Histology and histopathology最新文献

{"title":"Telocytes in skeletal muscle: Emerging players in homeostasis and repair/regeneration.","authors":"Irene Rosa, Eloisa Romano, Mirko Manetti","doi":"10.14670/HH-25-071","DOIUrl":"10.14670/HH-25-071","url":null,"abstract":"<p><p>Telocytes (TCs) have recently emerged as novel components of the skeletal muscle interstitium. They are distinguished from other stromal cells by their immunophenotypic profiles and, especially, unique ultrastructural traits. Specifically, TCs feature a small cell body and very long, thin telopodes with a moniliform appearance conferred by the alternation of slender segments (podomers) and small dilated portions (podoms). Experimental evidence suggests that, as part of the skeletal muscle stem cell niche, TCs may be involved in orchestrating satellite cell activation and myogenic differentiation through both direct physical interactions and paracrine signaling. Yet, further in-depth research is needed to uncover specific immunophenotypic signatures for skeletal muscle TCs within the niche, as well as to identify the signaling pathways by which they influence neighboring satellite cells and, possibly, other cellular components of the niche. In the present review, particular emphasis is placed on the putative strategic role of TCs in maintaining skeletal muscle tissue homeostasis, their involvement in muscle pathological alterations, and, most importantly, their possible role in the coordination of the regenerative response following injury. In perspective, the promising therapeutic potential of TC-based strategies to enhance skeletal muscle tissue repair/regeneration and restrain post-injury fibrosis is also discussed.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1635-1646"},"PeriodicalIF":2.2,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591947","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 clinical significance and mechanism of DCIS-like morphology of lymph node metastasis in breast cancer.","authors":"Xin Lin, Mingmei Fan, Jingquan Liu, Ting Long, Lingfang Gao, Haibin Wu, Yan Zhong, Wenwen Lin, Ruian Wang, Zuguo Li, Meihua Chen","doi":"10.14670/HH-25-145","DOIUrl":"https://doi.org/10.14670/HH-25-145","url":null,"abstract":"<p><strong>Background: </strong>During the practice of diagnostic pathology, we identified a case of invasive ductal carcinoma (IDC) of the breast with lung metastases exhibiting a ductal carcinoma in situ (DCIS)-like morphology. Immunohistochemistry confirmed the presence of CK5/6, P40 and P63-positive tumor cells at the periphery of the metastatic nests. Subsequent expansion of our sample revealed similar DCIS-like morphology in lymph node metastases of other IDC cases. This study aimed to preliminarily characterize the pathological features, significance, and mechanisms of this phenomenon.</p><p><strong>Methods: </strong>We collected 101 lymph node metastasis specimens of breast IDC. (1) DCIS-like metastases were identified, and their correlation with clinicopathological parameters was analyzed. (2) Immunohistochemistry for basal/myoepithelial markers (CK5/6, P63, SMA, Calponin) was performed to assess their expression in relation to DCIS-like morphology. (3) Stemness markers (ALDH1A1, CD44, SOX2) were detected, and their expression was correlated with clinicopathological parameters, DCIS-like morphology, and basal/myoepithelial differentiation.</p><p><strong>Results: </strong>(1) DCIS-like morphology was observed in 24.8% (25/101) of lymph node metastases. Its presence correlated with higher nodal burden and non-luminal molecular subtypes (HER2-enriched and triple-negative). The recurrence rate of the DCIS-like metastasis group was higher than that of the non-DCIS-like metastasis group. (2) A subset of cases showed tumor cell expression of P63, CK5/6, or SMA in metastases, while none expressed Calponin. The proportion of cases expressing basal/myoepithelial markers was higher in the DCIS-like metastasis group, with a significant correlation between DCIS-like morphology and CK5/6 expression. (3) High stemness marker expression correlated significantly with higher histological grade, increased numbers of lymph node metastases, advanced pTNM stage, the presence of DCIS-like morphology, and basal/myoepithelial differentiation.</p><p><strong>Conclusion: </strong>The presence of DCIS-like morphology and basal/myoepithelial marker expression in lymph node metastases of breast IDC is associated with enhanced tumor stemness. DCIS-like metastases may serve as a valuable morphological indicator of higher tumor aggressiveness and increased recurrence risk.