scholarly journals A novel population of subepithelial platelet-derived growth factor receptor α-positive cells in the mouse and human colon

2013 ◽  
Vol 304 (9) ◽  
pp. G823-G834 ◽  
Author(s):  
Masaaki Kurahashi ◽  
Yasuko Nakano ◽  
Lauren E. Peri ◽  
Jared B. Townsend ◽  
Sean M. Ward ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Fluorescent Protein ◽  
Purinergic Receptor ◽  
Smooth Muscle Actin ◽  
Quantitative Polymerase Chain Reaction ◽  
Receptor Gene ◽  
Nerve Fibers ◽  
Platelet Derived Growth Factor ◽  
Close Proximity

Recently platelet-derived growth factor-α-positive cells (PDGFRα+ cells), previously called “fibroblast-like” cells, have been described in the muscle layers of the gastrointestinal tract. These cells form networks and are involved in purinergic motor neurotransduction. Examination of colon from mice with enhanced green fluorescent protein (eGFP) driven from the endogenous Pdgfra (PDGFRα-eGFP mice) revealed a unique population of PDGFRα+ cells in the mucosal layer of colon. We investigated the phenotype and potential role of these cells, which have not been characterized previously. Expression of PDGFRα and several additional proteins was surveyed in human and murine colonic mucosae by immunolabeling; PDGFRα+ cells in colonic mucosa were isolated from PDGFRα-eGFP mice, and the gene expression profile was analyzed by quantitative polymerase chain reaction. We found for the first time that PDGFRα was expressed in subepithelial cells (subepithelial PDGFRα+ cells) forming a pericryptal sheath from the base to the tip of crypts. These cells were in close proximity to the basolateral surface of epithelial cells and distinct from subepithelial myofibroblasts, which were identified by expression of α-smooth muscle actin and smooth muscle myosin. PDGFRα+ cells also lay in close proximity to varicose processes of nerve fibers. Mouse subepithelial PDGFRα+ cells expressed Toll-like receptor genes, purinergic receptor genes, 5-hydroxytryptamine (5-HT) 4 receptor gene, and hedgehog signaling genes. Subepithelial PDGFRα+ cells occupy an important niche in the lamina propria and may function in transduction of sensory and immune signals and in the maintenance of mucosal homeostasis.

scholarly journals Resveratrol Inhibits Phenotype Modulation by Platelet Derived Growth Factor-bb in Rat Aortic Smooth Muscle Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Mi Hee Lee ◽  
Byeong-Ju Kwon ◽  
Hyok Jin Seo ◽  
Kyeong Eun Yoo ◽  
Min Sung Kim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
Pathway Activation ◽  
Dependent Inhibition

Dedifferentiated vascular smooth muscle cells (VSMCs) are phenotypically modulated from the contractile state to the active synthetic state in the vessel wall. In this study, we investigated the effects of resveratrol on phenotype modulation by dedifferentiation and the intracellular signal transduction pathways of platelet derived growth factor-bb (PDGF-bb) in rat aortic vascular smooth muscle cells (RAOSMCs). Treatment of RAOSMCs with resveratrol showed dose-dependent inhibition of PDGF-bb-stimulated proliferation. Resveratrol treatment inhibited this phenotype change and disassembly of actin filaments and maintained the expression of contractile phenotype-related proteins such as calponin and smooth muscle actin-alpha in comparison with only PDGF-bb stimulated RAOSMC. Although PDGF stimulation elicited strong and detectable Akt and mTOR phosphorylations lasting for several hours, Akt activation was much weaker when PDGF was used with resveratrol. In contrast, resveratrol only slightly inhibited phosphorylations of 42/44 MAPK and p38 MAPK. In conclusion, RAOSMC dedifferentiation, phenotype, and proliferation rate were inhibited by resveratrol via interruption of the balance of Akt, 42/44MAPK, and p38MAPK pathway activation stimulated by PDGF-bb.

Platelet-Derived Growth Factor Enhances Sp1 Binding to the LDL Receptor Gene

1995 ◽  
Vol 15 (8) ◽  
pp. 1248-1254 ◽  
Author(s):  
Khaja Basheeruddin ◽  
Xiaoli Li ◽  
Carol Rechtoris ◽  
Theodore Mazzone
Keyword(s):  
Growth Factor ◽  
Receptor Gene ◽  
Ldl Receptor ◽  
Platelet Derived Growth Factor

scholarly journals LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 117-127
Author(s):  
Hongmei Gao ◽  
Zhaohui Guo
Keyword(s):  
Smooth Muscle ◽  
Muscle Protein ◽  
Umbilical Vein ◽  
Smooth Muscle Actin ◽  
Quantitative Polymerase Chain Reaction ◽  
Density Lipoprotein ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Western Blot Assay ◽  
Lactate Dehydrogenase Activity

Abstract Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.

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