Histology and histopathology Vol.40, nº2 (2025)
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- PublicationOpen AccessBPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Pan, Yanling; Yuan, Feng; Lin, Zhiren; Li, YijieGlioma is the most prevalent malignant tumor of the brain, and the study of the molecular mechanisms associated with its development has important clinical significance. Our previous study found that BPTF promotes the malignant phenotype of glioma and is significantly associated with poor prognosis; the downstream regulatory mechanisms are explored in this study. Western blot and immuno-histochemical staining were used to detect protein expression in cells or tissues. BPTF knockdown as well as FOXC1-overexpressing lentiviruses were used in combination for the construction of the U251 cell model, leading to functional rescue experiments. CCK8 assay, flow cytometry, scratch assay, and Transwell assay were used to detect cell proliferation, apoptosis, and migration, respectively. Finally, immuno-precipitation assays, combined with western blot (WB), were used to detect the interaction between proteins as well as the level of ubiquitination modification. The obtained results suggested that BPTF knockdown may inhibit the malignant behavior of glioma cells by downregulating FOXC1 expression. Moreover, FOXC1 expression was significantly higher in glioma tissues than in normal brain tissues and was significantly associated with higher tumor stage and worse patient prognosis. Finally, the mechanism of FOXC1 regulation by BPTF was found to result from the affected protein stability of FOXC1 through USP34-mediated de-ubiquitylation. In conclusion, the BPTF/FOXC1 axis was identified as a key promotor in glioma development and may be a potential target in the inhibition of glioma development.
- PublicationOpen AccessDifferential expression of HIF-1α and its hypoxia-related inducers in the spleens of plateau yaks and plain yellow cattle(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Zhou, Manlin; Dong, Shihui; Wang, Jun; Luo, Xuehui; Li, Rui; Zhang, Yiyang; Ding, Haie; Tan, Xiao; Qiao, Zilin; Yang, Kun; Chen, WeijiThe present study aims to investigate the distribution and expression characteristics of HIF-1α, VEGF, VEGFR-2, VCAM-1, and IL-4 in the spleen of plateau yaks and plain yellow cattle and to speculate the possible regulatory role of HIF-1α and its related hypoxia-inducible factors in the adaptation of the yak spleen to the plateau hypoxic environment. Histological features were observed using H&E and PAS stains. Immunohistochemical staining and optical density analysis were applied to investigate the distribution and differences in the expression of HIF-1α, VEGF, VEGFR-2, VCAM-1, and IL-4 in the spleen of yaks and cattle. The results showed that the area of splenic trabeculae and splenic nodules was significantly larger in the yak than in yellow cattle (P<0.05). Glycogen was mainly distributed in splenic arterial endothelial cells, vascular smooth muscle cells, splenic blood sinusoidal endothelial cells, and fibroblasts, and the distribution was significantly higher in the spleen of yaks than in cattle (P<0.05). HIF-1α, VEGF, VEGFR-2, VCAM-1, and IL-4 were mainly expressed in lymphocytes, arterial endothelial cells, vascular smooth muscle cells, splenic blood sinusoidal endothelial cells, and fibroblast cytoplasm, with higher expression in yak spleen (P<0.05). In conclusion, combining the differences in spleen tissue structure, glycogen distribution, and expression distribution of several hypoxia-related factors between yaks and cattle, we suggest that HIF-1α, VEGF, VEGFR-2, VCAM-1, and IL-4 may be important factors in the adaptation of yak spleen to the plateau environment, which provides a theoretical basis for further exploring the adaptation mechanism of plateau hypoxia in yaks.
