanna Suszynska-Zajczyk, Andrzej Plawski, Adam Plewinski, Andrea Porzionato, Ludwik K Malendowicz, Marcin Rucinski","doi":"10.5603/fhc.108988","DOIUrl":"10.5603/fhc.108988","url":null,"abstract":"<p><strong>Introduction: </strong>. The adrenal glands are central regulators of endocrine homeostasis and stress adaptation. Despite decades of research, the molecular mechanisms governing adrenal zonation and cortical renewal remain incompletely understood.</p><p><strong>Material and methods: </strong>. Here, the 10x Genomics Visium CytAssist platform was applied to generate a high-resolution atlas of the adult CD1 IGS male mouse adrenal gland. The study employed a range of analytical approaches, including unsupervised clustering, differential gene expression analysis, pathway and Gene Ontology enrichment, cell-type deconvolution, and pseudotime trajectory inference. These approaches collectively facilitated the comprehensive characterization of transcriptional signatures across the primary adrenal cortical zones and the medulla.</p><p><strong>Results: </strong>. Herein transcriptional signatures of distinct compartments were identified, including zona glomerulosa/adrenal capsule (ZG/capsule), outer and inner zona fasciculata (oZF, iZF), medulla, connective tissue, and surrounding brown and white adipose depots. Deconvolution analysis further delineated contributions from stromal, immune, endothelial, and erythrocyte populations, highlighting the complexity of adrenal and periadrenal tissues. Pseudotime trajectory analysis validated the centripetal differentiation model of the adrenal cortex, demonstrating a continuum of transcriptional states from capsule and ZG/capsule through oZF to iZF, consistent with progressive acquisition of steroidogenic functions. Functional enrichment confirmed zone-specific pathways, including WNT and steroid biosynthesis in the cortex and neuroendocrine pathways in the medulla.</p><p><strong>Conclusions: </strong>. Together, this study provides the first spatially resolved transcriptomic reference map of the adult male mouse adrenal gland, revealing the cellular and molecular framework underlying zonation, renewal, and inter-compartment interactions. This atlas constitutes a valuable resource for advancing the understanding of adrenal physiology and pathology.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"162-176"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145631635","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":"Nintedanib alleviates hyperoxia-induced lung injury via targeting NF-κB signalling pathway in rat model of bronchopulmonary dysplasia.","authors":"Rui Hao, Yuping Li, Junhui Li, Zirui Guo, Zhi Yang, Wei Lu","doi":"10.5603/fhc.105218","DOIUrl":"10.5603/fhc.105218","url":null,"abstract":"<p><strong>Introduction: </strong>Bronchopulmonary dysplasia (BPD) is a common chronic respiratory disease in premature infants. Hyperoxia is the main pathogenic factor of BPD. Nintedanib is a small-molecule tyrosine kinase inhibitor that has been confirmed to affect several cellular processes in different diseases. The aim of this study was to explore the function of nintedanib in the treatment of BPD.</p><p><strong>Material and methods: </strong>Newborn Sprague-Dawley rats (postnatal day 1) were used to establish an in vivo BPD model by hyperoxia induction. Nintedanib was intraperitoneally injected into rats. Haematoxylin and eosin (H&E) staining was applied to detect lung injury in BPD rats. Cell apoptosis was determined by TUNEL (TdT-mediated dUTP nick end labelling) assay. Western blotting was applied to detect level changes of inflammatory factors IL-1β (interleukin-1 beta), CXCL-1 (C-X-C motif chemokine ligand 1), MCP-1 (monocyte chemotactic protein-1), as well as the phosphorylation of IkB (NF kappa B inhibitor) and NF-kB (nuclear factor kappa-B) in lung samples.</p><p><strong>Results: </strong>Hyperoxia resulted in lung injury in neonatal rats, while nintedanib treatment relieved the injury. Furthermore, nintedanib alleviated hyperoxia-induced apoptosis in rat lungs. It was further observed that an inflammatory response caused by hyperoxia in lung samples was attenuated by nintedanib administration. Additionally, nintedanib inactivated the NF-κB pathway in BPD rats.</p><p><strong>Conclusions: </strong>Nintedanib alleviates hyperoxia-induced lung injury via targeting the NF-κB signalling pathway.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"79-87"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149442","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}