scholarly journals Cartilage Oligometric Matrix Protein-Angiopoietin-1 Promotes Revascularization Through Increased Survivin Expression in Dermal Endothelial Cells of Skin Grafts in Mice

2007 ◽  
Vol 171 (5) ◽  
pp. 1682-1690 ◽  
Author(s):  
Seung-Jae Byun ◽  
Kyu-Sil Choi ◽  
Sung Hoon Park ◽  
Nam Woo Cho ◽  
Chang Hyun Yoo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Matrix Protein ◽  
Survivin Expression ◽  
Skin Grafts ◽  
Angiopoietin 1

scholarly journals HIV-1 Matrix Protein p17 Promotes Lymphangiogenesis and Activates the Endothelin-1/Endothelin B Receptor Axis

2014 ◽  
Vol 34 (4) ◽  
pp. 846-856 ◽  
Author(s):  
Francesca Caccuri ◽  
Christine Rueckert ◽  
Cinzia Giagulli ◽  
Kai Schulze ◽  
Daniele Basta ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lymph Node ◽  
Structure Formation ◽  
Highly Active Antiretroviral Therapy ◽  
Matrix Protein ◽  
Lymphatic Endothelial Cells ◽  
Endothelin 1 ◽  
Tumor Dissemination ◽  
Hiv 1

Objective— AIDS-related lymphomas are high grade and aggressively metastatic with poor prognosis. Lymphangiogenesis is essential in supporting proliferation and survival of lymphoma, as well as tumor dissemination. Data suggest that aberrant lymphangiogenesis relies on action of HIV-1 proteins rather than on a direct effect of the virus itself. HIV-1 matrix protein p17 was found to accumulate and persist in lymph nodes of patients even under highly active antiretroviral therapy. Because p17 was recently found to exert a potent proangiogenic activity by interacting with chemokine (C-X-C motif) receptors 1 and 2, we tested the prolymphangiogenic activity of the viral protein. Approach and Results— Human primary lymph node–derived lymphatic endothelial cells were used to perform capillary-like structure formation, wound healing, spheroids, and Western blot assays after stimulation with or without p17. Here, we show that p17 promotes lymphangiogenesis by binding to chemokine (C-X-C motif) receptor-1 and chemokine (C-X-C motif) receptor-2 expressed on lymph node–derived lymphatic endothelial cells and activating the Akt/extracellular signal–regulated kinase signaling pathway. In particular, it was found to induce capillary-like structure formation, sprout formation from spheroids, and increase lymph node–derived lymphatic endothelial cells motility. The p17 lymphangiogenic activity was, in part, sustained by activation of the endothelin-1/endothelin receptor B axis. A Matrigel plug assay showed that p17 was able to promote the outgrowth of lymphatic vessels in vivo, demonstrating that p17 directly regulates lymphatic vessel formation. Conclusions— Our results suggest that p17 may generate a prolymphangiogenic microenvironment and plays a role in predisposing the lymph node to lymphoma growth and metastasis. This finding offers new opportunities to identify treatment strategies in combating AIDS-related lymphomas.

Systemic Analysis of Tyrosine Phosphorylated Proteins in Angiopoietin-1 Induced Signaling Pathway of Endothelial Cells

2007 ◽  
Vol 6 (8) ◽  
pp. 3278-3290 ◽  
Author(s):  
Young Mee Kim ◽  
Jawon Seo ◽  
Yung Hee Kim ◽  
Jaeho Jeong ◽  
Hye Joon Joo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Phosphorylated Proteins ◽  
Systemic Analysis ◽  
Angiopoietin 1

Proliferation and functionality of human umbilical vein endothelial cells on angiopoietin-1 immobilized 316L stainless steel

2015 ◽  
Vol 3 (44) ◽  
pp. 8717-8728 ◽  
Author(s):  
Xin Li ◽  
Shuheng Yuan ◽  
Si Chen ◽  
Rifang Luo ◽  
Kaiqin Xiong ◽  
...  
Keyword(s):  
Stainless Steel ◽  
Endothelial Cells ◽  
316L Stainless Steel ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
And Function ◽  
Functionalized Surface ◽  
Angiopoietin 1

An angiopoietin-1 functionalized surface was establishedviapolydopamine coating and regulated HUVECs survival, proliferation and function.