- PublicationOpen AccessCORRIGENDUM TO: "LncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis" Histol Histopathol. 2022 Nov;37(11):1113-1125. doi: 10.14670/HH-18-489(Universidad de Murcia. Servicio de publicaciones, 2025) Fu, Jiding; Huang, Yunbo; Xian, Lewu
- PublicationOpen AccessGlucan-rich polysaccharides obtained from split gill mushroom [Schizophyllum commune (Fr.)] ameliorate hyperglycemia by enhancing insulin and GLUT2 pancreas in type 2 diabetic rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Matsathit, Udomlak; Sermwittayawong, Decha; Komolkriengkrai, Manaras; Khimmaktong, WipapanAims. Abnormalities in the secretion of insulin are the cause of pathology and complications in diabetic patients. The aim of this study was to investigate the anti-diabetic effect of polysaccharide extracts from the split gill mushroom in type 2 diabetes rats administered a low dose of streptozotocin (STZ) in combination with a high-fat diet. Methods. The rats were divided into 6 groups: the control group (ND), the control group fed with polysaccharide extract from split gill (ND240), the diabetes group (HFD+DM), the diabetic group fed 120 (HFD+S120) and 240 mg/kg BW polysaccharide extract (HFD+S240), and the diabetic group receiving metformin (HFD+Met). Subsequently, the Islets of Langerhans of pancreatic tissue were studied using a light microscope and transmission electron microscopy (TEM). Immunofluorescence for the detection of insulin and glucose transporter 2 (GLUT2) proteins, and malondialdehyde (MDA) were also detected in pancreatic tissue. Results. In the diabetic and HFD+120 groups, the tissues harbored various pathologies. The HFD+S240 and HFD+Met groups were found to have lower blood sugar levels. The levels of insulin and GLUT2 increased compared with the diabetic group. Additionally, the levels of MDA were reduced. Conclusions. The use of polysaccharide extract from split gill mushrooms (240 mg/kg BW) is an alternative to treating various pathologies in the relief or treatment of diabetes mellitus
- PublicationOpen AccessAromadendrin alleviates LPS-induced kidney apoptosis and inflammation by inhibiting phosphorylation of MAPK and NF-κB signaling pathways(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Ma, Xiaohong; Liu, Wenhua; Wang, Bin; Shi, FeizhuangBackground. Excessive inflammation and apoptosis in kidneys are critical players in the pathogenesis of acute kidney injury (AKI). Aromadendrin is a natural flavonoid characterized by anti-inflammatory, anti-apoptotic, and antioxidant actions. Thus, we investigated the roles and mechanisms of aromadendrin in the development of AKI. Methods. Lipopolysaccharide (LPS) was used to induce AKI mice, and one hour after LPS challenge, the mice received oral administration of aromadendrin or vehicle. Renal functions were assessed by measuring blood urea nitrogen and creatinine in serum. Histological changes were determined by hematoxylin and eosin staining. Apoptotic cells of renal tissues were detected by TUNEL staining. Gene expression was measured by western blotting and RT-qPCR. Results. Aromadendrin alleviated LPS-induced renal dysfunctions and histological defects in mice. Additionally, aromadendrin suppressed excessive inflammation and tissue apoptosis in the kidneys of LPS-induced AKI mice. Mechanistically, aromadendrin blocked the activation of NF-κB and MAPK pathways in LPS-induced AKI mice. Conclusion. Aromadendrin alleviates LPS-stimulated inflammation and tissue cell apoptosis in kidneys by inactivating the NF-κB and MAPK pathways
- PublicationOpen AccessTROP2 regulates cisplatin sensitivity of triple-negative breast cancer cells by regulating endoplasmic reticulum stress(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Zhang, Mingqi; Xu, Jianzhong; Liu, Qing; Yan, Xi; Li, NingTriple-negative breast cancer (TNBC) is a kind of breast cancer with a high metastasis rate and poor prognosis. As a transmembrane glycoprotein, tumor-associated calcium signal transducer 2 (TROP2) plays a certain role in the cancers. This study aimed to explore the potential mechanism of TROP2 affecting cisplatin (CDDP) resistance in TNBC from endoplasmic reticulum stress (ERS). MDA-MB-231 and CDDP-resistant cell lines MDA-MB-231/CDDP were used in this study, and the expression of TROP2 was detected by western blotting. After transfecting with the interference sequence of siRNA targeting TROP2, cell proliferation and apoptosis were detected by the cell counting kit-8, colony formation, and flow cytometry, and the expression of ERS-marker proteins was detected by western blotting. Furthermore, the effects of ERS in TROP2 on drug resistance of TNBC cells were explored by using ERS inhibitor 4-phenylbutyric acid (4-PBA). Results found that TROP2 expression in MDA-MB-231/CDDP was significantly upregulated compared with MDA-MB-231. The expression of TROP2 in MDA-MB-231/CDDP was significantly decreased after transfection with siRNA-TROP2, and the proliferation of MDA-MB-231 and MDA-MB-231/CDDP cells was significantly decreased after further induction with CDDP. TROP2 significantly affected TNBC cell cloning, apoptosis, and the expression of ERS-related marker proteins, while 4-PBA reversed the promoting effects of siRNA-TROP2 on apoptosis and ERS, as well as the inhibitory effects on cell proliferation, suggesting that TROP2 affected the resistance of TNBC cells to CDDP through ERS. In conclusion, TROP2 inhibited apoptosis of TNBC cells, improved the cell cloning ability, and regulated the sensitivity of TNBC cells to CDDP through ERS.