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25145"},"PeriodicalIF":2.2,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149080486","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":"High expression of glycoprotein non-metastatic melanoma protein B is associated with resistance to neoadjuvant chemotherapy in triple-negative breast cancer.","authors":"Xiaofan Xu, Yuanyuan Cao, Xueying Kong, Jingyi Wang, Ziwei Wu, Qiurong Li","doi":"10.14670/HH-25-144","DOIUrl":"https://doi.org/10.14670/HH-25-144","url":null,"abstract":"<p><strong>Aims: </strong>This retrospective single-center study aimed to investigate the expression of glycoprotein non-metastatic melanoma protein B (GPNMB) and its association with clinicopathological parameters, Miller-Payer (MP) grading, neoadjuvant chemotherapy (NAC), and prognosis in triple-negative breast cancer (TNBC).</p><p><strong>Methods: </strong>A total of 50 female patients with TNBC, who were subjected to NAC followed by surgery between January 2010 and March 2024 at Jinling Hospital (Nanjing Medical University, China), were included in this study. The formalin-fixed and paraffin-embedded (FFPE) core biopsy and excision samples of these patients were obtained from the pathology department. The FFPE samples were subjected to histological analysis using hematoxylin and eosin (H&amp;E) staining and immunohistochemistry (IHC) staining of the estrogen receptor, progesterone receptor, human epidermal growth factor receptor-2, proliferation marker Ki-67, and GPNMB. The response of excision FFPE samples to NAC was evaluated by H&amp;E staining with an MP grading system. Finally, the relationship between GPNMB expression and clinicopathological parameters, MP grade, and prognosis of patients with TNBC was statistically analyzed using univariable and multivariable logistic regression methods. Functional experiments of GPNMB in TNBC cells were carried out <i>in vitro</i>.</p><p><strong>Results: </strong>Positive expression of GPNMB was significantly associated with low MP grade and poor prognosis of patients with TNBC. Knockdown of GPNMB suppressed proliferation and migration, promoted apoptosis, and enhanced chemosensitivity in TNBC cells.</p><p><strong>Conclusions: </strong>These results indicate that GPNMB expression can serve as a potential biomarker for predicting the pathological response to NAC (in addition to MP grading) and as a prognostic marker for TNBC. The important limitation of this study is the small number of patients; further validation is needed.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25144"},"PeriodicalIF":2.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074594","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":"Structural and metabolic signatures of cardiac aging in African turquoise killifish <i>(Nothobranchius furzeri)</i>.","authors":"Ryuichi Hishida, Takayoshi Otsuka, Shinya Toyokuni, Hideaki Matsui","doi":"10.14670/HH-25-143","DOIUrl":"https://doi.org/10.14670/HH-25-143","url":null,"abstract":"<p><p>Aging induces profound structural remodeling of the heart, yet experimental investigation of cardiac aging remains limited due to the long lifespan of most vertebrate models. The African turquoise killifish <i>(Nothobranchius furzeri)</i> provides a unique opportunity to analyze age-related cardiac changes within an experimentally accessible timeframe. While previous studies have primarily focused on the short-lived GRZ strain, cardiac aging in long-lived strains remains poorly characterized. In this study, we examined cardiac aging in the long-lived MZCS strain of <i>N. furzeri</i> using histological analyses combined with quantitative image analysis. Age-related changes in cardiac morphology, myocardial structure, extracellular matrix remodeling, accumulation of PAS-positive (glycogen-like) material, and senescence-associated β-galactosidase (SA-β-Gal) activity were evaluated by comparing young (1.5 months) and old (7-10 months) fish of both sexes. Old fish exhibited ventricular enlargement, epicardial thickening, valvular abnormalities, and prominent interstitial myocardial fibrosis. In contrast to mammals and zebrafish, cardiomyocyte hypertrophy was not observed; instead, myocardial density was reduced, with marked thinning of peripheral trabeculae, indicating a species-specific mode of cardiac remodeling. Accumulation of glycogen-like material tended to be more pronounced in young fish, whereas the expression of most glucose metabolism-related genes showed no marked age-dependent changes. Notably, SA-β-Gal activity was robustly detected from early life onward, suggesting that elevated SA-β-Gal activity represents an intrinsic characteristic of the killifish heart rather than a simple marker of chronological aging. Together, these findings establish the long-lived MZCS strain of <i>N. furzeri</i> as a valuable histological model for investigating conserved and species-specific features of cardiac aging.