Endothelial cells derived extracellular vesicles promote diabetic arterial calcification via circ_0008362/miR-1251-5p/Runx2 axial.

Introduction: Arterial calcification, an independent predictor of cardiovascular events, increases morbidity and mortality in patients with diabetes mellitus (DM), but its mechanisms remain unclear. Extracellular vesicles (EVs) play an important role in intercellular communication. The study investigates the role and potential mechanisms of EVs derived from endothelial cells (ECs) in regulating vascular smooth muscle cell (VSMC) calcification under high glucose (HG) condition, with a goal of developing effective prevention and treatment strategies for diabetic arterial calcification.

Impact of cerebral small vessel disease on symptomatic in-stent restenosis in intracranial atherosclerosis.

Objective: Cerebral small vessel disease (CSVD) commonly coexists with intracranial atherosclerotic stenosis (ICAS). In-stent restenosis (ISR) affects the nonprocedural outcome of severe symptomatic ICAS after intracranial stenting. However, only 8%-27% of ISR patients are symptomatic, which highlights the importance of the investigation of risk factors associated with symptomatic ISR (SISR) to improve long-term functional outcome.

Melatonin alleviates vascular calcification and ageing through exosomal miR-204/miR-211 cluster in a paracrine manner.

In the elderly with atherosclerosis, hypertension and diabetes, vascular calcification and ageing are ubiquitous. Melatonin (MT) has been demonstrated to impact the cardiovascular system. In this study, we have shown that MT alleviates vascular calcification and ageing, and the underlying mechanism involved.

Aberrant DNA methylation of synaptophysin is involved in adrenal cortisol-producing adenoma.

Cortisol-producing adenoma (CPA) is the main cause of Adrenal Cushing syndrome. However, its molecular mechanism is not fully understood. Previous study revealed Synaptophysin () is ubiquitously expressed in adrenocortical tumors, but its function in CPA still need to be discovered.

Aberration methylation of miR-34b was involved in regulating vascular calcification by targeting Notch1.

Vascular calcification is one of the most important factors for cardiovascular and all-cause mortality in patients with end-stage renal diseases (ESRD). The current study was aimed to investigate the function and mechanisms of miR-34b on the calcification of vascular smooth muscle cells (VSMCs) both and . We found that the expression of miR-34b was significantly suppressed in VSMCs with high inorganic phosphate (Pi) treatment, as well as mouse arteries derived from 5/6 nephrectomy with a high-phosphate diet (0.

miR‑124 regulates the osteogenic differentiation of bone marrow‑derived mesenchymal stem cells by targeting Sp7.

MicroRNAs (miRNAs) are novel key regulators of cellular differentiation. miR‑124 has been reported to regulate osteogenic differentiation of bone marrow‑derived mesenchymal stem cells (BMSCs). However, the specific mechanisms involved have not yet been fully elucidated.

Exosomes increased angiogenesis in papillary thyroid cancer microenvironment.

Tumour-derived exosomes under hypoxic conditions contain informative miRNAs involved in the interaction of cancer and para-carcinoma cells, thus contributing to tissue remodelling of the tumour microenvironment (TME). Exosomes isolated from hypoxic papillary thyroid cancer cells, BCPAP cells and KTC-1 cells enhanced the angiogenesis of human umbilical vein endothelial cells (HUVECs) compared with exosomes isolated from normal thyroid follicular cell line (Nthy-ori-3-1), normoxic BCPAP or KTC-1 cells both in vitro and in vivo. miR-21-5p was significantly upregulated in exosomes from papillary thyroid cancer BCPAP cells under hypoxic conditions, while the exosomes isolated from hypoxic BCPAP cells with knockdown of miR-21-5p attenuated the promoting effect of angiogenesis.

Fine Tuning of Emission Behavior, Self-Assembly, Anion Sensing, and Mitochondria Targeting of Pyridinium-Functionalized Tetraphenylethene by Alkyl Chain Engineering.

