Histology and histopathology Vol.37,nº11 (2022)
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- PublicationOpen AccessNOL4 is a novel nuclear marker of small cell carcinoma and other neuroendocrine neoplasms(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Lee, Jung Hee; Shin, Dong Hoon; Lee, Sang Yull; Park, Jun Young; Kim, So Young; Hwang, Chung Su; Lee, Hyun Jung; Na, Joo Young; Kim, Jee YeonNeuroendocrine neoplasms (NENs) such as small cell lung cancer (SCLC) and large cell neuroendocrine carcinoma (LCNEC) have characteristic histologies, but immunohistochemistry using neuroendocrine markers is still desirable to confirm diagnosis. CD56 is the most sensitive marker, but also stains various normal tissues and other tumors. Recently, we reported that nucleolar protein 4 (NOL4) is present in the blood of SCLC patients and found it was stained in the SCLC nuclei. In this study, we compared expressions of NOL4 and CD56, using 64 cases of SCLC, 18 cases of LCNEC, 6 cases of atypical carcinoid tumor, 7 cases of typical carcinoid tumor, 68 cases of lung adenocarcinoma, and 62 cases of lung squamous cell carcinoma. For primary lung NENs, sensitivity, specificity, positive predictive value (PPV) and negative predictive value of NOL4 were 77.5%, 95.8%, 93.2%, and 85.1%, respectively, while those of CD56 were 92.1%, 93.3%, 91.1%, and 94.1%. The specificity and PPV of NOL4 were higher than those of CD56, although the differences were not statistically significant. However, NOL4 retains its nuclear immunoreactivity in areas of crush artifact or necrosis. Furthermore, NOL4 was not expressed in adjacent normal tissues including bronchial cells and pneumocytes. Therefore, a combination of NOL4 staining with other cytoplasmic or membranous neuroendocrine markers might enhance diagnostic utility for SCLC and other NENs.
- PublicationOpen AccessUpregulation of lncRNA HITT promotes cell apoptosis by suppressing the maturation of miR-602 in gastric cancer(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Chen, Yun; Ouyang, Canhui; Liao, Lingyun; Zhou, Yun; Meng, Fan; Liu, Yao; Ye, JingIt has been reported that HITT can inhibit colon cancer. However, the role of HITT in gastric cancer (GC) is unknown. Our preliminary sequencing data revealed the altered expression of HITT in GC and its close correlation with miR-602, suggesting the involvement of HITT and its potential interaction with miR-602 in GC. This study explored the role of HITT and its crosstalk with miR-602 in GC. In this study, the expression of HITT, premature and mature miR-602 in paired GC and normal tissues (62 patients) was detected by RT-qPCR. RNA pull-down assay was performed to evaluate the direct interaction between HITT and mature miR-602. The subcellular location of HITT was assessed by nuclear fractionation assay. The role of HITT in regulating miR-602 maturation was explored by overexpression assay. Cell apoptosis was analyzed by flow cytometry. Our data illustrated that HITT was highly upregulated and mature miR-602 was downregulated in GC. No alteration in premature miR602 in GC was observed. HITT was located in both nucleus and cytoplasm, and it can directly interact with miR-602. In addition, overexpression of HITT in GC cells increased the expression levels of mature miR-602 but not premature miR-602. Overexpression of HITT further increased GC cell apoptosis and suppressed the role of miR-602 in inhibiting GC cell apoptosis. In conclusion, HITT may promote GC cell apoptosis by suppressing the maturation of miR-602.
- PublicationOpen AccessExploring the relationship of brown adipose tissue to bone microarchitecture using 7T MRI and micro-CT(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Ping; Yu, Baohai; Shao, Shuying; Zhang, Ranxu; Zeng, Yan; Li, Jujia; Ren, Congcong; Zhou, Xiaoyue; Zhao, JianBackground. Brown adipose tissue (BAT) is involved both in energy production and bone metabolism. The purpose of this study was to analyze the relationship between BAT and microarchitecture at cancellous and cortical bone using Kunming mice and the methods of 7T magnetic resonance imaging (MRI) combined with micro-CT. Methods. Twenty-four female Kunming mice were examined by 7T MRI and measured T2* relaxation time on the deep and superficial interscapular BAT (iBAT) and subcutaneous white adipose tissue (sWAT). Cancellous bone microarchitecture of the distal femur and cortical bone of the middle femur were examined by micro-CT. A paired t-test was used to analyze the differences in T2* values between iBAT and sWAT. The correlation between BAT T2* values and bone microstructure parameters were analyzed using Pearson’s correlation. Results. T2* values of the deep and superficial iBAT (6.36±3.31 ms and 6.23±2.61 ms) were significantly shorter than those of sWAT (16.30±3.05 ms, tdeep iBAT=- 10.816), tsuperficial iBAT=-12.276, p<0.01). Deep iBAT T2* values were significantly and negatively correlated with bone volume, cancellous thickness, and bone thickness (Th) and trabecular thickness (Tb.Th) of the cancellous bone of femur. Deep iBAT T2* values were significantly and positively correlated with the structural model index of cancellous bone of femur. Deep iBAT T2* values were significantly and negatively correlated with bone mineral density of the cortical bone of femur. Conclusions. MRI can distinguish the two adipose tissues from each other. T2* values of BAT were lower than WAT on MRI. BAT related bone remodeling was more correlated with the microstructure of cancellous bone than that of cortical bone.
