Synonyms for pericytes or Related words with pericytes

pericyte              vsmc              endothelia              vsmcs              angioblasts              angioblast              endothelium              astrocytes              microvessels              smcs              myofibroblasts              astrocyte              endothelialcells              hemogenic              mesenchyme              microglia              astroglial              myoblasts              stroma              myocardiocyte              glomeruli              glia              osteocytes              microvasculature              oligodendrocytes              cardiomyocytes              tubulogenesis              trophoblast              fibrocytes              osteoblasts              podocytes              periendothelial              astrocytic              fibroblastic              schwann              epcs              myocytes              huvecs              peritubular              chondroblast              myogenic              hepatoblasts              oligodendroglia              cardiomyocyte              arterioles              osteocyte              chondrocyte              cytotrophoblasts              chondrocytes              cytotrophoblast             

Examples of "pericytes"
Alpha-7 integrin pericytes (AIPs)express several types of integrin chains which generate heterodimers. Integrin chains allow integrin pericytes to interact with hematopoietic cells and promote their migration.
Increasing evidence suggests that pericytes can regulate blood flow at the capillary level. For the retina, movies have been published showing that pericytes constrict capillaries when their membrane potential is altered to cause calcium influx, and in the brain it has been reported that neuronal activity increases local blood flow by inducing pericytes to dilate capillaries before upstream arteriole dilation occurs. This area is controversial, with a recent study claiming that pericytes do not express contractile proteins and are not capable of contraction in vivo, although the latter paper has been criticised for using a highly unconventional definition of pericyte which explicitly excludes contractile pericytes. It appears that different signaling pathways regulate the constriction of capillaries by pericytes and of arterioles by smooth muscle cells
Pericytes are contractile cells that wrap around the endothelial cells that line the capillaries and venules throughout the body. Also known as Rouget cells or mural cells, pericytes are embedded in basement membrane where they communicate with endothelial cells of the body's smallest blood vessels by means of both direct physical contact and paracrine signaling. In the brain, pericytes help sustain the blood–brain barrier as well as several other homeostatic and hemostatic functions of the brain. These cells are also a key component of the "neurovascular unit", which includes endothelial cells, astrocytes, and neurons. Pericytes regulate capillary blood flow, the clearance and phagocytosis of cellular debris, and the permeability of the blood–brain barrier. Pericytes stabilize and monitor the maturation of endothelial cells by means of direct communication between the cell membrane as well as through paracrine signaling. A deficiency of pericytes in the central nervous system can cause the blood–brain barrier to break down.
In vitro studies using cultured cells indicate that endothelial cells secrete PDGF, which recruits PDGFRβ-expressing pericytes that stabilize nascent blood vessels. Mice harboring a single activated allele of pdgfrb show a number of postnatal phenotypes including reduced differentiation of aortic vascular smooth muscle cells and brain pericytes. Similarly, differentiation of adipose from pericytes and mesenchymal cells is suppressed. Misregulation of the PDGFRβ's kinase activity (typically activation) contributes to endemic diseases such as cancer and cardiovascular disease.
Both pericytes and endothelial cells share a basement membrane where a variety of intercellular connections are made. Many types of integrin molecules facilitate communication between pericytes and endothelial cells separated by the basement membrane. Pericytes can also form direct connections with neighboring cells by forming peg and socket arrangements in which parts of the cells interlock, similar to the gears of a clock. At these interlocking sites, gap junctions can be formed which allow the pericytes and neighboring cells to exchange ions and other small molecules. Important molecules in these intercellular connections include N-cadherin, fibronectin, connexin and various integrins.