- PublicationOpen AccessLymph node or lymphoid aggregate? Impact on cancer resection quality, clinical prognosis, and tumor staging(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Gocht, Andreas; Watermann, Christian; Melzer, Madelaine; Schumacher, UdoThe clinical outcome of most cancer patients depends on the stage of the primary tumor, the lymph node status, and if distant metastases are present. According to the Union for International Cancer Control (UICC) and the American Joint Committee on Cancer (AJCC), the Tumor Node Metastasis (TNM) classifi-cation of malignant tumors requires the examination of a minimum number of regional lymph nodes for each type of cancer to fulfill the criteria of high-quality surgical oncology. Due to the daily challenge of collecting an appropriate number of lymph nodes and time constraints when processing and assessing tissue samples, pathologists may be tempted to identify every histological lymphoid structure mimicking a lymph node as a “true” lymph node. Faced with this issue, we propose to resolve it by specifying histological characteristics to differentiate lymphoid aggregates from “true” lymph nodes. To find a minimum consensus, we suggest defining as lymph nodes only those lymphoid structures composed of lymphoid cells encapsulated by a complete or incomplete fibrous capsule.
- PublicationOpen AccessMechanism of PTPN18 for regulating the migration and invasion of endometrial cancer cells via the MYC/PI3K/AKT pathway(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Suo, Shiqi; Chen, Song; Zhou, Liyuan; Xu, Ruili; Li, Jingxia; Li, WeiObjective. Endometrial cancer (EC) is a prevalent gynecologic malignancy. The critical role of PTPN18 in EC has been reported, while its role in the aerobic glycolysis of EC cells remains unclear. Our current study focused on the mechanism of PTPN18 in the regulation of aerobic glycolysis in EC. Methods. PTPN18 expression levels in endometrial stromal cells (KC02-44D) and EC cells (KLE, HEC-1-A, HEC-1B, and HEC-50) were determined. Following transfection of sh-PTPN18 in HEC-1-A cells, the changes in cell migratory and invasive abilities were assessed by the Transwell assay, and the changes in glucose consumption, lactic acid secretion, and ATP levels were detected using kits. The expression levels of glycolysis-related proteins HIF-1α, PKM2, and LDHA and the activation of the MYC/PI3K/AKT pathway were detected by Western blot. Additionally, sh-PTPN18 and pcDNA3.1-MYC were transfected into HEC-1-A cells to further explore their roles in the changes in aerobic glycolysis, migration, and invasion ability of EC cells. Results. Expression of PTPN18 in EC cells was up-regulated (HEC-1-A>HEC-1B>HEC-50>KLE). PTPN18 knockdown suppressed EC cell migration and invasion. Additionally, PTPN18 knockdown reduced glucose consumption, lactate production, ATP levels, and glycolysis-related protein levels (HIF-1α, PKM2, LDHA). PTPN18 knockdown inhibited the activation of the MYC/PI3K/AKT pathway in EC cells. MYC overexpression partially annulled the inhibitory effects of PTPN18 knockdown on aerobic glycolysis, migration, and invasion of EC cells. Conclusion. Our present study provided evidence that the knockdown of PTPN18 inhibited the aerobic glycolysis, migration, and invasion of EC cells by suppressing the MYC/PI3K/AKT pathway
- PublicationOpen AccessProspects of induced pluripotent stem cells in treating advancing Alzheimer’s disease: A review(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Park, Juyoun Janis; Rim, Yeri Alice; Sohn, Yeowon; Nam, Yoojun; Ju, Ji HyeonThe World Health Organization has identified Alzheimer’s disease (AD), the leading cause of dementia globally, as a public health priority. However, the complex multifactorial pathology of AD means that its etiology remains incompletely understood. Despite being recognized a century ago, incomplete knowledge has hindered the development of effective treatments for AD. Recent