Histology and histopathology Vol.37, nº2 (2022)
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- PublicationOpen AccessPathological diagnosis, differential diagnosis and origin investigation of easily misdiagnosed adult gastric duplication cysts(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Liu, Fangfang; Zhao, HuiminObjectives. To study diagnosis, differential diagnosis, and origin of easily misdiagnosed adult gastric duplication cysts. Methods. Six cases with GDCs were studied using immunohistochemical methods to research the expression of tumor markers. Results. Most GDCs were located in the abdominal cavity outside the digestive organs. The cyst wall tissues included a repetition of the full-thickness structure of the stomach wall that was lined by a variety of different epithelia. The expression of CK7 was positive in all epithelia (6/6), while CK7 expression was positive in cardia glands in 5/5 and positive in fundus glands in 1/5. CK 20 was 100% (4/4) positively expressed in the SCE, 100% (3/3) negative in the CCE, and in the SE. It was also expressed positively 100% (5/5) in fundus glands and 80% (4/5) in cardia glands. Both CK7 and CK20 were negatively expressed in the pyloric glands in case 3. The expression of MUC1 was positive in all epithelia and glands, whereas MUC2 expression was negative. MUC5AC was expressed differently in epithelia and glands. Conclusions. GDCs can originate from the antrum or the fundus of the stomach. Tumor markers can help diagnosis and differential diagnosis. This study may help to improve clinical precision treatment.
- PublicationOpen AccessAnterior cruciate ligament innervation in primary knee osteoarthritis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Guerra González, Adrián; Casa, Carmen da; Crespo, Íñigo; Pescador, David; Benito Garzón, Lorena; Blanco, Juan FObjective. To relate the Anterior Cruciate Ligament (ACL) innervation and histologic degeneration status to the knee osteoarthritis radiologic and functional status. Design. Prospective observational study including 30 consecutive patients affected by primary knee osteoarthritis undergoing Total Knee Arthroplasty (TKA). All patients suffering secondary knee osteoarthritis, an antecedent of an infectious process, malignant process, autoimmune disorder, or previous knee surgery were excluded. We recorded biodemographic, clinical, and radiologic variables of all participants previous to the TKA procedure. ACL tissue was harvested during TKA standard procedure and the obtained sample was fixed in 4% formalin and paraffinembedded. ACL cross-sections were stained by haematoxylin-eosin and Gallego staining for elastic and collagen fibers, and Sevier-Munger silver staining for nervous tissue. Results. ACL samples histologic degeneration classification reported 15.4% normal, 23.1% slight, 26.9% mild, 11.5% moderate and 23.1% marked. We noted 46.2% large nervous fascicles, 15.4% medium fascicles, 3.8% small fascicles, and no nerve fibers were found in 34.6% ACL samples. No significant correlation was found between the histologic degeneration and the nervous fiber quantification (p>0.05, in all cases). We noted a significant histologic degeneration inverse correlation with the VAS scale (p=0.016), and nervous fiber quantification correlation with Lequesne maximum distance walked punctuation (p=0.043). We also noted greater nervous fiber quantification with minor radiological knee osteoarthritis (Kellgren-Lawrence grade II). Conclusions. ACL degeneration and innervation deficit may play a role in primary knee osteoarthritis onset, but the lack of a defining relationship among the different parameters assessed justifies further research in greater populations.