It has been well established that smooth muscle-like pericytes play an important role in stabilizing newly formed blood vessels. Pericytes present in the stroma of tumors of breast cancer patients express MMP-9. Animal models deficient of MMP-9 display disturbed recruitment of pericytes. The inability to recruit pericytes severely affects the stability of vessels and the degree of vascularization of neuroblastomas. Aminopeptidase A also may be involved in pericyte recruitment due to its increased expression by activated pericytes in various pathological conditions associated with angiogenesis. The mechanism by which this protease facilitates vessel maturation has not yet been determined. Angiogenesis requires a fine balance between proteolytic activity and proteinase inhibition. Pericytes secrete TIMP-3 which inhibits MT1-MMP dependent MMP-2 activation on endothelial cell, thus facilitating stabilization of newly formed microvessels. Co-cultures consisting of pericytes and endothelial cells induce the expression of TIMP-3 by pericytes, while endothelial cells produce TIMP-2. Together, these inhibitors stabilize the vasculature by inhibiting a variety of MMPs, ADAMs, and VEGF receptor 2.
There are several pathways of communication between the endothelial cells and pericytes. The first is transforming growth factor (TGF) signaling, which is mediated by endothelial cells. This is important for pericyte differentiation. Angiopoietin 1 and Tie-2 signaling is essential for maturation and stabilization of endothelial cells. Platelet-derived growth factor (PDGF) pathway signaling from endothelial cells recruits pericytes, so that pericytes can migrate to growing vessels. If this pathway is blocked, it leads to pericyte deficiency. Sphingosine-1-phosphate (S1P) signaling also aides in pericyte recruitment by communication through G protein-coupled receptors. S1P signals through GTPases that promote N-cadherin trafficking to endothelial membranes. This trafficking strengthens contacts with pericytes.
Intraglomerular mesangial cells are specialized pericytes located among the glomerular capillaries within a renal corpuscle of a kidney.
Pericytes are important in maintaining circulation. In a study involving adult pericyte-deficient mice, cerebral blood flow was diminished with concurrent vascular regression due to loss of both endothelia and pericytes. Significantly greater hypoxia was reported in the hippocampus of pericyte-deficient mice as well as inflammation, and learning and memory impairment.
Communication between endothelial cells and pericytes is important. Inhibiting the PDGF pathway leads to pericyte deficiency. This causes endothelial hyperplasia, abnormal junctions, and diabetic retinotropy. A lack of pericytes also causes an upregulation of vascular endothelial growth factor (VEGF), leading to vascular leakage and hemorrhage. Also, angiopoietin 2 can act as an antagonist to Tie-2. This destabilizes the endothelial cells, which accounts for less endothelial cell and pericyte interaction. This can actually lead to the formation of tumors. Similar to the inhibition of the PDGF pathway, angiopoietin 2 reduces levels of pericytes, leading to diabetic retinopathy.
Aside from creating and remodeling blood vessels in a viable fashion, pericytes have been found to protect endothelial cells from death via apoptosis or cytotoxic elements. It has been studied "in vivo" that pericytes release a hormone known as pericytic aminopeptidase N/pAPN that may help to promote angiogenesis. When this hormone was mixed with cerebral endothelial cells as well as astrocytes, the pericytes grouped into structures that resembled capillaries. Furthermore, if experimental group contained all of the following with the exception of pericytes, the endothelial cells would undergo apoptosis. That being said, it was concluded that pericytes must be present to assure the proper function of endothelial cells and astrocytes must be present to assure that both remain in contact. If not, then proper angiogenesis cannot occur. In addition, it has been found that pericytes contribute to the survival of endothelial cells because they secrete the protein Bcl-w during cellular crosstalk. Bcl-w is an instrumental protein in the pathway that enforces VEGF-A expression and discourages apoptosis. Although there is some speculation as to why VEGF is directly responsible for preventing apoptosis, it is believed to be responsible for modulating apoptotic signal transduction pathways and inhibiting activation of apoptosis inducing enzymes. Two biochemical mechanisms utilized by VEGF to accomplish such would be phosphorylation of extracellular regulatory kinase 1 (ERK-1) which sustains cell survival over time and inhibition of stress-activated protein kinase/c-jun-NH2 kinase which also promotes apoptosis.
Inhibition of subtype A pericyte generation caused improper closing of spinal cord incisions, which supports the idea that pericytes are important for scarring.
