scholarly journals Large-Scale Phosphoproteomics Reveals Shp-2 Phosphatase-Dependent Regulators of Pdgf Receptor Signaling

Cell Reports ◽  
2018 ◽  
Vol 22 (10) ◽  
pp. 2784-2796 ◽  
Author(s):  
Tanveer S. Batth ◽  
Moreno Papetti ◽  
Anamarija Pfeiffer ◽  
Maxim A.X. Tollenaere ◽  
Chiara Francavilla ◽  
...  
2017 ◽  
Vol 23 (13) ◽  
pp. 3442-3452 ◽  
Author(s):  
Yukihiro Otaka ◽  
Susumu Rokudai ◽  
Kyoichi Kaira ◽  
Michiru Fujieda ◽  
Ikuko Horikoshi ◽  
...  

2008 ◽  
Vol 28 (18) ◽  
pp. 5646-5657 ◽  
Author(s):  
Wendy J. French ◽  
Esther E. Creemers ◽  
Michelle D. Tallquist

ABSTRACT Complete loss of platelet-derived growth factor (PDGF) receptor signaling results in embryonic lethality around embryonic day 9.5, but the cause of this lethality has not been identified. Because cardiovascular failure often results in embryonic lethality at this time point, we hypothesized that a failure in cardiovascular development could be the cause. To assess the combined role of PDGF receptor α (PDGFRα) and PDGFRβ, we generated embryos that lacked these receptors in cardiomyocytes and vascular smooth muscle cells (VSMC) using conditional gene ablation. Deletion of either PDGFRα or PDGFRβ caused no overt vascular defects, but loss of both receptors using an SM22α-Cre transgenic mouse line led to a disruption in yolk sac blood vessel development. The cell population responsible for this vascular defect was the yolk sac mesothelial cells, not the cardiomyocytes or the VSMC. Coincident with loss of PDGF receptor signaling, we found a reduction in collagen deposition and an increase in MMP-2 activity. Finally, in vitro allantois cultures demonstrated a requirement for PDGF signaling in vessel growth. Together, these data demonstrate that PDGF receptors cooperate in the yolk sac mesothelium to direct blood vessel maturation and suggest that these effects are independent of their role in VSMC development.


2008 ◽  
Vol 22 (7) ◽  
pp. 2214-2222 ◽  
Author(s):  
Alfiya Akhmetshina ◽  
Clara Dees ◽  
Margarita Pileckyte ◽  
Britta Maurer ◽  
Roland Axmann ◽  
...  

1998 ◽  
Vol 8 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Jian-xin Yang ◽  
Karen Symes ◽  
Mark Mercola ◽  
Stuart L. Schreiber

2018 ◽  
Author(s):  
Zhaohu Yuan ◽  
Qianyu Wu ◽  
Xiaojie Chen ◽  
Yaming Wei

ABSTRACTAlthough platelet is anucleate cell, it contains a large amount miRNAs. This study aims to explore the relationship between miRNAs expression profles and platelets function, as well as miRNAs potential roles during platelet storage lesions. Platelets were collected from 15 healthy men with O blood types. MiRNAs profiles in platelets were detected by Agilent Human miRNA Array Differential miRNA levels were studied using human platelets after apheresis and stored for 2, 5 and 8 days using microarray. There were 167 and 230 altered miRNAs during the 5 and 8 day storage, respectively. In addition, the number of reduced miRNAs was much greater than that of increased. And many of them are involved in functions of platelet activation, degranulation, PDGF receptor signaling pathway and cell differentiation. The results of RT-PCR showed that the expression of miR-21-5p, miR-21-3p and miR-155 decreased on the 5th day, while miR-223, miR-3162 and let-7b increased. Flow cytometry results revealed that with increase of storage time, the expression of P2Y12 increased and phosphorylation level of VASP reduced. Meanwhile, the platelet reactivity index (PRI) decreased from 72.7% to 18.2%, while the apoptotic percentage of platelet significantly increased. For the first time, we found altered miRNAs are closely related to platelet aggregation, including P2Y12, VASP and GPⅡb/Ⅲa. Through KEGG database prediction, we verified there were many miRNAs impacting the pathway of platelet aggregation, such as miR-223, miR-21 and let-7b, which indicated miRNAs might serve as potential biomarkers of storage lesion in platelet. These target miRNAs are related to activation, degranulation and PDGF receptor signaling pathway of platelet.


Sign in / Sign up

Export Citation Format

Share Document