scholarly journals AngiotensinII Preconditioning Promotes AngiogenesisIn Vitrovia ERKs Phosphorylation

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Aili Guan ◽  
Yunzeng Zou ◽  
Hui Gong ◽  
Yuhong Niu ◽  
Yong Ye ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cardiac Hypertrophy ◽  
Protein Kinases ◽  
Cardiac Remodeling ◽  
Microvascular Endothelial Cells ◽  
Long Period ◽  
Extracellular Signal ◽  
Short Period ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

AngiotensinII (AngII) is involved in not only the formation of cardiac hypertrophy but also the development of cardiac remodeling both of which are associated with myocardial angiogenesis. This study was therefore performed to clarify the effects of AngII on the formation of vasculatures by cultured cardiac microvascular endothelial cells (CMVECs) after a long-period stimulation with or without the AngII preconditioning. Incubation with AngII for 18 hrs significantly impaired the formation of capillary-like tubes comparing to that without AngII. CMVECs with AngII pretreatment for 5 and 10 min formed more capillary-like tubes than those without AngII pretreatment, suggesting that preconditioning with AngII at a lower dose for a short period could prevent the further damage of CMVECs by a higher concentration of AngII. Moreover, AngII (10-7 M) stimulation for 5 and 10 min significantly induced the increase in extracellular signal-regulated protein kinases (ERKs) phosphorylation, and an ERKs inhibitor, PD98059, abrogated the increase in the formation of capillary-like tubes induced by the AngII-pretreatment. In conclusion, preconditioning with a lower concentration of AngII for a short period prevents the subsequent impairment of CMVECs by a higher dose of AngII, at least in part, through the increase in ERKs phosphorylation.

Isolation and characterization of human and rat cardiac microvascular endothelial cells

1993 ◽  
Vol 264 (2) ◽  
pp. H639-H652 ◽  
Author(s):  
M. Nishida ◽  
W. W. Carley ◽  
M. E. Gerritsen ◽  
O. Ellingsen ◽  
R. A. Kelly ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelium ◽  
Adult Rat ◽  
Isolation And Characterization ◽  
Ventricular Tissue ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Although reciprocal intercellular signaling may occur between endocardial or microvascular endothelium and cardiac myocytes, suitable in vitro models have not been well characterized. In this report, we describe the isolation and primary culture of cardiac microvascular endothelial cells (CMEC) from both adult rat and human ventricular tissue. Differential uptake of fluorescently labeled acetylated low-density lipoprotein (Ac-LDL) indicated that primary isolates of rat CMEC were quite homogeneous, unlike primary isolates of human ventricular tissue, which required cell sorting based on Ac-LDL uptake to create endothelial cell-enriched primary cultures. The endothelial phenotype of both primary isolates and postsort subcultured CMEC and their microvascular origin were determined by characteristic histochemical staining for a number of endothelial cell-specific markers, by the absence of cells with fibroblast or pericyte-specific cell surface antigens, and by rapid tube formation on purified basement membrane preparations. Importantly, [3H]-thymidine uptake was increased 2.3-fold in subconfluent rat microvascular endothelial cells 3 days after coculture with adult rat ventricular myocytes because of release of an endothelial cell mitogen(s) into the extracellular matrix, resulting in a 68% increase in cell number compared with CMEC in monoculture. Thus biologically relevant cell-to-cell interactions can be modeled with this in vitro system.

Autophagy inhibits high glucose induced cardiac microvascular endothelial cells apoptosis by mTOR signal pathway

APOPTOSIS ◽  
2017 ◽  
Vol 22 (12) ◽  
pp. 1510-1523 ◽  
Author(s):  
Zheng Zhang ◽  
Shenwei Zhang ◽  
Yong Wang ◽  
Ming Yang ◽  
Ning Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Signal Pathway ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Basal Nonselective Cation Permeability in Rat Cardiac Microvascular Endothelial Cells

2002 ◽  
Vol 64 (2) ◽  
pp. 187-197 ◽  
Author(s):  
Francesco Moccia ◽  
Roberto Berra-Romani ◽  
Silvana Baruffi ◽  
Santina Spaggiari ◽  
David J. Adams ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Microvascular Endothelial Cells ◽  
Cation Permeability ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Abstract 269: Exendin-4 Prevents Glucose-induced Secretion of Tissue Transglutaminase-2 from Cardiac Microvascular Endothelial Cells: Potential Role in the Prevention of Matrix Remodeling in Diabetes

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Ali S Shihab ◽  
Vanitra A Richardson ◽  
Betsy B Dokken
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
High Glucose ◽  
Tissue Transglutaminase ◽  
Vascular Complications ◽  
Transglutaminase 2 ◽  
Conditioned Media ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Cardiac Microvascular Endothelial Cells

Diabetes causes endothelial dysfunction, which is the initial trigger for vascular complications in diabetic patients. Hyperglycemia initiates a cascade of events that alters protein expression and secretion by endothelial cells. Tissue transglutaminase-2 (tTG2) is an enzyme that under physiologic conditions is sequestered inside the endothelial cell, but under pathologic conditions causing decreased bioavailability of nitric oxide, tTG2 is secreted, activated, and catalyzes irreversible crosslinking of proteins in the extracellular matrix (ECM). Exendin-4 (Ex-4) is a glucagon-like peptide-1 receptor (GLP-1R) agonist, used in the treatment of type 2 diabetes, which has vasculo-protective effects. We hypothesized that hyperglycemic stress would induce secretion of tTG2, and that this effect would be attenuated by Ex-4. Mouse cardiac microvascular endothelial cells (MCECs) were serum-starved and exposed to control (5.5 mM glucose) or hyperglycemic (25 mM glucose) conditions, with or without Ex-4 (10 nM) x 72 hrs. Proteins from conditioned media were isolated, trypsinized, and analyzed using LC-MS/MS (LTQ Orbitrap Velos). Immunoblots from cell homogenate were probed for tTG protein expression. Conditioned media from MCECs exposed to high-glucose but not Ex-4 contained tTG2, which was absent in media from cells exposed to high-glucose and Ex-4, as well as in media from control cells, suggesting that Ex-4 prevented the secretion of tTG2 induced by hyperglycemic stress. Protein expression in cell lysate was not different. These findings may have important implications for the etiology of diabetic vascular complications, and for the role of Ex-4 to prevent the pathologic ECM remodeling associated with diabetic vasculopathy. Further studies are ongoing to determine the mechanisms of glucose-induced secretion of tTG2, as well as the mechanisms by which Ex-4 prevents this effect.

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