scientific advancements, particularly in induced pluripotent stem cell (iPSC) technology, show great promise in elucidating the fundamental mechanisms of AD. iPSCs play a dual role in regenerating damaged cells for therapeutic purposes and creating disease models to understand AD pathology and aid in drug screening. Nevertheless, as an emerging field, iPSC technology requires further technological advancement to develop effective AD treatments in the future. Thus, this review summarizes recent advances in stem cell therapies, specifically iPSCs, aimed at understanding AD pathology and developing treatments
- PublicationOpen AccessAdvances in 3D bioprinting to enhance translational applications in bone tissue engineering and regenerative medicin(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Ortega, Miguel A; Leon Oliva, Diego De; Liviu Boaru, Diego; Fraile-Martínez, Oscar; Garcia Montero, Cielo; Casanova, Carlos; García Honduvilla, Natalio; Buján, Julia; Saez, Miguel A; Álvarez Mon, Melchor; Velazquez De Castro, Amador; Acero, Julio; Barrena Blázquez, Silvestra; Diaz, Raul; López González, LauraBone defects are due to trauma, infections, tumors, or aging, including bone fractures, bone metastases, osteoporosis, or osteoarthritis. The global burden of these demands research into innovative strategies that overcome the limitations of conventional autografts. In this sense, the development of three-dimensional (3D) bioprinting has emerged as a promising approach in the field of tissue engineering and regenerative medicine (TERM) for the on-demand generation and transplantation of tissues and organs, including bone. It combines biological materials and living cells, which are precisely positioned layer by layer. Despite obtaining some promising results, 3D bioprinting of bone tissue still faces several challenges, such as generating an effective vascular network to increase tissue viability. In this review, we aim to collect the main knowledge on methods and techniques of 3D bioprinting. Then, we will review the main biomaterials, their composition, and the rationale for their application in 3D bioprinting for the TERM of bone.
- PublicationOpen AccessEndometrial epithelial cell organoids as tools for studying the CD39 family of enzymes and for validating enzyme inhibitors(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Rodríguez Martínez, Aitor; Torrejón Escribano, Benjamín; Eritja, Núria; Dorca Arévalo, Jonatan; Gabaldón, Clara; Sévigny, Jean; Matias Guiu, Xavier; Martín Satué, MireiaExtracellular adenosine triphosphate (ATP) conducts a complex dynamic system of broadly represented cell signaling. Ectonucleotidases are the enzymes with nucleotide hydrolytic ability that regulate ATP levels in physiological and pathological conditions, thus playing a key role in the so-called purinergic signaling. Altered ectonucleotidase expression has been reported in cancer, and the ectonucleoside triphosphate diphosphohydrolase (NTPDase) family of enzymes, with its best-known form NTPDase1 (CD39), is targeted in cancer immunotherapy. The tandem of enzymes CD39-CD73 is responsible for the generation of immuno-suppressive adenosine in the tumor microenvironment, and inhibition strategies are of great interest. Organoids have emerged as very convenient models for the study of tumors since they are three-dimensional cultures that retain many of the features of tissue. The present study aims to contribute to improving the methodology and the molecular tools needed for the study of ecto-nucleotidases in healthy and disease conditions. The study, performed in an endometrial cancer cell model, could be extended to other types of tumors and pathologies in which the purinergic system is involved. We generated organoids from endometrial cancer cells overexpressing NTPDase2 (CD39L1) and NTPDase3 (CD39L3) as fusion proteins with EGFP, and we performed functional assays by adapting in situ cytochemistry protocols. This allowed us to simultaneously detect enzyme activity and protein expression and to demonstrate that organoids can be used to test ectonucleotidase inhibitors—a result that can be used to develop new cancer treatment options
