LncRNA FOXC2-AS1 protects cardiomyocytes from doxorubicin-induced cardiotoxicity through activation of WNT1-inducible signaling pathway protein-1

Doxorubicin (Dox) is an anthracycline antibiotic that has been used to treat different cancers. Dox-induced cardiotoxicity is common in clinical practice, while its mechanism is unknown. It has been proved that lncRNA FOXC2-AS1 may promote doxorubicin resistance and WNT1-inducible signaling pathway protein-1 (WISP1) blocks doxorubicin-induced cardiomyocyte death. Our study aimed to investigate the involvement of lncRNA FOXC2-AS1 and WISP1 in doxorubicin-induced cardiotoxicity and to explore their interactions. In our study we observed that FOXC2-AS1 and WISP1 mRNA were downregulated in heart tissues of mice with Dox-induced cardiotoxicity. FOXC2-AS1 and WISP1 mRNA expression were positively correlated in mice with Dox-induced cardiotoxicity but not in healthy mice. Overexpression of FOXC2-AS1 promoted to viability of mice cardiomyocytes under Dox treatment and also increased the expression level of WISP1. In contrast, WISP1 overexpression showed no significant effect on FOXC2-AS1. We therefore conclude that lncRNA FOXC2-AS1 may upregulate WISP1 to protect cardiomyocytes from doxorubicin-induced cardiotoxicity.     

Identification of Candidate Genes Related to Stem Development in Brassica napus Using RNA-Seq

Plant Molecular Biology Reporter - Plant stems are involved in supporting the entire plant body, thus having an important effect on the yield of oilseed rape. The current understanding of the...     

小地老虎食诱剂糖醋酒液配方筛选及发酵增效作用

【目的】为筛选和规范诱集小地老虎Agrotis ipsilon成虫的最佳糖醋酒液配方及最佳发酵时间,确定发酵液中的挥发物成分。【方法】优选以单一纯物质糖、醋、酒和水进行混配的配方A, B, C和D, 其配比分别为蔗糖(g)∶乙酸(mL)∶无水乙醇(mL)∶纯水(mL)(m/v/v/v)=3∶1∶3∶80, 3∶1∶3∶160, 3∶1∶6∶80和1∶1∶3∶80及常见配方E［白糖(g)∶白醋(mL)∶白酒(mL)∶自来水(mL)= 6∶3∶1∶10(m/v/v/v)］,分别并采用Y型嗅觉仪及GC-MS测试和分析小地老虎成虫对发酵1~15 d后的糖醋酒液的趋性及发酵液中的挥发物成分。【结果】趋性试验结果表明,糖醋酒液B配方对小地老虎诱集效果显著优于A, C, D和E配方,C配方次之。小地老虎成虫对B和C这两种配方发酵8 d发酵液的选择反应率均显著高于对未发酵及发酵5 d和7 d外的其他发酵时间发酵液的选择反应率。挥发物成分组成分析结果显示,糖醋酒液B配方发酵8 d发酵液的挥发物共有41种化合物,主要包括17种烃类化合物、8种醛类化合物、2种酮类化合物、4种醇类化合物、5种酯类化合物和5种醚类化合物。而且发酵8 d的糖醋酒液B配方与其未发酵以及发酵4 d和发酵12 d的糖醋酒液B配方之间的挥发物成分差异较大。【结论】优选并明确单一物质糖、醋、酒和水进行混配的小地老虎食诱剂配方(3∶1∶3∶160, m/v/v/v),其糖醋酒液通过发酵可以产生增效作用,最佳发酵时间为8 d。     

Retracted: The protective effects of TGR5 against ultraviolet B irradiation in epidermal stem cells

Repetitive exposure to ultraviolet radiation (UVR) results in continuous insults to the skin, including continuous loss of the capacities of epidermal stem cells (ESCs). Takeda G-protein-coupled receptor-5 (TGR5) participates in a variety of physiological activities, but its biological function in skin has not been reported. In this study, we report that TGR5 could be detected in ESCs and its expression was reduced after ultraviolet B (UV-B) irradiation. Treatment with the specific TGR5 agonist 3-(2-chlorophenyl)-N-(4-chlorophenyl)-N,5-dimethylisoxazole-4-carboxamide (GPBARA) prevented UV-B-induced oxidative stress by reducing 4-hydroxy-2-nonenal and increasing the level of glutathione. We also found that the presence of GPBARA improved UV-B irradiation-induced mitochondrial dysfunction by elevating mitochondrial membrane potential. Interestingly, our results indicate that GPBARA pretreatment suppressed UV-B irradiation-induced reduced cell viability, release of lactic dehydrogenase, and secretion of high mobility group box 1. Notably, GPBARA pretreatment inhibited UV-B irradiation-induced decrease in integrin β1 and Krt19, dependent on TGR5. Mechanistically, we found that the activation of TGR5 by GPBARA increased Wnt1, Wnt3a, Myc, and cyclin D1 in ESCs. Our data suggest a new function of TGR5 in regulating ESCs.     