Angiopoietin-1 promotes endothelial cell proliferation and migration through AP-1–dependent autocrine production of interleukin-8

Blood ◽  
2008 ◽  
Vol 111 (8) ◽  
pp. 4145-4154 ◽  
Author(s):  
Nelly A. Abdel-Malak ◽  
Coimbatore B. Srikant ◽  
Arnold S. Kristof ◽  
Sheldon A. Magder ◽  
John A. Di Battista ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Interleukin 8 ◽  
Endothelial Cell Migration ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration ◽  
Angiopoietin 1

Abstract Angiopoietin-1 (Ang-1), ligand for the endothelial cell–specific Tie-2 receptors, promotes migration and proliferation of endothelial cells, however, whether these effects are promoted through the release of a secondary mediator remains unclear. In this study, we assessed whether Ang-1 promotes endothelial cell migration and proliferation through the release of interleukin-8 (IL-8). Ang-1 elicited in human umbilical vein endothelial cells (HUVECs) a dose- and time-dependent increase in IL-8 production as a result of induction of mRNA and enhanced mRNA stability of IL-8 transcripts. IL-8 production is also elevated in HUVECs transduced with retroviruses expressing Ang-1. Neutralization of IL-8 in these cells with a specific antibody significantly attenuated proliferation and migration and induced caspase-3 activation. Exposure to Ang-1 triggered a significant increase in DNA binding of activator protein-1 (AP-1) to a relatively short fragment of IL-8 promoter. Upstream from the AP-1 complex, up-regulation of IL-8 transcription by Ang-1 was mediated through the Erk1/2, SAPK/JNK, and PI-3 kinase pathways, which triggered c-Jun phosphorylation on Ser63 and Ser73. These results suggest that promotion of endothelial migration and proliferation by Ang-1 is mediated, in part, through the production of IL-8, which acts in an autocrine fashion to suppress apoptosis and facilitate cell proliferation and migration.

scholarly journals Suppressive Effects of Sulforaphane on TGFBIp-mediated Sepsis

2017 ◽  
Vol 12 (10) ◽  
pp. 1934578X1701201 ◽  
Author(s):  
In-Chul Lee ◽  
Jong-Sup Bae
Keyword(s):  
Endothelial Cells ◽  
Matrix Protein ◽  
Transforming Growth Factor ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Cecal Ligation ◽  
Transforming Growth Factor Β ◽  
Extracellular Matrix Protein ◽  
Experimental Sepsis

Sulforaphane (SFN) is produced when the enzyme myrosinase transforms glucoraphanin upon damage to the plant such as from chewing and effective in preventing carcinogenesis, diabetes, and inflammatory responses. Transforming growth factor β-induced protein (TGFBIp) is an extracellular matrix protein whose expression in several cell types is greatly increased by TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. We hypothesized that SFN could reduce TGFBIp-mediated severe inflammatory responses in human endothelial cells and mice. Here, we investigated the anti-septic effects and underlying mechanisms of SFN against TGFBIp-mediated septic responses. SFN effectively inhibited lipopolysaccharide-induced release of TGFBIp and suppressed TGFBIp-mediated septic responses. In addition, SFN suppressed cecal ligation and puncture (CLP)-induced sepsis lethality and pulmonary injury. In conclusion, SFN suppressed TGFBIp-mediated and CLP-induced septic responses. Therefore, SFN could be a potential therapeutic agent for treatment of various severe vascular inflammatory diseases via inhibition of the TGFBIp signaling pathway.

COMP-Ang-1 Improves Glucose Uptake in db/db Mice with Type 2 Diabetes

2020 ◽  
Vol 52 (09) ◽  
pp. 685-688
Author(s):  
Petra Baum ◽  
Sabine Paeschke ◽  
Nora Klöting ◽  
Matthias Blüher ◽  
Matthias Kern ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Matrix Protein ◽  
Molecular Mechanisms ◽  
Therapeutic Potential ◽  
Vascular Endothelial ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Hba1c Levels ◽  
Angiopoietin 1

AbstractCartilage oligomeric matrix protein (COMP)-Angiopoietin-1 is a potent angiopoietin-1 (Ang-1) variant that possesses therapeutic potential in angiogenesis and vascular endothelial dysfunction. Noteworthy, we have shown that COMP-Ang-1 improves hyperglycemia and neuroregeneration in ob/ob mice. However, the mechanism of the antidiabetic effect of COMP-Ang-1 is completely unknown. Therefore, we elucidated the diabetes protective molecular mechanisms of COMP-Ang-1 in diabetic db/db mouse model. COMP-Ang-1 (0.5 ng/g body weight) or aqueous NaCl solution was injected intraperitoneally per day in 21 consecutive days into 3-month old, male db/db mice (n=10 per group). Blood glucose and HbA1c levels were determined at baseline and 21 days after COMP-Ang-1 or NaCl treatment. The effect of COMP-Ang-1 on glucose uptake was investigated by euglycemic-hyperinsulinemic clamp studies and key genes of glucose metabolism were studied by Western blot analysis. Our findings indicate that COMP-Ang-1 improves glucose metabolism in a tissue specific manner by regulating HIF-1α transcriptional genes of GLUT-1 expression.

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