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25143"},"PeriodicalIF":2.2,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069555","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":"FOXC1-FTO axis regulates cardiomyocyte hypertrophy and mitochondrial dysfunction during cardiac hypertrophy in mice.","authors":"Xiao Kong, Xuan Li, Yanpeng Zhang, Chao Li, Kaiyao Shi","doi":"10.14670/HH-25-142","DOIUrl":"https://doi.org/10.14670/HH-25-142","url":null,"abstract":"<p><p>Cardiomyocyte hypertrophy and mitochondrial dysfunction represent the primary outcomes of pathological myocardial hypertrophy. Although FOXC1 has been reported to be associated with myocardial injury, its functional role in cardiac hypertrophy remains unclear. FOXC1 was found to be upregulated in both transverse aortic constriction (TAC)-induced cardiac hypertrophy mice and angiotensin II (Ang II)-induced cardiomyocytes (AC16 cells), suggesting that high expression of FOXC1 might serve as a risk factor in the progression of myocardial hypertrophy. To investigate the effect of FOXC1 on cardiomyocyte injury, FOXC1 siRNA was designed and transfected into cardiomyocytes. Knocking down FOXC1 suppressed the occurrence of hypertrophic responses, including the reduction in the levels of hypertrophic markers (atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP)) and the increase in cardiomyocyte surface area. Additionally, FOXC1 knockdown alleviated mitochondrial dysfunction in cardiomyocytes, as evidenced by the decrease in oxidative stress levels and mitochondrial membrane potential. Mechanistically, FOXC1 was found to inhibit the transcriptional activity of FTO, and FTO inhibition exacerbated the myocardial injury relieved by FOXC1 knockdown. Collectively, our study highlighted the functional role of FOXC1 in the pathogenesis of myocardial hypertrophy and provided a potential target for the prevention and treatment of pathological myocardial hypertrophy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25142"},"PeriodicalIF":2.2,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038374","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":"Acupuncture alleviates form-deprivation myopia by promoting dopamine secretion and suppressing ferroptosis, potentially involving the PACAP-AC/cAMP pathway.","authors":"Bifeng Chen, Mengdi Yan, Qiqi Pan, Juntao Zhang, Shiming Wang","doi":"10.14670/HH-25-141","DOIUrl":"https://doi.org/10.14670/HH-25-141","url":null,"abstract":"<p><strong>Introduction: </strong>Acupuncture has shown potential in the clinical treatment of myopia. The research aimed to elucidate the underlying mechanism of acupuncture in treating myopia.</p><p><strong>Material and methods: </strong>Guinea pigs were randomly divided into five groups: Control, form-deprivation myopia (FDM), FDM + sham acupuncture, FDM + acupuncture (BL1 \"<i>Jingming</i>\" and BL2 \"<i>Cuanzhu</i>\"), and FDM + acupuncture + SQ22536 (an adenylyl cyclase (AC) inhibitor). Retinal, choroidal, and scleral morphological changes and retinal apoptosis were assessed by hematoxylin and eosin (HE) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. Retinal dopamine, cyclic adenosine monophosphate (cAMP), Fe²⁺, reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) levels were measured using kits. Immunofluorescence and western blot were used to assess tyrosine hydroxylase (TH). Western blot was used to analyze retinal AC, pituitary adenylate cyclase-activating polypeptide (PACAP), solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), and scleral collagen type I alpha 1 chain (COL1A1).</p><p><strong>Results: </strong>Acupuncture significantly improved FDM-induced ocular biometric abnormalities, alleviated retinal, choroidal, and scleral alterations, and restored scleral COL1A1 expression. Moreover, acupuncture notably increased dopamine and TH levels in FDM guinea pigs. In addition, acupuncture partially restored the levels of cAMP, AC, and PACAP in FDM guinea pigs. Acupuncture markedly reduced Fe²⁺, ROS, and MDA levels, and increased GSH, SLC7A11, and GPX4 levels in FDM guinea pigs. These effects were reversed by SQ22536.