Pericytes in the skeletal striated muscle are of two distinct populations, each with its own role. The first pericyte subtype (Type-1) can differentiate into fat cells while the other (Type-2) into muscle cells. Type-1 characterized by negative expression for nestin (PDGFRβ+CD146+NG2-) and type-2 characterized by positive expression for nestin (PDGFRβ+CD146+NG2+). While both types are able to proliferate in response to glycerol or BaCl2-induced injury, type-1 pericytes give rise to adipogenic cells only in response to glycerol injection and type-2 become myogenic in response to both types of injury. The extent to which type-1 pericytes participate in fat accumulation is not known.
Studies have found that pericyte loss in the adult and aging brain leads to the disruption of proper cerebral perfusion and maintenance of the blood–brain barrier, which causes neurodegeneration and neuroinflammation. The apoptosis of pericytes in the aging brain may be the result of a failure in communication between growth factors and receptors on pericytes. Platelet-derived growth factor B (PDGFB) is released from endothelial cells in brain vasculature and binds to the receptor PDGFRB on pericytes, initiating their proliferation and investment in the vasculature.
Endothelial cells and pericytes are interdependent, so failure of proper communication between the two cells can lead to numerous human pathologies.
Pericytes are also associated with allowing endothelial cells to differentiate, multiply, form vascular branches (angiogenesis), survive apoptotic signals and travel throughout the body. Certain pericytes, known as microvascular pericytes, develop around the walls of capillaries and help to serve this function. Microvascular pericytes may not be contractile cells because they lack alpha-actin isoforms; structures that are common amongst other contractile cells. These cells communicate with endothelial cells via gap junctions and in turn cause endothelial cells to proliferate or be selectively inhibited. If this process did not occur, hyperplasia and abnormal vascular morphogenesis could occur. These types of pericyte can also phagocytose exogenous proteins. This suggests that the cell type might have been derived from microglia.
In the central nervous system, pericytes wrap around the endothelial cells that line the inside of the capillary. These two types of cells can be easily distinguished from one another based on the presence of the prominent round nucleus of the pericyte compared to the flat elongated nucleus of the endothelial cells. Pericytes also project finger-like extensions that wrap around the capillary wall, allowing the cells to regulate capillary blood flow.
A principal function of pericytes is to interact with astrocytes, smooth muscle cells, and other intracranial cells to form the blood brain barrier and to modulate the size of blood vessels to ensure proper delivery and distribution of oxygen and nutrients to neuronal tissues. Pericytes have both cholinergic (α2) and adrenergic (β2) receptors. Stimulation of the latter leads to vessel relaxation, while stimulation of the cholinergic receptors leads to contraction.
Mural cells have contractile function. As the progenitors of smooth muscle cells (SMCs) and pericytes, mural cells themselves derive from the mesenchyme. Invasive endothelial become surrounded by locally-derived mesenchymal cells, meaning the surrounding primordium itself contributes the mural cells to the developing vessels. This is advantageous as it can result in tissue-specific functional and regulatory properties of pericytes, and SMCs. In contrast, endothelial cells are thought to be of uniform origin.
The retina of diabetic individuals often exhibits loss of pericytes, and this loss is a characteristic factor of the early stages of diabetic retinopathy. Studies have found that pericytes are essential in diabetic individuals to protect the endothelial cells of retinal capillaries. With the loss of pericytes, microaneurysms form in the capillaries. In response, the retina either increases its vascular permeability, leading to swelling of the eye through a macular edema, or forms new vessels that permeate into the vitreous membrane of the eye. The end result is reduction or loss of vision. While it is unclear why pericytes are lost in diabetic patients, one hypothesis is that toxic sorbitol and advanced glycation end-products (AGE) accumulate in the pericytes. Because of the build-up of glucose, the polyol pathway increases its flux, and intracellular sorbitol and fructose accumulate. This leads to osmotic imbalance, which results in cellular damage. The presence of high glucose levels also leads to the buildup of AGE's, which also damage cells.