Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex

Long noncoding RNAs (lncRNAs) play important roles in the spatial and temporal regulation of muscle development and regeneration. Nevertheless, the determination of their biological functions and mechanisms underlying muscle regeneration remains challenging. Here, we identified a lncRNA named lncMREF (lncRNA muscle regeneration enhancement factor) as a conserved positive regulator of muscle regeneration among mice, pigs and humans. Functional studies demonstrated that lncMREF, which is mainly expressed in differentiated muscle satellite cells, promotes myogenic differentiation and muscle regeneration. Mechanistically, lncMREF interacts with Smarca5 to promote chromatin accessibility when muscle satellite cells are activated and start to differentiate, thereby facilitating genomic binding of p300/CBP/H3K27ac to upregulate the expression of myogenic regulators, such as MyoD and cell differentiation. Our results unravel a novel temporal-specific epigenetic regulation during muscle regeneration and reveal that lncMREF/Smarca5-mediated epigenetic programming is responsible for muscle cell differentiation, which provides new insights into the regulatory mechanism of muscle regeneration.     

An insight into planarian regeneration

BackgroundPlanarian has attracted increasing attentions in the regeneration field for its usefulness as an important biological model organism attributing to its strong regeneration ability. Both the complexity of multiple regulatory networks and their coordinate functions contribute to the maintenance of normal cellular homeostasis and the process of regeneration in planarian. The polarity, size, location and number of regeneration tissues are regulated by diverse mechanisms. In this review we summarize the recent advances about the importance genetic and molecular mechanisms for regeneration control on various tissues in planarian.MethodsA comprehensive literature search of original articles published in recent years was performed in regards to the molecular mechanism of each cell types during the planarian regeneration, including neoblast, nerve system, eye spot, excretory system and epidermal.ResultsAvailable molecular mechanisms gave us an overview of regeneration process in every tissue. The sense of injuries and initiation of regeneration is regulated by diverse genes like follistatin and ERK signaling. The Neoblasts differentiate into tissue progenitors under the regulation of genes such as egfr‐3. The regeneration polarity is controlled by Wnt pathway, BMP pathway and bioelectric signals. The neoblast within the blastema differentiate into desired cell types and regenerate the missing tissues. Those tissue specific genes regulate the tissue progenitor cells to differentiate into desired cell types to complete the regeneration process.ConclusionAll tissue types in planarian participate in the regeneration process regulated by distinct molecular factors and cellular signaling pathways. The neoblasts play vital roles in tissue regeneration and morphology maintenance. These studies provide new insights into the molecular mechanisms for regulating planarian regeneration.

Genetic and molecular mechanisms for regeneration control on various tissues in planarian.     

Effects of highly selective sensory/motor nerve injury on bone metabolism and bone remodeling in rats

Objectives:This work aimed to investigate the mechanism of selective sensory/motor nerve injury in affecting bone metabolism and remodeling.Methods:The selective sensory/motor nerve injury rat model was constructed through posterior rhizotomy (PRG), anterior rhizotomy (ARG), or anterior combined with posterior rhizotomy (APRG) at the L_4-6 sensory/motor nerves on the right side of rats. Sham-operated (SOG) rats served as control. At 8 weeks after surgery, the sciatic nerves, spinal cord segments L₅ and tibial tissues were collected for analysis.Results:the integrity of trabecular bone was damaged, the number of trabecular bone was decreased and the number of osteoclasts were increased in ARG group. ARG activated NF-κβ and PPAR-γ pathways, and inhibited Wnt/β-catenin pathway. ARG group exhibited high turnover bone metabolism. In PRG group, the trabecular bone morphology became thinner, and the number of osteoclasts was increased. NF-κβ pathway was activated and OPG/RANKL ratio was decreased in PRG group. The activated osteoclasts, reduced osteoblasts activity and lower turnover bone metabolism were observed in PRG group. Additionally, the bone metabolism in APRG group was similar to ARG group.Conclusion:The posterior rhizotomy and anterior rhizotomy induced the different degree of osteoporosis in rats, which may attribute to regulate Wnt/β-catenin, NF-κβ and PPAR-γ signalling pathways.     

A comparative study of the ability of recombinant oncolytic adenovirus,doxorubicin and tamoxifen to inhibit the proliferation of breast cancer cells

In this study, we compared the inhibitory effects of recombinant oncolytic adenovirus (Ad‐apoptin‐hTERTp‐E1a, Ad‐VT) with that of doxorubicin (DOX), a first‐line chemotherapy drug, and tamoxifen (TAM), an endocrine therapy drug, on the proliferation of breast cancer cells. We found that Ad‐VT could effectively inhibit the proliferation of breast cancer cells (p < 0.01); the inhibition rate of Ad‐VT on normal mammary epithelial MCF‐10A cells was less than 20%. DOX can effectively inhibit the proliferation of breast cancer cells and also has a strong inhibitory effect on MCF‐10A cells (p < 0.01). TAM also has a strong inhibitory effect on breast cancer cells, among which the oestrogen‐dependent MCF‐7 cell inhibition was stronger (p < 0.01), At higher concentrations, TAM also had a high rate of inhibition (>70%) on the proliferation of MCF‐10A cells. We also found that both recombinant adenovirus and both drugs could successfully induce tumour cell apoptosis. Further Western blot results showed that the recombinant adenovirus killed breast cancer cells through the endogenous apoptotic pathway. Analysis of the nude mouse subcutaneous breast cancer model showed that Ad‐VT significantly inhibited tumour growth (the luminescence rate of cancer cells was reduced by more than 90%) and improved the survival rate of tumour‐bearing mice (p < 0.01). Compared with DOX and TAM, Ad‐VT has a significant inhibitory effect on breast cancer cells, but almost no inhibitory effect on normal breast epithelial cells, and this inhibitory effect is mainly through the endogenous apoptotic pathway. These results indicate that Ad‐VT has significant potential as a drug for the treatment of breast cancer.     