</p><p><strong>Conclusions: </strong>Acupuncture stimulation at BL1 and BL2 alleviates myopia by promoting dopamine secretion and inhibiting ferroptosis, which may be associated with the PACAP-AC/cAMP signaling pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25141"},"PeriodicalIF":2.2,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030270","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":"Comprehensive review on adult neurogenesis through immunological studies in the brain regions of vertebrate classes.","authors":"Hemlata Arya, Kavita Tamta, Adarsh Kumar, Meghana Mehta, Ram Chandra Maurya","doi":"10.14670/HH-25-140","DOIUrl":"https://doi.org/10.14670/HH-25-140","url":null,"abstract":"<p><p>Adult neurogenesis is the process in which new neurons are produced, mature, and integrated into the neural circuits of adult vertebrate brains- fish, amphibians, reptiles, aves, and mammals. All vertebrate groups exhibit a great capacity for neurogenesis, which is dependent upon the number of neurogenic zones in the brain. The fish brain is known to have the highest neurogenic rate because they acquire the maximum number of neurogenic zones, such as the olfactory bulb, telencephalon, preoptic area, cerebellum, thalamus, hypothalamus, optic tectum, and medulla oblongata. The amphibian brain is also known for its high number of proliferative zones similar to fish, whereas reptilian, avian, and mammalian brains show adult neurogenesis primarily in the telencephalon. The process is affected by aging and hormones but is highly sensitive to environmental factors, such as stress, seasonal changes, and temperature, which subsequently control (increase or decrease) the neurogenesis rate. However, aging is the most common factor known to suppress neurogenesis. Various stages of adult neurogenesis were distinguished by a number of molecular markers, like 5-Bromo-2'-deoxyuridine, Doublecortin, nestin, glial fibrillary acidic protein, etc. The study of neurogenesis in various organisms aids in the better understanding of the capacity of the brain to modify itself according to the changing environment, to form new synaptic connections by replacing old neurons with new ones. The new synaptic connections help with memory and cognition.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25140"},"PeriodicalIF":2.2,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024744","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":"<i>CDKN2A</i> alterations in solid tumors: From biological mechanisms to clinical applications, with special emphasis on central nervous system tumors.","authors":"Thibaut Wolf, Nissrine Berry, Lucas Geyer, Noelle Weingertner, Erwan Pencreach, Georges Noel, Roland Schott, Julien Todeschi, Natacha Entz-Werlé, Marie-Pierre Chenard, Sophie Martin, Damien Reita, Benoît Lhermitte","doi":"10.14670/HH-25-139","DOIUrl":"https://doi.org/10.14670/HH-25-139","url":null,"abstract":"<p><p><i>CDKN2A</i> encodes the tumor suppressor p16^INK4a protein, inactivated in up to 50% of human cancers, most commonly through homozygous deletion (HD). <i>CDKN2A</i> HD carries major diagnostic, prognostic, and grading implications across several central nervous system (CNS) tumor types and subtypes, as well as in other solid neoplasms, including melanoma and mesothelioma. Screening for this deletion is therefore part of the pathologist's daily routine. Multiple approaches are currently available for detecting <i>CDKN2A</i> alterations. In addition to fluorescence <i>in situ</i> hybridization (FISH) and comparative genomic hybridization (CGH), several other molecular techniques have emerged, each with distinct strengths and limitations, underscoring the need for integrated diagnostic strategies. Here, we review the current literature on the diagnostic, grading and prognostic significance of <i>CDKN2A</i> HD in solid tumors with a focus on CNS neoplasms. We also review the emerging evidence on the clinical impact of alternative gene inactivation mechanisms, including hemizygous deletions and point mutations, and discuss the performance and limitations of currently available diagnostic assays for their detection. We finally propose a practical diagnostic workflow for achieving a reliable <i>CDKN2A</i> alteration assessment to support patient management and therapeutic decision-making.