- PublicationOpen AccessInhibition of dendritic cell autophagy alleviates the progression of allergic rhinitis by inhibiting Th1/Th2/Th17 immune imbalance and inflammation(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Xiao, Changwu; Feng, Lizhi; Yang, WeiIntroduction. Immune imbalance is a fundamental immunological feature of allergic rhinitis (AR). The autophagy in CD11c+ dendritic cells (DCs), the strongest antigen-presenting cells, was reported to induce the occurrence of AR by facilitating CD4+ T cell immune imbalance and subsequent inflammation. Our study was designed to confirm that inhibition of DC autophagy can alleviate the progression of AR by inhibiting the T cell immune imbalance. Methods. The AR mouse model was established by using ovalbumin (OVA). OVA-induced mouse models were then injected intraperitoneally with the autophagy inhibitor Baf-A1. Levels of OVA-specific IgE, PGD2, ECP, LTC4, and Th1/Th2/Th17 cell-related cytokines in serum or nasal lavage fluid (NLF) were examined using the corresponding commercial ELISA kits. Morphological changes in the nasal mucosa were observed by HE staining. Nasal mucosa tissues were collected for western blotting to assess the expression of autophagy markers (LC3, P62, and Beclin 1) in each group of mice. Results. Baf-A1 treatment alleviated the allergic symptoms, mitigated inflammatory immune cell infiltration in the nasal mucosa, decreased IgE, LTC4, ECP, and PGD2 levels in both serum and NLF, impaired CD11c+ DC autophagy, and restored Th1/Th2/Th17 cytokine imbalance in OVA-induced AR mice. Furthermore, Baf-A1 treatment also reversed the immune imbalance of CD4+ T cell subtypes and attenuated Th1/Th2/Th17 cytokine imbalance in vitro. Conclusion. Inhibition of CD11c+ DC autophagy suppressed the immune imbalance of CD4+ T cell subsets and attenuated the subsequent inflammatory response, thereby ameliorating the progression of AR.
- PublicationOpen AccessGATA4 is diagnostically useful for distinguishing primary ovarian mucinous carcinomas from metastatic colorectal adenocarcinomas to the ovary(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Mochizuki, Kunio; Inoue, Tomohiro; Kasai, Kazunari; Kondo, TetsuoAim. Determining the primary origin of an ovarian mucin-producing carcinoma can be challenging at times because some metastases of primary colorectal origin may exhibit gross, microscopic, and/or immunohistochemical features that overlap with those of primary ovarian mucinous carcinomas (OMCs). We hypothesized that GATA binding protein 4 (GATA4) might be a novel, useful marker for differentiating primary OMCs from metastatic colorectal adeno-carcinomas to the ovary. Methodology. For comparison with the usefulness of other markers (special AT-rich sequence-binding protein 2 (SATB2) and caudal type homeobox 2 (CDX2)), we elucidated the expression profiles of GATA4 in OMCs, colorectal non-mucinous adenocarcinomas (CNMACs), and colorectal mucinous adenocarcinomas (CMACs) using immunohistochemistry. Results. We confirmed GATA4 expression (H-score ≥50 points) in 93%, SATB2 in 0%, and CDX2 in 64% of 14 OMCs. GATA4 was expressed in 13%, SATB2 in 90%, and CDX2 in 93% of 30 CNMACs. GATA4 was expressed in 20%, SATB2 in 73%, and CDX2 in 100% of 30 CMACs. Conclusion. The expression of GATA4 in a mucus-producing ovarian tumor strongly supports it being a primary OMC rather than a metastatic colorectal carcinoma: GATA4 expression indicates OMC and SATB2 expression indicates colorectal adenocarcinoma. However, three cases of colorectal adenocarcinoma were GATA4-positive and SATB2-negative, so the GATA4/ SATB2 marker combination is not absolute for determining the primary site. Further research for more markers is necessary to find the ideal combination.