Histology and histopathology Vol.36,nº11 (2021)
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- PublicationOpen AccessThe differential expression of perilipin-2 in hepatoblastoma and its association with prognosis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Azukisawa, Sadafumi; Zheng, Jianbo; Guo, Xin; Ura, Hiroki; Niida, Yo; Itoh, Tohru; Yamada, SohsukePerilipin-2, a lipid droplet (LD) coating protein, has been found to be involved in cancer progression. However, its role in hepatoblastoma (HB) is undefined. We collected 87 HB samples and the corresponding clinical data. Immunohistochemistry (IHC) staining was performed to detect perilipin-2 and the association of the perilipin-2 expression with clinical characteristics and prognosis was analyzed. The expression of perilipin-2 was increased in fetal HB components in comparison to embryonal HB components. The predominant staining pattern was vesicular in fetal HB cells, while it was granular in embryonal HB cells. Furthermore, strong expression of perilipin-2 was associated with the histopathological type of fetal predominant HB. Although event-free survival (EFS) did not differ to a statistically significant extent between the strong and weak expression groups in a univariate survival analysis, a multivariate survival analysis revealed that EFS was significantly improved in the strong perilipin-2 expression group. In conclusion, perilipin-2 is differentially expressed in HB and the strong exp
- PublicationOpen AccessMiR-222-3p promotes the proliferation, migration and invasion of papillary thyroid carcinoma cells through targeting SLC4A4(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Zhang, Chunying; Chang, Qing; Hu, Yaojie; Chang, Wang; Guo, Xin; Fu, Liru; Tang, Guoshuai; Chen, ChunyouObjective. An increasing number of studies indicate that miR-222-3p is upregulated in various cancers and can regulate tumor progression. This study aimed to explore the regulatory mechanism of miR-222- 3p in papillary thyroid carcinoma (PTC). Methods. TCGA database was used to dig differentially expressed miRNAs and mRNAs in PTC tissue. Relevant references were searched to determine target miRNA. StarBase, TargetScan and miRDB were applied to predict mRNAs that had binding sites with the target miRNA. Then, the mRNAs were intersected with differentially downregulated mRNAs in TCGA to determine the target mRNA. qRT-PCR was exerted to evaluate gene expression of miR-222-3p and SLC4A4 in PTC. Western blot was performed out to evaluate the protein expression of SLC4A4 in PTC cells. CCK-8, wound healing assay and cell invasion assay were undertaken to observe the proliferative, migratory, and invasive abilities of PTC cells. Dual-luciferase assay was employed to test the binding relationship between miR222-3p and SLC4A4. Results. MiR-222-3p was highly expressed in PTC while SLC4A4 was lowly expressed. Moreover, miR222-3p was able to promote the proliferation, invasion, and migration of PTC cells. SLC4A4 was able to reverse these promotive effects of miR-222-3p. Conclusion. MiR-222-3p can promote the proliferation, migration and invasion of PTC cells through targeting SLC4A4. MiR-222-3p is expected to be a molecular therapeutic target for PTC patients.
- PublicationOpen AccessEnhanced IL-10 inhibits proliferation and promotes apoptosis of HUVECs through STAT3 signaling pathway in sepsis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Xie, Zuohua; Lin, Bing; Jia, Xinju; Su, Ting; Wei, Ying; Tang, Jiping; Yang, Chengzhi; Cui, Chuanbao; Liu, JinxiangAims. The present study aims to determine the expression of interleukin (IL)-10 in peripheral blood of patients with sepsis, and investigate its effects on the biological function of vascular endothelial cells. Methods. Thirty-six sepsis patients and 20 healthy subjects were included. Peripheral blood was collected from all subjects. ELISA was used to determine IL-10 content in serum. A ratio of IL-10+ T cells was determined by flow cytometry. CCK-8 assay was used to investigate proliferation. Cell cycle and apoptosis were analyzed by flow cytometry. Western blotting was used to examine the expression of phosphorylated STAT3 protein. Results. The content of IL-10 and the ratio of IL-10+ T cells were enhanced in pa-tients with sepsis. Serum from patients with sepsis inhibited the proliferation of HU-VECs, and addition of IL-10 antibody reversed this effect. IL-10 in the serum from patients with sepsis promoted the apoptosis of HUVECs. IL-10 inhibited the proliferation and promoted the apoptosis of HUVECs by enhancing the phosphorylation of STAT3. Conclusions. The present study demonstrates that the content of IL-10 and the ratio of IL-10+ T cells in peripheral blood of patients with sepsis are up-regulated, and this inhibits HUVEC proliferation and promotes HUVEC apoptosis through STAT3 sig-naling pathway. The results in this study provide a new experimental basis for further understanding the molecular mechanism of sepsis-induced vascular injury.