- PublicationOpen AccessTherapeutic effect of adipose-derived mesenchymal stem cells (AD-MSCs) compared to pirfenidone on corticosteroid resistance in a mouse model of acute exacerbation of idiopathic pulmonary fibrosis(2022) Fikry, Heba; Saleh, Lobna A.; Gawad, Sara AbdelIntroduction. Acute exacerbation-idiopathic pulmonary fibrosis (AE-IPF) is a life-threatening condition. In the treatment of AE-IPF, corticosteroid medication is commonly utilized. However, there is insufficient evidence to justify its usage. Pirfenidone (PFD) has recently been discovered to be effective in the treatment of AE-IPF patients. However, regenerative therapy, such as stem cell therapy or tissue engineering, is necessary due to ineffective and limited therapies. Combining MSC transplantation with pharmacological therapy may also give additional benefits; nevertheless, its use must be proven experimentally. As a result, the goal of this study was to assess the therapeutic effects of adipose-derived mesenchymal stem cells (AD-MSCs) on corticosteroid resistance in an animal model of AE-IPF caused by bleomycin compared to PFD. Materials and methods. Seventy C57BL/6J male mice were randomly divided into seven groups, control, BLM, methylprednisolone (MP), PFD, AD-MSCs, PFD +MP, and AD-MSCs +MP. Results. In terms of survival, collagen deposition, the acute lung injury score (ALI), and the Ashcroft score, AD-MSCs exceeded PFD. AD-MSCs + MP provided protection and preserved the lung's architecture in BLM-induced AE. In addition, AD-MSCs successfully decreased chemokine (CC motif) ligand-2 (CCL2) positive cells and lower pro-fibrotic and proinflammatory cytokines. Conclusions. AD-MSCs enhanced histological structure, Ashcroft and ALI scores, lung collagen deposition, survival, and cytokines in an animal model of AE-IPF. As a result, we believe that AD-MSCs may be more therapeutically helpful for AE-IPF than presently available therapies, either alone or in conjunction with MP.
- PublicationOpen AccessLncRNA SNHG15 regulates hypoxic-ischemic brain injury via miR-153-3p/SETD7 axis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Fu, Jiding; Huang, Yunbo; Xian, LewuHypoxic-ischemic encephalopathy (HIE) is a leading cause of fatality and morbidity in newborns. Long non-coding RNAs (lncRNAs) Small Nucleolar RNA Host Gene 15 (SNHG15) was elevated in the peripheral blood of patients with acute cerebral ischemia, but its role in HI brain injury remained elusive. Hence, this study aimed to investigate the effect of SNHG15 on HI brain injury and study the precise mechanism of action. In this study, a mouse model of HI brain injury was established through ligating right carotid arteries. The oxygen-glucose deprivation (OGD) model was established in PC12 cells. Results showed that SNHG15 was elevated in brain tissues of mice with HI brain injury, and knockdown of SNHG15 attenuated HI-induced impairment of neurobehavioral function, brain edema, brain injury, and cell apoptosis. Besides, SNHG15 acted as a miR-153-3p sponge. SETD7 was identified to be a target of miR-153-3p. Furthermore, down-regulation of SNHG15 inhibited the OGD-induced increase in SETD7 expression in PC12 cells. Moreover, SNHG15 modulated OGD-induced cell apoptosis and decrease of cell viability through the miR-153- 3p/SETD7 axis. In conclusion, knockdown of SNHG15 alleviated HI brain injury through modulating the miR153-3p/ SETD7 axis. SNHG15 may be a prospective target for HIE therapy