Histology and histopathology, Vol.40, Nº11, (2025)

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http://hdl.handle.net/10201/179731

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Open Access
Histological and transcriptomic analysis of paravaginal and central defects in anterior vaginal wall prolapse: Insights from DeLancey's pelvic floor theory
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Zhang Chun; Tang Qingxia; Zhou Yan; Fu Xuemei; Hu Pan; Liu Lubin; Biología Celular e Histología
Background. This study aimed to pre-liminarily explore the differences between paravaginal and central defect types of anterior vaginal wall prolapse based on DeLancey's pelvic floor theory. Methods. Seventy-eight patients with normal, paravaginal, or central defect vaginal wall tissues were collected and stained using hematoxylin and eosin (HE) and immunofluorescence staining to analyze and identify the expression of vimentin and phosphohistone H3 (PH3). Ribonucleic acid from fresh tissues was extracted for transcriptome sequencing to analyze differences between paravaginal and central defect types of anterior vaginal wall prolapse. Results. Significant differences were found in age, menopausal status, body mass index, pregnancy, and delivery among the control, paravaginal, and central defect groups. Histological analysis revealed that the distribution of interstitium in the normal HE staining group was compact and continuous. In the paravaginal defect interstitium, fiber morphology was altered, while central defect interstitial fibers were fragmented. PH3 expression was significantly lower in the central defect type than in the normal and paravaginal defect groups, suggesting degenerative lesions in the vaginal mucosa with central defects. Vimentin distribution in the normal group was tightly packed and continuous, whereas, in the paravaginal defect interstitium, vimentin filaments were fragmented into small spots and micro-aggregates. In the central defect interstitium, vimentin micro-aggregates exhibited altered coalescence and cell shape, appearing punctate. These findings indicated degenerative lesions in the anterior vaginal interstitium of both paravaginal and central defect types. KEGG enrichment analysis of differential genes revealed their involvement in proteinaceous extracellular matrix (ECM)-related signaling pathways, with increased expression of matrix metalloproteinase 13 (MMP13), MMP3, MMP12, and MMP7 in the paravaginal defect type compared with the central defect type. Conclusion. The differences between paravaginal and central defect types of anterior vaginal wall prolapse may be related to the expression of MMP-related proteins; KEGG enrichment analysis of differential genes indicated that they were closely related to the protein ECM pathway. Moreover, delineative lesions appeared in the paravaginal defect interstitium, and degenerative lesions appeared in the central defect mucosa and interstitium, which further enriched the DeLancey three-level theory
Open Access
Astragaloside IV suppression of chronic atrophic gastritis by upregulating PAR-1 in vitro and in vivo
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Duan Bensong; Bao Zhewei; Yang Jingya; Wang Zhenzhen; Li Aoxiang; Yang Jin; Lv Mengke; Zhang Haibin; Biología Celular e Histología
Background. Astragaloside IV (AS-IV) has demonstrated a protective effect against gastrointestinal tract injury induced by various factors. However, its potential mechanism against chronic atrophic gastritis (CAG) remains unknown. Purpose. The objective of the present study was to investigate the impact of AS-IV on CAG and elucidate its molecular mechanism. Methods. The mRNA and protein levels of protease-activated receptor-1 (PAR-1) and related proteins were assessed using reverse transcription-polymerase chain reaction and western blot analyses, respectively. In addition, the levels of inflammatory factors were measured via enzyme-linked immunosorbent assay in GES-1 cells following treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The CAG model was established in rats induced with MNNG and concurrently treated with AS-IV for 10 weeks. Subsequently, serum samples were collected to assess the expression levels of proteins reflecting inflammatory markers. The gastric tissue sections were used for hematoxylin and eosin staining, immunohistochemical analysis, and the assessment of p-NF-κB p65 and PAR-1 signaling. Results. In-vitro experiments demonstrated that the mRNA levels of PAR-1 were upregulated following treatment with AS-IV and MNNG. Conversely, inhibition of PAR-1 expression reversed the therapeutic effects of AS-IV on MNNG-treated GES-1 cells, leading to increased expression of cyclooxygenase-2 and p-NF-κB p65. In addition, PAR-1 inhibition notably reversed MNNG-induced inflammatory factors, including IL increase. In-vivo experimental validation further confirmed that the upregulation of PAR-1 expression following treatment with AS-IV exerted a protective effect on the gastric mucosa of CAG rats. Conclusion. In conclusion, the findings of the present study suggested that AS-IV exhibited therapeutic efficacy against CAG induced by MNNG; its mechanism may be closely associated with the thrombin/PAR-1 signaling pathway. The present study provides a theoretical foundation for further exploration of the pharmacological effects of AS-IV on the treatment of human CAG
