ABSTRACT
Coastal zone ecosystems in Jiangsu have produced different degrees of spatial response and degradation characteristics under complex external disturbances, especially significant spatiotemporal evolution of landscape pattern in recent decades. It is urgent to carry out comprehensive assessment on landscape ecology covering landscape composition, configuration, and function at multiple scales. We analyzed the spatial and temporal variations of landscape ecological condition index (LECI) in large-scale coastal zone of Jiangsu Province from 1990 to 2020, assessed landscape ecological conditions of 14 county-level districts, and selected evaluation units with side lengths of 100, 200, , 1000 m to understand the spatial scale effects of LECI. The results showed that the indicators of landscape composition, configuration and function could sensitively reflect the changes of LECI, which could comprehensively evaluate landscape ecological condition of Jiangsu coastal zone during the study period, with 300 m evaluation unit being the best spatial scale. The LECI value in the study area fluctuated. Landscape ecological condition was the best in 1990 and the worst in 2020. Landscape composition and configuration had a greater impacts on the changes of landscape ecological condition. The fluctuation of LECI in different counties and cities was closely related to intense human activities. Human activities, such as industrial development and urban expansion, had damaged landscape ecological status. The establishment of nature reserves had restored landscape ecological status to a certain extent. LECI could effectively indicate the changes of landscape ecological status of large-scale coastal zone, and provide multi-perspective suggestions for space utilization and protection.
Subject(s)
Anthropogenic Effects , Ecosystem , China , Cities , Conservation of Natural Resources/methods , Ecology , Industrial DevelopmentABSTRACT
Recent studies demonstrate that RNA species could regulate each other by competing for shared microRNA response elements (MREs). This regulatory model is called competing endogenous RNA (ceRNA). Currently, the identified ceRNAs cover coding and non-coding RNAs. The latter includes pseudogene transcripts, long non-coding RNAs (lncRNAs), circular RNAs (circRNAs) and so on. In this review, we summarize the biological functions of regulatory networks consisting of various types of ceRNAs and their roles in the pathological and physiological processes. Additionally, several factors that may regulate ceRNAs were discussed.
Subject(s)
Pseudogenes/physiology , RNA, Long Noncoding/physiology , RNA/physiology , Animals , Gene Regulatory Networks , Humans , MicroRNAs/physiology , RNA, Circular , RNA, Messenger/physiologyABSTRACT
EGC was prepared from green tea polyphenols through column chromatography of a polyamide (3.6 × 40 cm). Three dosages of EGC (0.25, 0.5, 1.0 g kg(-1) d(-1)) were ingested respectively by ICR mice via gavage. Compared with the control group, group EGC0.5 (dosage, 0. 5 g kg(-1) d(-1)) and group EGC1.0 (dosage, 1.0 g kg(-1) d(-1)) presented significant inhibition on platelet aggregation in mice accompanied by 18.4 and 25.6% of inhibition ratio, respectively. The bleeding times (BT) of mice in group EGC0.5 and group EGC1.0 were significantly prolonged (P < 0.01) as well as blood clotting time (BCT) in group EGC1.0 (P < 0.05). All three dosages of EGC prolonged activated partial thromboplastin time (APTT) significantly (P < 0.01), but had no prominent effect on prothrombin time (PT) and fibrinogen level which indicated that the anticoagulation of EGC could not be attributed to the level decrease of coagulation factor such as fibrinogen. The results demonstrated that EGC had prominent antiplatelet activity and blood anticoagulation in a dose-dependent manner.