Compared to the many studies that focus on the development of novel molecular frameworks pertaining to functionalized fluorescent materials, there is lesser emphasis on side chains even though they have a significant impact on the properties and applications of fluorescent materials. In this study, a series of pyridinium-functionalized tetraphenylethene salts (TPEPy-1 to TPEPy-4) possessing different alkyl chains are synthesized, and the influence of chain length on their optical performance and applications is thoroughly investigated. By changing the alkyl chain, the fluorogens exhibit opposite emission behavior in aqueous media because of their distinct hydrophobic nature, and their solid-state emission can be fine-tuned from green to red owing to their distinct molecular configuration.

Arterial Calcification Is Regulated Via an miR-204/DNMT3a Regulatory Circuit Both In Vitro and in Female Mice.

Arterial calcification is a common cardiovascular disease that initiates from a process of osteoblastic differentiation of vascular smooth muscle cells (VSMCs). Accumulating evidence has demonstrated that microRNAs play an important role in regulating arterial calcification. miR-204 was significantly downregulated in calcified human renal arteries from patients with uremia; calcified arteries of mice, due to 5/6 nephrectomy with a high-phosphate diet (5/6 NTP); and in VSMCs induced by high phosphate concentration.

Mammalian sterile 20-like kinase 1 expression and its prognostic significance in patients with breast cancer.

Mammalian sterile 20-like kinase 1 (Mst1) is a major inhibitor of cell proliferation, and is involved in apoptosis, oncogenesis and organ growth via its ubiquitously encoded serine threonine kinase. Previous studies have demonstrated that Mst1 has a tumor suppressor function in human breast cancer. Mst1 deletion or mutation is associated with tumorigenesis, whereas Mst1 overexpression leads to tumor cell apoptosis and decreases proliferation of tumor cells.

Oestrogen Inhibits Arterial Calcification by Promoting Autophagy.

Arterial calcification is a major complication of cardiovascular disease. Oestrogen replacement therapy in postmenopausal women is associated with lower levels of coronary artery calcification, but its mechanism of action remains unclear. Here, we show that oestrogen inhibits the osteoblastic differentiation of vascular smooth muscle cells (VSMCs) in vitro and arterial calcification in vivo by promoting autophagy.

Leptin promotes the osteoblastic differentiation of vascular smooth muscle cells from female mice by increasing RANKL expression.

Arterial calcification is a complex and active regulated process, which results from a process of osteoblastic differentiation of vascular smooth muscle cells (VSMCs). Leptin, the product of the ob gene, mainly regulates food intake and energy expenditure and recently has been considered to be correlated with the arterial calcification. However, the mechanisms of the effects of leptin on osteoblastic differentiation of VSMCs are unknown.

Ghrelin inhibits the apoptosis of MC3T3-E1 cells through ERK and AKT signaling pathway.

Ghrelin is a 28-amino-acid peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR) and strongly stimulates the release of growth hormone from the hypothalamus-pituitary axis. Previous studies have identified the important physiological effects of ghrelin on bone metabolism, such as regulating proliferation and differentiation of osteoblasts, independent of GH/IGF-1 axis. However, research on effects and mechanisms of ghrelin on osteoblast apoptosis is still rare.

Puerarin Suppress Apoptosis of Human Osteoblasts via ERK Signaling Pathway.

Puerarin, the main isoflavone glycoside extracted from Radix Puerariae, is an isoflavone traditional Chinese herb. Previous studies have demonstrated that puerarin could regulate osteoblast proliferation and differentiation to promote bone formation. However, the effect of puerarin on the process of human osteoblasts (hOBs) apoptosis is still unclear.

MiR-133a modulates osteogenic differentiation of vascular smooth muscle cells.

