scholarly journals T3 enhances Ang2 in rat aorta in myocardial I/R: comparison with left ventricle

2016 ◽  
Vol 57 (3) ◽  
pp. 139-149 ◽  
Author(s):  
Laura Sabatino ◽  
Claudia Kusmic ◽  
Giuseppina Nicolini ◽  
Rosario Amato ◽  
Giovanni Casini ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Tyrosine Kinase ◽  
Thoracic Aorta ◽  
Ischemia Reperfusion ◽  
Capillary Density ◽  
Tyrosine Kinase Receptor ◽  
Remote Zone ◽  
Angiopoietin 2 ◽  
Significant Increment ◽  
Angiopoietin 1

Angiogenesis is important for recovery after tissue damage in myocardial ischemia/reperfusion, and tri-iodothyronine (T3) has documented effects on angiogenesis. The angiopoietins 1/2 and tyrosine kinase receptor represent an essential system in angiogenesis controlling endothelial cell survival and vascular maturation. Recently, in a 3-day ischemia/reperfusion rat model, the infusion of a low dose of T3 improved the post-ischemic recovery of cardiac function. Adopting this model, our study aimed to investigate the effects of T3 on the capillary index and the expression of angiogenic genes as the angiopoietins 1/2 and tyrosine kinase receptor system, in the thoracic aorta and in the left ventricle. In the thoracic aorta, T3 infusion significantly improved the angiogenic sprouting and angiopoietin 2 expression. Instead, Sham-T3 group did not show any significant increment of capillary density and angiopoietin 2 expression. In the area at risk (AAR) of the left ventricle, T3 infusion did not increase capillary density but restored levels of angiopoietin 1, which were reduced in I/R group. Angiopoietin 2 levels were similar to Sham group and unchanged by T3 administration. In the remote zone, T3 induced a significant increment of both angiopoietin 1/2. In conclusion, T3 infusion induced a different response of angiopoietin 1/2 between the ventricle (the AAR and the remote zone) and the thoracic aorta, probably reflecting the different action of angiopoietin 1/2 in cardiomyocytes and endothelial cells. Overall, these data suggest a new aspect of T3-mediated cardioprotection through angiogenesis.

Angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2) and Tie-2 (a receptor tyrosine kinase) concentrations in peripheral blood of patients with thyroid cancers

Cytokine ◽  
2006 ◽  
Vol 36 (5-6) ◽  
pp. 291-295 ◽  
Author(s):  
Sebastian Niedźwiecki ◽  
Tomasz Stępień ◽  
Krzysztof Kopeć ◽  
Krzysztof Kuzdak ◽  
Jan Komorowski ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Peripheral Blood ◽  
Thyroid Cancers ◽  
Angiopoietin 2 ◽  
Angiopoietin 1

Angiogenic factors and alveolar vasculature: development and alterations by injury in very premature baboons

2002 ◽  
Vol 282 (4) ◽  
pp. L811-L823 ◽  
Author(s):  
William M. Maniscalco ◽  
Richard H. Watkins ◽  
Gloria S. Pryhuber ◽  
Abhay Bhatt ◽  
Colleen Shea ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Capillary Density ◽  
Normal Lung ◽  
Tyrosine Kinase Receptor ◽  
Angiogenic Growth Factor ◽  
Angiogenic Growth Factors ◽  
Chronic Injury ◽  
Platelet Endothelial Cell Adhesion

Proper formation of the pulmonary microvasculature is essential for normal lung development and gas exchange. Lung microvascular development may be disrupted by chronic injury of developing lungs in clinical diseases such as bronchopulmonary dysplasia. We examined microvascular development, angiogenic growth factors, and endothelial cell receptors in a fetal baboon model of chronic lung disease (CLD). In the last third of gestation, the endothelial cell marker platelet endothelial cell adhesion molecule (PECAM)-1 increased 7.5-fold, and capillaries immunostained for PECAM-1 changed from a central location in airspace septa to a subepithelial location. In premature animals delivered at 67% of term and supported with oxygen and ventilation for 14 days, PECAM-1 protein and capillary density did not increase, suggesting failure to expand the capillary network. The capillaries of the CLD animals were dysmorphic and not subepithelial. The angiogenic growth factor vascular endothelial growth factor (VEGF) and its receptor fms-like tyrosine kinase receptor (Flt-1) were significantly decreased in CLD. Angiopoietin-1, another angiogenic growth factor, and its receptor tyrosine kinase with immunoglobulin and epidermal growth factor homology domains were not significantly changed. These data suggest that CLD impairs lung microvascular development and that a possible mechanism is disruption of VEGF and Flt-1 expression.