Subject(s)
Anticoagulants/pharmacology , Antioxidants/pharmacology , Blood Coagulation/drug effects , Blood Platelets/drug effects , Camellia sinensis/chemistry , Catechin/analogs & derivatives , Plant Extracts/pharmacology , Animals , Anticoagulants/chemistry , Antioxidants/chemistry , Blood Platelets/physiology , Catechin/chemistry , Catechin/pharmacology , Fibrinogen/metabolism , Mice , Mice, Inbred ICR , Plant Extracts/chemistryABSTRACT
Though continuous development and progress have been made in the early diagnosis and treatment of cancer, it is still difficult to find a sensitive, accurate and minimally invasive biomarker for cancer diagnosis and treatment. MicroRNA (miRNA) is a class of non-coding small endogenous RNAs of 21-24 nucleotides in length. As a novel molecular biomarker, extracellular miRNA (ec-miRNA) has the potential to be a minimally invasive, highly sensitive and highly specific marker in cancer diagnosis. Many research achievements of ec-miRNA have been accumulated in recent years. In this paper, the origin, function and detection of ec-miRNA, its role in lung cancer diagnosis as a novel molecular biomarker, and some issues are reviewed.
Subject(s)
Biomarkers, Tumor/genetics , Biomarkers, Tumor/metabolism , Extracellular Matrix/genetics , Extracellular Matrix/metabolism , Lung Neoplasms/genetics , Lung Neoplasms/metabolism , MicroRNAs/metabolism , HumansABSTRACT
Profilin-1 has recently been linked to vascular hypertrophy and remodeling. Here, we assessed the hypothesis that angiotensin (Ang) II type I receptor antagonist telmisartan improves vascular hypertrophy by modulation of expression of profilin-1 and angiotensin-converting enzyme 2 (ACE2). Ten-week-old male spontaneously hypertensive rats (SHR) were received oral administration of telmisartan (5 or 10mg/kg; daily) or saline for 10 weeks. Compared with Wistar-Kyoto (WKY) rats, there were marked increases in systolic blood pressure and profilin-1 expression and reduced ACE2 and peroxisome proliferator activated receptor-γ (PPARγ) levels in aorta of SHR, associated with elevated extracellular-signal regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) phosphorylation signaling and aortic hypertrophy characterized with increased media thickness, which were strikingly reversed by telmisartan. In cultured human umbilical artery smooth muscle cells (HUASMCs), Ang II induced a dose-dependent increase in profilin-1 expression, along with decreased ACE2 protein expression and elevated ERK1/2 and JNK phosphorylation. In addition, blockade of ERK1/2 or JNK by either specific inhibitor was able to abolish Ang II-induced ACE2 downregulation and profilin-1 upregulation in HUASMCs. Importantly, treatment with telmisartan (1 or 10 µM) or recombinant human ACE2 (2mg/ml) largely ameliorated Ang II-induced profilin-1 expression and ERK1/2 and JNK phosphorylation and augmented PPARγ ï expression in the cultured HUASMCs. In conclusion, telmisartan treatment attenuates vascular hypertrophy in SHR by the modulation of ACE2 and profilin-1 expression with a marked reversal of ERK1/2 and JNK phosphorylation signaling pathways.
Subject(s)
Aorta/pathology , Benzimidazoles/therapeutic use , Benzoates/therapeutic use , Peptidyl-Dipeptidase A/biosynthesis , Profilins/biosynthesis , Angiotensin-Converting Enzyme 2 , Animals , Aorta/drug effects , Cells, Cultured , Humans , Hypertrophy/metabolism , Hypertrophy/prevention & control , JNK Mitogen-Activated Protein Kinases/metabolism , Male , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Muscle, Smooth, Vascular/cytology , PPAR gamma/biosynthesis , Peptidyl-Dipeptidase A/metabolism , Profilins/drug effects , Rats , Rats, Inbred SHR , Rats, Inbred WKY , Signal Transduction/drug effects , TelmisartanABSTRACT
Cyclin-dependent kinase 2 (CDK2) is a member of serine/ threonine protein kinases, which initiates the principal transitions of the eukaryotic cell cycle and is a promising target for cancer therapy. The present study was designed to inhibit cdk2 gene expression to induce cell cycle arrest and cell proliferation suppression. Here, we constructed a series of RNA interference (RNAi) plasmids which can successfully express small interference RNA (siRNA) in the transfected human cells. The results showed that the RNAi plasmids containing the coding sequences for siRNAs down-regulated the cdk2 gene expression in human cancer cells at the mRNA and the protein levels. Furthermore, we found that the cell cycle was arrested at G0G1 phases and the cell proliferation was inhibited by different siRNAs. These results demonstrate that suppression of CDK2 activity by RNAi may be an effective strategy for gene therapy in human cancers.