Arterial calcification is a key pathologic component of vascular diseases such as atherosclerosis, coronary artery disease, and peripheral vascular disease. A hallmark of this pathological process is the phenotypic transition of vascular smooth muscle cells (VSMCs) to osteoblast-like cells. Several studies have demonstrated that microRNAs (miRNAs) regulate osteoblast differentiation, but it is unclear whether miRNAs also regulate VSMC-mediated arterial calcification.

Omentin-1 Stimulates Human Osteoblast Proliferation through PI3K/Akt Signal Pathway.

It has been presumed that adipokines deriving from adipose tissue may play important roles in bone metabolism. Omentin-1, a novel adipokine, which is selectively expressed in visceral adipose tissue, has been reported to stimulate proliferation and inhibit differentiation of mouse osteoblast. However, little information refers to the effect of omentin-1 on human osteoblast (hOB) proliferation.

Photochemical properties and phototoxicity of Pazufloxacin: a stable and transient study.

Photochemical properties and phototoxicity of Pazufloxacin (PAX) were systematically investigated in aqueous solutions using UV-Vis, fluorescence, laser flash photolysis, pulse radiolysis and SDS-PAGE gel electrophoresis techniques. PAX triplet-state ((3)PAX(*)) absorption spectra (λ(max)=570 nm) was determined. (3)PAX(*) was quenched by PAX and O(2), with rate constants of 6.

Vaspin attenuates the apoptosis of human osteoblasts through ERK signaling pathway.

It has been hypothesized that adipocytokines originating from adipose tissue may have an important role in bone metabolism. Vaspin is a novel adipocytokine isolated from visceral white adipose tissue, which has been reported to have anti-apoptotic effects in vascular endothelial cells. However, to the best of our knowledge there is no information regarding the effects of vaspin on osteoblast apoptosis.

MicroRNA-204 regulates vascular smooth muscle cell calcification in vitro and in vivo.

Aims: Medial artery calcification is a common macroangiopathy that initiates from a cell-regulated process similar to osteogenesis. Although the mechanisms governing this process remain unclear, epigenomic regulation by specific microRNAs might play a role in vascular smooth muscle cell (VSMC) calcification. In this study, we aimed to investigate whether miR-204 participates in the regulation of VSMC calcification.

Apelin-APJ induces ICAM-1, VCAM-1 and MCP-1 expression via NF-κB/JNK signal pathway in human umbilical vein endothelial cells.

Apelin receptor (APJ) deficiency has been reported to be preventive against atherosclerosis. However, the mechanism of this effect remains unknown. In this study, quantitative real-time RT-PCR, Western blotting and ELISA analyses revealed a significant increase in the expression of intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) treated with apelin.

Ghrelin attenuates the osteoblastic differentiation of vascular smooth muscle cells through the ERK pathway.

Vascular calcification results from osteoblastic differentiation of vascular smooth muscle cells (VSMCs) and is a major risk factor for cardiovascular events. Ghrelin is a newly discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagog receptor (GHSR). Several studies have identified the protective effects of ghrelin on the cardiovascular system, however research on the effects and mechanisms of ghrelin on vascular calcification is still quite rare.

RANKL is a downstream mediator for insulin-induced osteoblastic differentiation of vascular smooth muscle cells.

Several reports have shown that circulating insulin level is positively correlated with arterial calcification; however, the relationship between insulin and arterial calcification remains controversial and the mechanism involved is still unclear. We used calcifying vascular smooth muscle cells (CVSMCs), a specific subpopulation of vascular smooth muscle cells that could spontaneously express osteoblastic phenotype genes and form calcification nodules, to investigate the effect of insulin on osteoblastic differentiation of CVSMCs and the cell signals involved. Our experiments demonstrated that insulin could promote alkaline phosphatase (ALP) activity, osteocalcin expression and the formation of mineralized nodules in CVSMCs.

Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.

Vascular calcification, which results from a process osteoblastic differentiation of vascular smooth muscle cells (VSMCs), is a major risk factor for cardiovascular morbidity and mortality. Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled receptor, APJ. Several studies have identified the protective effects of apelin on the cardiovascular system.