Vascular Pharmacology, Journal Year: 2018, Volume and Issue: 114, P. 76 - 92
Published: Oct. 7, 2018
Language: Английский
Vascular Pharmacology, Journal Year: 2018, Volume and Issue: 114, P. 76 - 92
Published: Oct. 7, 2018
Language: Английский
Frontiers in Molecular Biosciences, Journal Year: 2017, Volume and Issue: 4
Published: July 17, 2017
The process of intercellular communication seems to have been a highly conserved evolutionary process. Higher eukaryotes use several means address both the changing physiological demands body and fight against diseases. In recent years, there has an increasing interest in understanding how cell-derived nanovesicles, known as extracellular vesicles (EVs), can function normal paracrine mediators communication, but also elicit disease progression may be used for innovative therapies. Over last decade, large evidence accumulated show that cells cytoplasmic extensions comprising open-ended channels called tunneling nanotubes (TNTs) connect at long distance facilitate exchange material. TNTs are different classical gap junctions or cell fusions; since they characterized by bridging transfers organelles intracellular between represent heteroplasmy. role EVs is relatively well-understood, fit into this just emerging. aim review describe relationship EVs, discuss synergies these two crucial processes context cellular cross-talk, roles, modulation immune responses, development diseases, their combinatory effects tissue repair. At present time appears first summary implications overlapping roles EVs. We believe better appreciation parallel will improve our on nanoscale conduits utilized novel tools targeted
Language: Английский
Citations
110Circulation Research, Journal Year: 2019, Volume and Issue: 124(2), P. 211 - 224
Published: Jan. 17, 2019
Maintaining endothelial cells (EC) as a monolayer in the vessel wall depends on their metabolic state and gene expression profile, features influenced by contact with neighboring such pericytes smooth muscle (SMC). Failure to regenerate normal EC response injury can result occlusive neointima formation diseases atherosclerosis pulmonary arterial hypertension.We investigated nature functional importance of contact-dependent communication between SMC maintain integrity.We found that cocultures, BMPR2 (bone morphogenetic protein receptor 2) is required both cell types produce collagen IV activate ILK (integrin-linked kinase). This enzyme directs p-JNK (phospho-c-Jun N-terminal kinase) membrane, where it stabilizes presenilin1 releases N1ICD (Notch1 intracellular domain) promote proliferation. necessary for regeneration after carotid artery injury. It deficient EC-SMC Bmpr2 double heterozygous mice association reduced production, decreased N1ICD, attenuated proliferation, but be rescued targeting EC. Deletion EC- Notch1 transgenic worsens hypoxia-induced hypertension, impaired regenerative function associated loss precapillary arteries. We further determined maintains proliferative capacity increasing mitochondrial mass inducing phosphofructokinase PFKFB3 (fructose-2,6-bisphosphatase 3). Chromatin immunoprecipitation sequencing analyses showed citrate-dependent H3K27 acetylation at enhancer sites genes regulated acetyl transferase p300 or target MYC proliferation homeostasis.Thus, SMC-EC activation BMPR2, coordinate metabolism chromatin remodeling enable regeneration, integrity vascular homeostasis
Language: Английский
Citations
104Frontiers in Cell and Developmental Biology, Journal Year: 2020, Volume and Issue: 8
Published: March 20, 2020
Cardiovascular diseases (CVDs), especially those involving a systemic inflammatory process such as atherosclerosis, remain the leading cause of morbidity and mortality in patients with chronic kidney disease (CKD). CKD is condition affecting approximately 10% general population. The prevalence has increased over past decades because aging population worldwide. Indeed, CVDs constitute premature form CVD observed Multiple studies indicate that renal undergo accelerated aging, which precipitates appearance pathologies, including CVDs, usually associated advanced age. In this review, we discuss several aspects characterize CKD-associated etiopathogenic elements share population, changes cellular balance reactive oxygen species (ROS), senescence. Uremia-associated linked numerous at molecular level. These are similar to normal physiologic aging. We also new perspectives study epigenetic alterations intercellular signaling, mediated by microRNAs and/or extracellular vesicles (EVs), promote vascular damage subsequent development CVD. Understanding processes factors involved senescence other abnormal signaling will identify therapeutic targets lead improved methods diagnosis monitoring for CVDs.
Language: Английский
Citations
102Current Hypertension Reports, Journal Year: 2016, Volume and Issue: 18(12)
Published: Nov. 11, 2016
Language: Английский
Citations
101Vascular Pharmacology, Journal Year: 2018, Volume and Issue: 114, P. 76 - 92
Published: Oct. 7, 2018
Language: Английский
Citations
101