scholarly journals Natural killer T cells from peripheral blood of patients with pregnancy-induced hypertension inhibit the proliferation and migration of vascular endothelial cells by secreting interleukin-17

2019 ◽  
Vol 33 (1) ◽  
pp. 347-358
Author(s):  
Aixin Zhao ◽  
Kun Liu ◽  
Yunfang Qi
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Natural Killer T Cells ◽  
Interleukin 17 ◽  
Vascular Endothelial ◽  
Pregnancy Induced Hypertension ◽  
Induced Hypertension ◽  
And Migration ◽  
Killer T Cells ◽  
Proliferation And Migration

scholarly journals Inhibition of the JAK2/STAT3/SOSC1 Signaling Pathway Improves Secretion Function of Vascular Endothelial Cells in a Rat Model of Pregnancy-Induced Hypertension

2016 ◽  
Vol 40 (3-4) ◽  
pp. 527-537 ◽  
Author(s):  
Jian-Ying Luo ◽  
Dan Fu ◽  
Ya-Qin Wu ◽  
Ying Gao
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Rat Model ◽  
Vascular Endothelial Cells ◽  
Serum Levels ◽  
Vascular Endothelial ◽  
Pregnancy Induced Hypertension ◽  
Pregnant Rats ◽  
Tnf Α ◽  
Induced Hypertension

Background/Aims: The present study aimed to investigate the effects of the JAK2/STAT3/SOSC1 signaling pathway on the secretion function of vascular endothelial cells (VECs) in a rat model of pregnancy-induced hypertension (PIH). Methods: A PIH rat model was established. Forty-eight pregnant Sprague-Dawley female rats were selected and assigned into four groups: the normal group (normal non-pregnant rats), the non-PIH group (pregnant rats without PIH), the PIH group (pregnant rats with PIH) and the AG490 group (pregnant rats with PIH treated with AG490). Systolic blood pressure (SBP) and urinary protein (UP) were measured. The expressions of JAK2/STAT3/SOSC1 signaling pathway-related proteins in placenta tissues were detect by Western blotting. Radioimmunoassay was applied to detect serum levels of nitric oxide (NO), super oxide dismutase (SOD), placental growth factor (PGF), thromboxane B2 (TXB2) and endothelin (ET). Enzyme-linked immunosorbent assay (ELISA) was used to determine serum levels of interleukin-6 (IL-6), interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α). Results: Compared with the normal and non-PIH groups, the PIH and AG490 groups had higher SBP and UP levels at 17th and 25th day of pregnancy. The expressions of p/t-JAK2, p/t-STAT3 and SOSC1 in the PIH and AG490 groups were higher than those in the non-PIH group, while the expressions of p/t-JAK2, p/t-STAT3 and SOSC1 in the AG490 group were lower than those in the PIH group. Compared with the non-PIH group, serum levels of ET, TXB2, IL-6 and TNF-α were increased in the PIH and AG490 groups, while serum levels of NO, SOD, 6-keto-PGF1a and IL-10 levels were reduced. Furthermore, the AG490 had lower serum levels of ET, TXB2, IL-6 and TNF-α and higher serum levels of NO, SOD, 6-keto-PGF1a and IL-10 than those in the PIH group. Conclusion: Our study provides evidence that inhibition of the JAK2/STAT3/SOSC1 signaling pathway could improve the secretion function of VECs in PIH rats.

The Novel Platelet Activation Receptor CLEC-2 Regulates Blood/Lymphatic Vessel Separation by Inhibiting Proliferation and Migration of Lymphatic Endothelial Cells

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 160-160 ◽  
Author(s):  
Makoto Osada ◽  
Osamu Inoue ◽  
Guo Ding ◽  
Masanori Hirashima ◽  
Katsue Suzuki-Inoue ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Cells ◽  
Tumor Metastasis ◽  
Lymphatic Vessel ◽  
Conflicts Of Interest ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
And Migration ◽  
Proliferation And Migration

Abstract Abstract 160 CLEC-2 has been described recently as playing crucial roles in thrombosis/hemostasis, tumor metastasis, and lymphangiogenesis. The snake venom rhodocytin is known as a strong platelet activator, and we have shown that this effect is mediated by CLEC-2. Podoplanin, which is expressed on the surface of tumor cells, is an endogenous ligand for CLEC-2 and facilitates tumor metastasis by inducing platelet aggregation. Mice deficient in podoplanin, which is also expressed on the surface of lymphatic endothelial cells, show abnormal patterns of lymphatic vessel formation. We have recently reported on the generation and phenotype of CLEC-2-deficient mice. These mice are lethal at the embryonic/neonatal stages associated with disorganized and blood-filled lymphatic vessels and severe edema, indicating that CLEC-2 is essential for blood/lymphatic vessel separation. However, CLEC-2 is expressed in both platelets and neutrophils in mice and whether CLEC-2 in platelets, but not that in other cells, plays a role in the separation has not been directly proved yet. Moreover, the mechanism how CLEC-2 regulates of blood/lymphatic vessel separation has not been elucidated to date. In the present study, we found that specific deletion of CLEC-2 from platelets mediated by PF4-Cre conferred the defect of blood/lymphatic vessel separation, identifying that CLEC-2 expressed in platelets is required to regulate lymphatic vascular development. Tube formation of lymphatic endothelial cells, but not that of vascular endothelial cells, was inhibited in the presence of platelets. Further, proliferation and migration of lymphatic endothelial cells, but not those of vascular endothelial cells, were inhibited by CLEC-2+/+ platelets, but not by CLEC-2−/− platelets. We propose that CLEC-2 regulates blood/lymphatic vessel separation by inhibiting proliferation and migration of lymphatic endothelial cells through the interaction between CLEC-2 in platelets and podoplanin in lymphatic endothelial cells. CLEC-2 may be a novel therapeutic target protein for lymphatic metastasis of tumor if the interaction of CLEC-2 and podoplanin also regulates lymphangiogenesis by tumor cells. Disclosures: No relevant conflicts of interest to declare.

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