- PublicationOpen AccessValproic acid during pregnancy decrease the number of spermatogenic cells and testicular volume in the offspring of mice: Stereological quantification(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Conei, Daniel; Rojas, Mariana; Santamaría, Luis; Risopatrón, JennieValproic acid (VPA) is a drug used to treat epilepsy, bipolar disorders and headaches. As a secondary effect, this antiepileptic drug can cause a decrease in androgens and gonadotropins, and dosedependent testicular defects, such as reduction of testicular weights, sperm motility and degeneration of the seminiferous tubules. In offspring exposed to VPA, its effects have not been evaluated, so the study aimed to determine the morphological effects of the use of VPA along testicular development in mice. 30 adult female BALB/c mice were crossed and divided by age, with embryos of 12.5 days post coitum (dpc), fetuses of 17.5 dpc and male mice 6 weeks postnatal. In each case, the pregnant mouse received 600 mg/kg of VPA, making up the VPA groups, or 0.3 mL of 0.9% physiological solution for the control groups, from the beginning to the end of the pregnancy, orally.t. A morpho-quantitative analysis was carried out on the gonadal development of the male offspring. In the groups treated with VPA, at all ages studied they had lower testicular volume. At 12.5 dpc, they showed less testicular development in the form of sex cords, with fewer gonocytes and somatic cells. At 17.5 dpc, they presented greater interstitial space, fewer spermatogonial, sustentacular Sertoli, peritubular and interstitial Leydig cells. At 6 weeks postnatal, they presented fewer spermatogonia, pachytene spermatocytes, elongated spermatids, sustentacular Sertoli and interstitial Leydig cells, with statistically significant differences. In conclusion, prenatal exposure to VPA causes histopathological alterations in the offspring of mice in testicular development, from the embryonic stage to 6 weeks postnatal.
- PublicationOpen AccessDeath-associated protein kinase 1 correlates with podocyte apoptosis and renal damage and can be mediated by miR-361(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Wu, Guang-jun; Zhao, Hong-biao; Zhang, Xiao-weiBackground. Herein, we aimed to determine whether DAPK1 and its post-transcriptional regulator miR-361 were implicated in high glucose (HG)-induced podocyte injury and renal damage in db/db mice. Materials and methods. Podocytes were incubated with normal glucose (NG; 5 mM) or HG (30 mM). Podocyte apoptosis was evaluated using TUNEL staining. Lentiviral-delivered specific short hairpin RNA (shRNA) was designed to silence DAPK1 expression in podocytes. miR-361 agomir was administrated by tail intravenous injection in db/db diabetic mice to investigate the renoprotection of miR-361 in vivo. Results. Exposure of podocytes to HG led to a significant increase in DAPK1 mRNA and protein levels and a decrease in miR-361 expression levels. Knockdown of DAPK1 attenuated HG-triggered growth inhibition, apoptosis, DNA damage and cell membrane damage in podocytes. Mechanically, DAPK1 was a direct target of miR-361. Transfection with miR-361 mimics into podocytes resulted in a significant decrease in the DAPK1 protein expression level. In addition, HGinduced the up-regulation of the DAPK1 protein expression level in podocytes was restrained by miR-361 mimics transfection. Intriguingly, overexpression of DAPK1 in HG-stimulated podocytes muted miR-361- mediated cytoprotection, including anti-apoptosis, resistance to DNA and membrane damage. In vivo, overexpression of miR-361 protected against hyperglycemia-induced podocyte loss, tubular atrophy and interstitial fibrosis in the kidney of db/db mice. Moreover, overexpression of miR-361 inhibited the protein expression of DAPK1 in the kidney of db/db mice. Conclusion. Our research presented a novel mechanism of HG-induced podocyte damage or renal lesion, supporting the miR-361/DAPK1 signaling pathway that could be used as a potential therapeutic target for the treatment of DN.