One night of sleep deprivation induces release of small extracellular vesicles into circulation and promotes platelet activation by small EVs

Extracellular vesicles (EVs) are emerging as key players in intercellular communication. Few studies have focused on EV levels in subjects with sleep disorders. Here, we aimed to explore the role of acute sleep deprivation on the quantity and functionality of circulating EVs, and their tissue distribution. EVs were isolated by ultracentrifugation from the plasma of volunteers and animals undergoing one night of sleep deprivation. Arterio‐venous shunt, FeCl₃ thrombus test and thrombin‐induced platelet aggregation assay were conducted to evaluate the in vivo and in vitro bioactivity of small EVs. Western blotting was performed to measure the expression of EV proteins. The fate and distribution of circulating small EVs were determined by intravital imaging. We found that one night of sleep deprivation triggers release of small EVs into the circulation in both healthy individuals and animals. Injection of sleep deprivation‐liberated small EVs into animals increased thrombus formation and weight in thrombosis models. Also, sleep deprivation‐liberated small EVs promoted platelet aggregation induced by thrombin. Mechanistically, sleep deprivation increased the levels of HMGB1 protein in small EVs, which play important roles in platelet activation. Furthermore, we found sleep deprivation‐liberated small EVs are more readily localize in the liver. These data suggested that one night of sleep deprivation is a stress for small EV release, and small EVs released here may increase the risk of thrombosis. Further, small EVs may be implicated in long distance signalling during sleep deprivation‐mediated adaptation processes.     

Positional behavior and canopy use of black snub-nosed monkeys Rhinopithecus strykeri in the Gaoligong Mountains,Yunnan, China

Studies on positional behavior and canopy use are essential for understanding how arboreal animals adapt their morphological characteristics and behaviors to the challenges of their environment. This study explores canopy and substrate use along with positional behavior in adult black snub-nosed monkeys Rhinopithecus strykeri, an endemic, critically endangered primate species in Gaoligong Mountains, southwest China. Using continuous focal animal sampling, we collected data over a 52-month period and found that R. strykeri is highly arboreal primarily using the high layers of the forest canopy (15–30 m), along with the terminal zone of tree crowns (52.9%), medium substrates (41.5%), and oblique substrates (56.8%). We also found sex differences in canopy and substrate use. Females use the terminal zones (56.7% versus 40.4%), small/medium (77.7% versus 60.1%), and oblique (59.9% versus 46.5%) substrates significantly more than males. On the other hand, males spend more time on large/very large (39.9% versus 22.3%) and horizontal (49.7% versus 35.2%) substrates. Whereas both sexes mainly sit (84.7%), and stand quadrupedally (9.1%), males stand quadrupedally (11.5% versus 8.3%), and bipedally (2.9% versus 0.8%) more often than females. Clamber, quadrupedalism, and leap/drop are the main locomotor modes for both sexes. Rhinopithecus strykeri populations never enter canopies of degenerated secondary forest and mainly use terminal branches in the middle and upper layers of canopies in intact mid-montane moist evergreen broadleaf forest and hemlock coniferous broadleaf mixed forests across their habitat.     

河岸带农田不同恢复年限对土壤碳氮磷生态化学计量特征的影响——以温榆河为例

弃耕地撂荒是土壤与植被向自然方向进行的次生演替,研究河岸带土壤撂荒后碳氮磷生态化学计量特征,是恢复和重建由农田干扰导致的退化河岸带生态系统的重要科学基础之一。以河岸带农地为对照,不同撂荒年限(撂荒2年、撂荒8年、撂荒10年)的土壤为研究对象,探索不同撂荒年限对土壤碳、氮、磷含量及相互关系的影响。结果表明:(1)土壤有机碳、氮的含量均呈现撂荒10年>撂荒8年>农田>撂荒2年;土壤中磷含量呈现撂荒10年>撂荒8年>撂荒2年>农田;农田和各撂荒年限的土壤碳、氮、磷含量,均随着土层深度的增加而呈降低的规律,但土壤碳和氮差异的显著性比磷明显。(2)河岸带土壤中C/N、C/P的均值均呈现:撂荒10年>农田>撂荒8年>撂荒2年趋势。N/P的均值呈现:撂荒10年(0.78)>农田(0.77)>撂荒8年(0.77)>撂荒2年(0.67),表明N是本研究区河岸带植被恢复的限制性营养元素。(3)河岸带农田和不同撂荒年限土壤碳、氮含量均存在极显著的耦合线性关系,而碳与磷、氮与磷之间的线性拟合程度相对较低。(4)在农田撂荒演替的初期阶段(2...     

基于生态系统服务和生态系统健康的生态风险评价——以长株潭城市群为例

基于生态系统服务和生态系统健康的生态风险评估框架为城市群生态风险管理和国土生态修复提供新的视角。以生态风险评估框架为基础,综合运用生态系统服务、生态系统健康评估模型以及相关分析法对长株潭城市群展开生态风险评价,并对风险程度进行分类。结果表明:(1)城市群的城市化水平提升,区域生态风险也随之增加。生态系统服务价值、生态系统组织、生态系统活力、生态系统弹性等生态指数呈现下降趋势。(2)人工表面比率和生态指数之间的Pearson相关系数表明,人工表面比率与生态指数之间存在负相关关系,人工表面比率是生态风险提升的关键因素。(3)城市群人工表面比率要控制在36%以下,以进行生态风险管理和国土生态修复。总的来说,评价框架可以作为区域生态风险的评价终点。