Open Access
Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Chen Weina; Xue Diming; Feng Xia; Zhong Yinhang; Li Quanqing; Zhang Weihang; Jiang Guojun; Biología Celular e Histología
Objectives. The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro. Methods. The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured. Results. Pin alleviated lipid deposition, inflam-matory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2. Conclusion. Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway
Open Access
Venous vasculature drives neovascularization and stroma formation in pancreatic neuroendocrine tumors via intussusceptive angiogenesis and vein intravasation
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Díaz-Flores Lucio; Gutiérrez Ricardo; Pino García Maria; González-Gómez Miriam; Carrasco Jose Luis; Madrid Juan Francisco; Díaz-Flores Varela Lucio; Biología Celular e Histología
The microenvironment of pancreatic neuroendocrine tumors (PanNETs) has been extensively studied; however, research on their venous vasculature has largely focused on tumor invasion and metastasis. This study aims to (a) evaluate the role of veins/venules in PanNET neovascularization, tumor intravasation, and stromal tract (trabecula) formation, including the potential involvement of intussusceptive angiogenesis (IA); and (b) compare the trabeculae observed in PanNETs with those found in hepatic cavernous hemangiomas (HCHs) where IA in veins plays an important role. To achieve these objectives, we conducted an integrated morphological approach encompassing primary PanNETs (n=42), hepatic metastases of PanNETs (n=4), and HCHs (n=11). Our findings in both primary and metastatic PanNETs reveal (a) the involvement of veins/venules in tumor neovascularization, with IA acting synergistically with sprouting angiogenesis, through the formation of pillars, meshes, and complex meshes (vessels that encapsulate tumor clusters-endothelium-coated tumor clusters); (b) the development of connective tissue around the neo-vasculature, potentially involving adventitial CD34-positive stromal cells/telocytes; and (c) a notable architectural resemblance between the trabeculae of PanNETs and those of HCHs. In conclusion, this work highlights the pivotal role of the preexisting venous vasculature in PanNET neovascularization, tumor intravasation, and stroma formation, with active participation of IA. These findings provide a pathophysiological foundation for future in-depth molecular investigations and may pave the way for new studies on therapeutic strategies targeting angiogenic mechanisms
Open Access
Challenging diagnosis in pulmonary NUT carcinoma: A report of two cases with different histopathologic and molecular features and a novel SPECC1 :: NUTM1 gene fusion
(Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Xie Ling; Chen Jie; Ke Fei; Zheng YanYing; Li Hui; Biología Celular e Histología
Background. NUT carcinoma (NC), formerly known as NUT midline carcinoma, is a rare but highly aggressive cancer. It is a poorly differentiated carcinoma characterized by rearrangements of the NUTM1 (nuclear protein in Testis) gene with a member of the bromodomain-containing protein (BRD) family gene, usually BRD4. There is limited knowledge about primary pulmonary NC till now. It is probably underestimated or underdiagnosed because of its poorly differentiated character, misleading immunophenotype, and wide range of differential diagnoses. Method. We report here two cases of pulmonary NC with different clinicopathological and molecular presentations to draw attention to some atypical clinicopathologic features that can help clinicians and pathologists consider this rare entity. Results. The first case shows a nested pattern with small, uniform, blue epithelioid cells and aberrant expression of neuroendocrine markers, which has a known BRD3::NUTM1 fusion accompanied by a novel IGR (downstream ROR2)::NUTM1 fusion. The second case demonstrates solid sheets and cords of eosinophilic epithelioid-polygonal cells with a mucoid stroma and TTF1 expression, which has a novel SPECC1::NUTM1 gene fusion accompanied by TP53 and JAK1 gene oncogenic variants. Conclusion. As a result, our study contributes to expanding the variant spectrum of the NUTM1 gene. NUT carcinoma with different fusion partners seems to have unique clinicopathological characteristics, yet more cases need to accumulate experience

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