Subject(s)
Cyclin-Dependent Kinase 2/antagonists & inhibitors , Neoplasms/enzymology , RNA Interference , Cell Proliferation , Cyclin-Dependent Kinase 2/genetics , Cyclin-Dependent Kinase 2/metabolism , Down-Regulation , G1 Phase , HeLa Cells , Humans , RNA, Small Interfering/metabolism , Resting Phase, Cell Cycle , Tumor Cells, CulturedABSTRACT
AIM: The aim of this study was to investigate the effects of aloe-emodin, a natural compound from the root and rhizome of Rheum palmatum, on the growth of human cervical cancer cells, HeLa. METHODS: HeLa cells were treated with various concentrations of aloe-emodin for 1-5 d, and cell growth was measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide assay. The long-term growth effect was investigated by crystal violet assay. The distributions of the cell cycle and apoptosis were analyzed by flow cytometry. The alkaline phosphatase (ALP) activity was analyzed by a chemical analyzer. Finally, Western blotting was used to indicate the abundant changes of protein kinase C (PKC), c-myc, cyclins, cyclin-dependent kinases (CDK), and proliferating cell nuclear antigen (PCNA). RESULTS: Aloe-emodin inhibited the growth of HeLa cells in a dose-dependent manner at concentrations ranging between 2.5 and 40 micromol/L. The flow cytometric analysis showed that HeLa cells were arrested at the G2/M phase. This effect was associated with the decrease in cyclin A and CDK2, and the increase in cyclin B1 and CDK1. More importantly, the ALP activity was found to be increased by aloe-emodin treatment, and accompanied by the inhibition of PCNA expression. In addition, aloe-emodin suppressed the expression of PKCalpha and c-myc. CONCLUSION: These findings provide a possible mechanistic explanation for the growth inhibitory effect of aloe-emodin on HeLa, which includes cell cycle arrest and inducing differentiation.
Subject(s)
Anthraquinones/pharmacology , Cell Differentiation/drug effects , Cell Division/drug effects , G2 Phase/drug effects , Uterine Cervical Neoplasms/pathology , Female , HeLa Cells , HumansABSTRACT
The nontoxic B subunit of cholera toxin (CTB) can significantly increase the ability of proteins to induce immunological tolerance after oral administration, when it was conjugated to various proteins. Recombinant CTB offers great potential for treatment of autoimmune disease. Here we firstly investigated the feasibility of silkworm baculovirus expression vector system for the cost-effective production of CTB under the control of a strong polyhedrin promoter. Higher expression was achieved via introducing the partial non-coding and coding sequences (ATAAAT and ATGCCGAAT) of polyhedrin to the 5' end of the native CTB gene, with the maximal accumulation being approximately 54.4 mg/L of hemolymph. The silkworm bioreactor produced this protein vaccine as the glycoslated pentameric form, which retained the GM1-ganglioside binding affinity and the native antigenicity of CTB. Further studies revealed that mixing with silkworm-derived CTB increases the tolerogenic potential of insulin. In the nonconjugated form, an insulin : CTB ratio of 100 : 1 was optimal for the prominent reduction in pancreatic islet inflammation. The data presented here demonstrate that the silkworm bioreactor is an ideal production and delivery system for an oral protein vaccine designed to develop immunological tolerance against autoimmune diabetes and CTB functions as an effective mucosal adjuvant for oral tolerance induction.