Histology and histopathology Vol.37, nº1 (2022)
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- PublicationOpen AccessExpression of epithelial membrane protein (EMP) 1, EMP 2, and EMP 3 in thyroid cancer(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Kim, Eun Kyung; Koo, Ja SeungPurpose. Epithelial membrane protein (EMP) 1, EMP2, and EMP3 are expressed in various types of tumors and have been reported to be involved in carcinogenesis. In this study, we aimed to investigate the expression of these proteins in primary and metastatic thyroid cancer and its clinical implication. Methods. EMP1, EMP2, and EMP3 immunohistochemistry was performed using tissue microarrays of 545 primary thyroid carcinomas [338 papillary thyroid carcinoma (PTC), 111 follicular carcinoma (FC), 69 medullary carcinoma (MC), 23 poorly differentiated carcinoma (PDC), and 4 anaplastic carcinoma (AC)] and 59 recurrent or metastatic PTCs. Results. EMP1 showed high expression in AC, PTC, FC (P<0.001), and EMP2 was highly expressed in AC (P<0.001). EMP1 and EMP2 were not expressed in stromal cells. Expression of EMP3 in tumor cells [EMP3 (T)] was higher in PDC, PTC, and AC (P<0.001), and expression in stromal cells [EMP3 (S)] was observed only in AC and PTC (P=0.001). The expression of EMP1 (P=0.002) and EMP3 (T) (P<0.001) was higher in conventional PTC than in follicular variant PTC. PTC with BRAF V600E mutation showed higher expression of EMP1 (P<0.001), EMP3 (T) (P<0.001), and EMP3 (S) (P=0.012) than PTC without BRAF V600E mutation. In the PTC without BRAF V600E mutation group, expression of EMP3 (S) was associated with shorter disease free survival (P=0.004). Metastatic PTC showed higher EMP2 (3.4% vs. 0%, P=0.022) and lower EMP3 (T) (44.1% vs. 66%, P=0.001) than primary PTC. Conclusions. Expression of EMP1, EMP2, and EMP3 is different according to the subtypes of thyroid cancer. Further studies are needed to determine their role as prognostic markers and treatment target in thyroid cancer.
- PublicationOpen AccessMicroRNA-146b-5p/EPHA7 axis regulates cell invasion, metastasis, proliferation, and temozolomide-induced chemoresistance via regulation of IRAK4/TRAF6/NF-κB signaling pathway in aggressive pituitary adenoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Lou, Xiaohui; Cai, Yeyan; Zheng, Haijun; Zhang, YazhuoBackground. Aggressive pituitary adenoma (APA) is a huge challenge for neurosurgeons. Temozolomide (TMZ) is conventionally used in chemotherapy against APA, but acquired resistance developed during long-term therapy limits its benefits. MiRNA-146b-5p has been confirmed to inhibit tumor metastasis. This study aimed to explore the underlying biological functions of miRNA-146b-5p in APA. Methods. Sixty confirmed APA tissues and corresponding adjacent normal tissues were collected. We established a TMZ-resistant cell line (GH3/TMZ) by exposing GH3 cells to gradually increasing doses of TMZ for 5 months. Cell Counting Kit-8 assay, flow cytometric analysis, RNA pull-down assay, 5-ethynyl20-deoxyuridine assay, dual-luciferase reporter gene assay, wound healing assay, and invasion assay were used to explore the malignant biological characteristics of cells. Immunohistochemistry (IHC), western blotting analysis, and real-time quantitative PCR (qRT-PCR) were used to analyze the expression level of related proteins and nucleic acids. Results. The expression of miRNA-146b-5p was down-regulated not only in APA tissues but also in PA cell lines compared with the matched adjacent nontumor tissues or normal human astrocyte (NHA) cells. Low expression of miRNA-146b-5p was notably associated with poorer disease-free survival rate (P=0.032), overall survival rate (P=0.039), larger tumor size (P=0.028), poorer Knosp grade (P=0.020), and poorer Hardy grade (P=0.006) in APA patients. MiRNA146b-5p negatively regulated cell proliferation, invasion, migration, and induced apoptosis in GH3 cells. Overexpression of miRNA-146b-5p suppressed IRAK4 and TRAF6 protein expression and negatively regulated NF-κB phosphorylation. The restoration of EPHA7 expression in GH3 cells notably reversed the inhibitory effects of miRNA-146b-5p. MiRNA-146b-5p expression was significantly down-regulated and EPHA7 gene expression was significantly up-regulated in GH3/TMZ cells, compared to the parental cell line. Similarly, EPHA7 was up-regulated, while the miRNA-146b-5p level was down-regulated in chemoresistance tissues more than in chemosensitive tissues. The autophagic activity was decreased markedly with increasing miRNA-146b-5p expression, while it was enhanced after Lv-EPHA7 treatment in GH3/TMZ cells. Conclusions. MiRNA-146b-5p can inhibit EPHA7 expression, suppress the IRAK4/TRAF6/NF-κB signaling pathway, and weaken PA cell invasion, metastasis, proliferation, and TMZ-induced chemoresistance in vitro.