Study on the Physiological Mechanism of Early Flowering and Low Male Fertility of Limonium bicolor Mutant vrl15

As biennial recretohalophytes, Limonium bicolor plants need 2 years to complete their life cycle. A growth habit mutant Vernalization Requirement Loss 15 (vrl15) was obtained by ion implantation. However, the biological characteristics of the mutant were unclear. In the current study, the related traits of vrl15 and some possible reasons for these traits were examined. Compared with wild type (WT), vrl15 can bolt and flower in approximately four months without vernalization. Moreover, vrl15 needed much less time to bolting and flowering than wild-type L. bicolor under different vernalization treatments. After 20 days’ vernalization, bolting vrl15 plants had 24 rosette leaves and bolting WT had 31 rosette leaves. Moreover, the pollen number per anther, the proportion of active pollen, the seed setting rate and the 1000 seed weight of vrl15 were all lower than those of WT. The soluble sugar content and soluble protein content in leaves of the vrl15 were much higher than those of WT sowed at the same time. In addition, the GA content in the leaves of bolting vrl15 was higher than that of the non-bolting WT sowed at the same time and non-bolting vrl15, whereas the contents of ABA and BR were much lower than that of the non-bolting WT. These results indicate that to some extent the increase of GA and decrease of ABA and BR content may be involved in the growth habit and male fertility alteration of mutant vrl15 of L. bicolor.

     

Inhibition of miR-181b-5p protects cardiomyocytes against ischemia/reperfusion injury by targeting AKT3 and PI3KR3

Ischemic heart disease (IHD) is the most occurring cardiovascular-associated disease, which is a primary leading cause of cardiac disability and death worldwide. Myocardial ischemia/reperfusion injury (MI/RI) has been linked to IHD-induced cardiomyocytes apoptosis and tissue damage. The clinical studies have indicated that pathophysiologic mechanisms of MI/RI are associated with reactive oxygen species generation, calcium overload, energy metabolism disorder, neutrophil infiltration, and others. However, the genetic mechanism of MI/RI remains unclear. In this study, we successfully established the reproducing abnormal heart observed in rat, of IHD-induced MI/RI post operation. By using these rats, we illustrated that expression of miR-181b-5p was increased not only in both hypoxia/reoxygenation-cultured H9C2 but also heart of myocardial ischemia/reperfusion (MI/R) rat. Suppression of the miR-181b-5p cardiomyocytes apoptosis and rescued myocardial infarction. Additionally, our data indicated that miR-181b-5p negatively regulates the expression of AKT3 and PIK3R3 through directly binding with its 3′-untranslated region. More importantly, suppression of miR-181b-5p protects the cardiomyocytes apoptosis and tissue damage from MI/R via regulation of PIK3R3 and AKT3. Hence, our study indicates that miR-181b-5p is essential for MI/RI via regulation of PI3K/Akt signaling pathway and could be a potential therapeutic target in IHD.     

SNHG15 functions as a tumor suppressor in thyroid cancer

Small nucleolar RNA host gene 15 (SNHG15) has been suggested to be overexpressed, and function as an oncogenic long noncoding RNA (lncRNA) in various types of human malignancies. However, the expression status and function of SNHG15 were still unknown in thyroid cancer. In our study, we assessed the expression status and clinical value in thyroid cancer samples, and explored the effect of SNHG15 on thyroid cancer cell proliferation, migration, and invasion. In results, SNHG15 expression was downregulated in thyroid cancer tissues and cells, and correlated with age, pathology classification, clinical stage, tumor size, distant metastasis, and disease-free survival. The in vitro studies suggested SNHG15 overexpression suppressed cell proliferation, migration, and invasion in thyroid cancer. In summary, SNHG15 serves as tumor suppressive role in thyroid cancer.     

MicroRNA-329-mediated PTTG1 downregulation inactivates the MAPK signaling pathway to suppress cell proliferation and tumor growth in cholangiocarcinoma

Cholangiocarcinoma (CCA) is a severe malignancy usually producing a poor prognosis and high mortality rate. MicroRNAs (miRNAs) have been reported in association with CCA; however, the role miR-329 plays in the CCA condition still remains unclear. Therefore, this study was conducted to explore the underlying mechanism of which miR-329 is influencing the progression of CCA. This work studied the differential analysis of the expression chips of CCA obtained from the Gene Expression Omnibus database. Next, to determine both the expression and role of pituitary tumor transforming gene-1 (PTTG1) in CCA, the miRNAs regulating PTTG1 were predicted. In the CCA cells that had been intervened with miR-329 upregulation or inhibition, along with PTTG1 silencing, expression of miR-329, PTTG1, p-p38/p38, p-ERK5/ERK5, proliferating cell nuclear antigen (PCNA), Cyclin D1, Bcl-2-associated X protein (Bax), B-cell CLL/lymphoma 2 (Bcl-2), and caspase-3 were determined. The effects of both miR-329 and PTTG1 on cell proliferation, cell-cycle distribution, and apoptosis were also assayed. The miR-329 was likely to affect the CCA development through regulation of the PTTG1-mediated mitogen-activated protein kinase (MAPK) signaling pathway. The miR-329 targeted PTTG1, leading to inactivation of the MAPK signaling pathway. Upregulation of miR-329 and silencing of PTTG1 inhibited the CCA cell proliferation, induced cell-cycle arrest, and subsequently promoted apoptosis with elevations in Bax, cleaved caspase-3, and total caspase-3, but showed declines in PCNA, Cyclin D1, and Bcl-2. Moreover, miR-329 was also found to suppress the tumor growth by downregulation of PTTG1. To summarize, miR-329 inhibited the expression of PTTG1 to inactivate the MAPK signaling pathway, thus suppressing the CCA progression, thereby providing a therapeutic basis for the CCA treatment.