scholarly journals Study of the Role of the Tyrosine Kinase Receptor MerTK in the Development of Kidney Ischemia-Reperfusion Injury in RCS Rats

2021 ◽  
Vol 22 (22) ◽  
pp. 12103
Author(s):  
Thomas Pelé ◽  
Sebastien Giraud ◽  
Sandrine Joffrion ◽  
Virginie Ameteau ◽  
Adriana Delwail ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Kidney Tissue ◽  
Annexin V ◽  
Experimental Models ◽  
Tyrosine Kinase Receptor ◽  
Monocyte Chemoattractant Protein 1 ◽  
Major Player

Renal ischaemia reperfusion (I/R) triggers a cascade of events including oxidative stress, apoptotic body and microparticle (MP) formation as well as an acute inflammatory process that may contribute to organ failure. Macrophages are recruited to phagocytose cell debris and MPs. The tyrosine kinase receptor MerTK is a major player in the phagocytosis process. Experimental models of renal I/R events are of major importance for identifying I/R key players and for elaborating novel therapeutical approaches. A major aim of our study was to investigate possible involvement of MerTK in renal I/R. We performed our study on both natural mutant rats for MerTK (referred to as RCS) and on wild type rats referred to as WT. I/R was established by of bilateral clamping of the renal pedicles for 30′ followed by three days of reperfusion. Plasma samples were analysed for creatinine, aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH), kidney injury molecule -1 (KIM-1), and neutrophil gelatinase-associated lipocalin (NGAL) levels and for MPs. Kidney tissue damage and CD68-positive cell requirement were analysed by histochemistry. monocyte chemoattractant protein-1 (MCP-1), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS), and histone 3A (H3A) levels in kidney tissue lysates were analysed by western blotting. The phagocytic activity of blood-isolated monocytes collected from RCS or WT towards annexin-V positive bodies derived from cultured renal cell was assessed by fluorescence-activated single cell sorting (FACS) and confocal microscopy analyses. The renal I/R model for RCS rat described for the first time here paves the way for further investigations of MerTK-dependent events in renal tissue injury and repair mechanisms.

scholarly journals Expression of Angiopoietin-1, Angiopoietin-2, and the Tie-2 Receptor Tyrosine Kinase during Mouse Kidney Maturation

1999 ◽  
Vol 10 (8) ◽  
pp. 1722-1736
Author(s):  
HAI TAO YUAN ◽  
CHITRA SURI ◽  
GEORGE D. YANCOPOULOS ◽  
ADRIAN S. WOOLF
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Experimental Period ◽  
Mouse Kidney ◽  
Naturally Occurring ◽  
Vasa Recta ◽  
Kidney Maturation ◽  
Angiopoietin 2 ◽  
Angiopoietin 1

Abstract. The Tie-2 receptor tyrosine kinase transduces embryonic onic endothelial differentiation, with Angiopoietin-1 (Ang-1) acting as a stimulatory ligand and Ang-2 postulated to be a naturally occurring inhibitor. Expression of these genes was sought during mouse kidney maturation from the onset of glomerulogenesis (embryonic day 14 [E14]) to the end of nephron formation (2 wk postnatal [P2]), and during medullary maturation into adulthood (P8). Using Northern and slot blotting of RNA extracted from whole organs, these three genes were expressed throughout the experimental period with peak levels at P2 to P3. By in situ hybridization analysis at E18, P1, and P3, Ang-1 mRNA was found to localize to condensing renal mesenchymal cells, proximal tubules, and glomeruli in addition to maturing tubules of the outer medulla. In contrast, Ang-2 transcripts were more spatially restricted, being detected only in differentiating outer medullary tubules and the vasa recta bundle area. Using in situ hybridization and immunohistochemistry, Tie-2 was detected in capillaries of the nephrogenic cortex, glomerular tufts, cortical interstitium, and medulla including vessels in the vasa recta. Using Western blotting of protein extracted from whole organs, Tie-2 protein was detected between E14 and P8 with tyrosine phosphorylated Tie-2 evident from E18. These data are consistent with the hypothesis that Tie-2 has roles in maturation of both glomeruli and vasa rectae.

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