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25139"},"PeriodicalIF":2.2,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016742","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":"Jianpi Qingre Qushi Formula attenuates acute gouty arthritis through modulation of the Ras/Raf/MEK/ERK signaling pathway.","authors":"Nanfei Zhu, Yunxiang Cao, Amin Wang, Hui Wang, Yabing Wang, Jianing Wang","doi":"10.14670/HH-25-138","DOIUrl":"https://doi.org/10.14670/HH-25-138","url":null,"abstract":"<p><p>The global incidence of acute gouty arthritis (AGA) continues to increase, and its pathogenesis is closely associated with complex inflammatory signaling pathways. Jianpi Qingre Qushi Formula (JQR) has shown favorable therapeutic efficacy in clinical practice; however, its key bioactive components and underlying molecular mechanisms remain unclear. This study integrated network pharmacology, molecular docking, and <i>in vivo</i> experiments to systematically investigate the potential mechanisms of JQR in AGA treatment. We screened active components of JQR and their potential targets, and collected AGA-related disease targets. A compound-target network was then constructed, followed by protein-protein interaction (PPI) analysis. Subsequently, GO (Gene Ontology) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted on the overlapping targets. Molecular docking was performed to evaluate the binding affinities between core components and key signaling proteins. Additionally, a monosodium urate (MSU)-induced AGA rat model was established, and inflammatory responses and changes in key targets and signaling pathways were assessed using inflammatory scoring, histological examination, ELISA, immunofluorescence, western blotting, and quantitative PCR. JQR markedly alleviated inflammatory responses in AGA rats. Enrichment analyses indicated that the therapeutic effects of JQR were primarily associated with the Ras-dependent MAPK signaling pathway. Desacetylmatricarin, candletoxin A, dinatin, baicalein, and stigmasterol were identified as core active components and exhibited strong binding affinities to key proteins in the Ras/Raf/MEK/ERK signaling pathway. <i>In vivo</i> experiments further demonstrated that JQR notably reduced TNF-α and IL-1β levels, attenuated speck-like aggregation of the NLRP3 inflammasome, and downregulated the mRNA expression and protein levels of NLRP3, ASC, caspase-1, GSDMD, and IL-1β. In addition, JQR downregulated the protein level and mRNA expression of Ras, Raf, MEK, p-MEK, ERK, and p-ERK. These findings suggested that JQR exerted therapeutic effects on AGA via the coordinated regulation of multiple components and targets. This mechanism may be associated with the suppression of NLRP3 inflammasome activation and inflammatory responses through the Ras/Raf/MEK/ERK signaling pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25138"},"PeriodicalIF":2.2,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012237","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":"Nitrergic and secretagogin-expressing neurons in the olfactory neurogenic region of intact and maternally separated rats.","authors":"Alexandra Popovičová, Kamila Fabianová, Marcela Martončíková, Monika Žideková, Enikő Račeková","doi":"10.14670/HH-25-137","DOIUrl":"10.14670/HH-25-137","url":null,"abstract":"<p><p>Maternal separation (MS), a source of early-life stress, may influence postnatal neurogenesis, including proliferation, cell death, or migration of progenitor cells in the olfactory neurogenic region-the ventricular-subventricular zone (V-SVZ) and the rostral migratory stream (RMS). In this study, we investigated the impact of MS on populations of nitric oxide (NO)-producing neurons and neurons expressing secretagogin (SCGN) within the V-SVZ/RMS of adult rats. The aim was to obtain new morphological data on these neuronal populations in intact rats and rats subjected to MS during the first three neonatal weeks (3 hours/day). We analyzed their distribution, number, and mutual relationships within the V-SVZ and in specific anatomical subregions of the RMS. Double immunofluorescence labeling for neuronal nitric oxide synthase (nNOS) and SCGN confirmed the presence of nNOS+ and SCGN+ neurons in the V-SVZ/RMS, each exhibiting distinct morphological features and distribution patterns. The response to MS differed between the two neuronal populations. Quantitative analysis revealed an increased number of nNOS+ cells in the V-SVZ/RMS of MS rats, with a statistically significant increase observed specifically in the V-SVZ. In contrast, the typical caudo-rostral decrease in SCGN+ cell numbers-seen in intact rats, with the lowest count in the rostral part of the RMS-was absent in MS animals. Instead, MS rats showed a significant decrease in SCGN+ neuron numbers in the caudal part of the RMS and a significant increase in the rostral part of the migratory pathway. These findings indicate that nitrergic and SCGN-expressing neurons in the V-SVZ/RMS respond differently to early-life stress induced by MS, exhibiting distinct changes in both cell number and spatial distribution.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"25137"},"PeriodicalIF":2.2,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989920","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}