- PublicationOpen AccessMiR-124-3p attenuates brain microvascular endothelial cell injury in vitro by promoting autophagy(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhao, Jing; Wang, Yan; Wang, Dong; Yan, Wei; Zhang, Shishuang; Li, Dai; Han, Zhaoli; Chen, Fanglian; Le, Ping. Traumatic brain injury (TBI) can cause the pathological disruption of the blood-brain barrier (BBB) and associated neurological injury. Reducing the severity of such barrier disruption following TBI can decrease the degree of brain edema, suppress intracranial inflammation, and thereby protect against neurological damage. The BBB is made up of brain microvascular endothelial cells (BMVECs), neurons, pericytes, astrocytes, and extracellular matrix components. In prior analyses, we have demonstrated that miR-124-3p expression is enhanced in microglia-derived exosomes following TBI, with this miRNA being capable of promoting neural repair after such injury. Based upon these results, the present study was formulated to examine the impact of miR-124-3p on BMVEC function and to evaluatethe mechanistic basis for its activity by overexpressing miR-124-3p in these endothelial cells. We utilized a bEnd.3 cell scratch wound in vitro model to simulate TBI-associated brain microvascular endothelial cell injury. Lipofectamine3000 was used to transfect endothelial cells such that they overexpressed miR-124-3p. Fluorescence microscopy was used to observe the effects of miR-124-3p expression on these endothelial cells. TUNEL+CD31 immunofluorescence stainingwas employed to observe endothelial cell apoptosis. Tight junctions were observed via ionconductivity microscopy. Western blotting was used to detect the expression of tight junction proteins (occludin, ZO-1), autophagy-associated proteins (Beclin1, p62, LC3-II/LC3-I), and mTOR-associated proteins (p-mTOR, PDE4B). Chloroquine was used to treat these injured endothelial cells overexpressing miR-124-3p, and endothelial cell apoptosis was assessed via TUNEL+CD31 immunofluorescence staining. We found that the upregulation of miR-124-3p was sufficient to suppress bEnd.3 cell apoptotic death following in vitro scratch injury while promoting the upregulation of the tight junction proteins ZO-1 and occludin in these cells, thereby reducing the degree of leakage across the cerebral microvascular endothelial barrier. These protective effects may be related to the ability of miR124-3p to suppress mTOR signaling and to induce autophagic activity within BMVECs. These data support a model wherein miR-124-3p can inhibit mTOR signaling and promote autophagic induction in BMVECs, thereby protecting these cells against TBIinduced damage.
- PublicationOpen AccessThe role of TNFα/p53 pathway in endometrial cancer mouse model administered with apple seed extract(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Kim, Sang Hwany. Recent studies regarding the ability to relieve and reconstitute the endometrium in the treatment of endometrial cancer are limited. In this study, to analyze endometrial cancer, early endometrial cancer was induced by injecting a colon cancer cell line into the lower abdominal cavity of mice. Subsequently, the apple seed extract was administered orally to determine if the extract could affect the endometrial cancer. Administration of apple seed extract to the endometrial cancer model confirmed that the apoptosis suppressing mechanism was downregulated concurrently with the reduced expression of NF-κB. In contrast, the TNFα/p53 pathway upregulated the apoptosis. A number of clinical inferences could be derived from the results of this study; moreover, the administration of apple seed extract in a cancer metastasis model has not been reported in earlier toxicity induction studies. The results of this study indicated that the apple seed extract partially enhances apoptosis and the immune function related factors in endometrial cells. By improving tissue remodeling, the extract may help to restore the endometrium.
- PublicationOpen AccessFilamin-A expression in laryngeal squamous cell carcinoma and its clinical significance(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ouban, AbderrahmanBackground. Laryngeal squamous cell carcinomas (LSCCs) are tumours with a high incidence of treatment failure and recurrence. Recent strategies to improve the five-year survival rate and to decrease the rates of recurrence and metastases did not improve outcomes significantly. Research efforts in recent years have started focusing on discovering biomarkers of prognosis and management in LSCCs. Filamin-A reportedly has been associated with metastatic disease in a recent study. Analysis of this protein’s expression in LSCCs is lacking in the literature. Materials and Methods. This study analysed the expression of filamin-A, using immunohistochemistry, in a tissue microarray of 80 cases of laryngeal squamous cell cancers. Clinical-pathological parameters were analysed according to filamin-A expression in the tissue microarray. Furthermore, a review of possible mechanisms of this protein in cancer, in general, was presented, along with a review of the protein’s expression in other head and neck tumours. Results. A significant majority of laryngeal squamous cell cancers exhibited positive expression of filamin-A protein. All the filamin-A positive tumours expressed it in their cytoplasm. Significant correlation between filamin-A expression and grade, stage, lymph node status and metastases were found. Conclusion. The above may suggest an important role for filamin-A in LSCCs. Overall, filamin-A expression in laryngeal cancer is in line with evidence seen in other head and neck cancers. Further studies are in order to pinpoint the exact role of this protein in LSCCs, and its possible utilization in the management of these difficult-to-treat tumours.