- PublicationOpen AccessThe roles of microglia in neural remodeling during retinal degeneration(Retina remodeling is a consequence of many retinal degenerative diseases that are characterized by progressive photoreceptor death. Retina remodeling involves a series of complex pathological processes, consisting of photoreceptor degeneration and death, as well as retinal cell reprogramming and "rewiring". This rewiring alters retinal neural circuits that are centered on synaptic connections and lead to widespread death of retinal cells. Retinal remodeling, especially inner retinal remodeling, is the major factor that limits the effectiveness of various treatment strategies, including cell therapy; thus, it is important to elucidate the mechanisms involved in retinal remodeling during retinal degeneration. Microglia are the dominant immune cells in the retina. Microglia monitor the retinal microenvironment, are activated following retinal injury or degeneration, have powerful phagocytosis capabilities, and play a critical role in synaptic pruning during central neural system development. Analogously, microglia have been found to participate in the clearance of synaptic elements in a complement-dependent manner in the classic retinitis pigmentosa (RP) model, Royal College of Surgeons (RCS) rats, and retard the formation of ectopic neuritogenesis and the deterioration of visual function during retinal degeneration. Since previous research on microglia has rarely concentrated on synaptic remodeling during retinal degeneration, summarizing the microglial mechanisms involved in retinal remodeling is necessary in order to design compounds targeting microglia and retinal remodeling that might be promising therapeutic strategies for treating retinal degeneration., 2022) Gao, Hui; Huang, Xiaona; He, Juncai; Zou, Ting; Chen, Xuan; Xu, HaiweiRetina remodeling is a consequence of many retinal degenerative diseases that are characterized by progressive photoreceptor death. Retina remodeling involves a series of complex pathological processes, consisting of photoreceptor degeneration and death, as well as retinal cell reprogramming and "rewiring". This rewiring alters retinal neural circuits that are centered on synaptic connections and lead to widespread death of retinal cells. Retinal remodeling, especially inner retinal remodeling, is the major factor that limits the effectiveness of various treatment strategies, including cell therapy; thus, it is important to elucidate the mechanisms involved in retinal remodeling during retinal degeneration. Microglia are the dominant immune cells in the retina. Microglia monitor the retinal microenvironment, are activated following retinal injury or degeneration, have powerful phagocytosis capabilities, and play a critical role in synaptic pruning during central neural system development. Analogously, microglia have been found to participate in the clearance of synaptic elements in a complement-dependent manner in the classic retinitis pigmentosa (RP) model, Royal College of Surgeons (RCS) rats, and retard the formation of ectopic neuritogenesis and the deterioration of visual function during retinal degeneration. Since previous research on microglia has rarely concentrated on synaptic remodeling during retinal degeneration, summarizing the microglial mechanisms involved in retinal remodeling is necessary in order to design compounds targeting microglia and retinal remodeling that might be promising therapeutic strategies for treating retinal degeneration.
- PublicationOpen AccessAlterations in the von Ebner's gland secretion and implications for taste sensation in diabetic (db/db) mice(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Liao, Meng-Lin; Kung, Hsiu-Ni; Lu, Kuo-Shyan; Shen, Jia-Hong; Peng, Wei-HaoThe taste buds and associated glands, known as von Ebner's glands (VEGs), are involved in and augment gustatory function. The obese diabetic db/db mouse, which has defects in the leptin receptor, displays enhanced neural responses to, and an elevated behavioral preference for, sweet stimuli. However, the effect of diabetes on the morphology of circumvallate papilla (CVP) taste buds and the role of VEGs have not been investigated. The present study aimed to compare the CVP taste buds and VEGs in wildtype (Wt) and type 2 diabetic (db/db) mice. These mice were divided into control and isoproterenol-treated (at 1 h, 2 h, and 4 h after one day of fasting) groups, and were sacrificed for morphometric, immunohistochemical, and ultrastructural analyses. Morphometry revealed no significant difference in papilla size and the number of taste buds in the control and diabetic groups. Detection of PGP 9.5- immunoreactivity revealed nerve fibers in the trench wall of vallate papillae, but no significant differences were detected between groups. α-Amylase immunoreactivity levels in Wt and db/db mice were also similar. However, 1 h after isoproterenol injection, the majority of the VEG secretion of db/db mice was discharged, while the level of α-amylase was restored by 2 h after injection. The effect on α-amylase was in line with the quantitative ultrastructural analysis of the secretory granules. Our findings suggest diabetic metabolic disturbances in db/db mice do not alter the structure or innervation of CVP taste buds. However, the VEG secretory pattern was altered in db/db mice and might disrupt taste sensation.
- PublicationOpen AccessThe role of endocervical curettage in detection and treatment of cervical canal lesions(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Lang, Lin; Jia, Ying; Duan, Zhaoning; Luo, Jin Wu, Ming; Tian, PuObjective. To screen out high-risk groups of endocervical lesions, explore the effect of length of excision on margin status in women with abnormal endocervical curettage (ECC) and explore the role of ECC in the additional detection of high-grade squamous intraepithelial lesion or worse (HSIL+) under colposcopy and lesion-targeted biopsies. Methods. The study included 936 patients who underwent loop electrosurgical excision procedure (LEEP) for cervical lesions which were diagnosed by cervical biopsy and ECC at the cervical clinic of the First Affiliated Hospital of Chongqing Medical University from January 2014 and December 2018. The correlations among abnormal ECC, human papillomavirus (HPV) type, cytology, margin of excision, and age were analyzed by Pearson's χ2 test and multivariate logistic regression analysis. Results. Abnormal ECC was associated with HPV16 infection (P<0.001), or HSIL cervical cytology or worse (P<0.001), or aged 50 years old or older (P<0.001). Abnormal ECC was associated with positive margin of excision (P<0.001). For patients with abnormal ECC, the length of excision was independent of margin status (P=0.762). Among all the 491 patients with HSIL+ diagnosed by either cervical biopsy or ECC, the additional detection rate of HSIL+ by ECC was only 8.76% (43/491). Conclusion. In our study, ECC was recommended in women with HPV-16 infection, HSIL cervical cytology or worse, aged 50 or older, or invisible transformation zone in colposcopy. At the same time, our results suggested that ECC abnormalities were associated with positive margin of excision. The data did not support performing a longer length of excision in patients with abnormal ECC, especially in women with fertility needs. In summary, patients with abnormal ECC should be given more attention and follow-up to avoid missing residual lesions.