PDGF receptor protein tyrosine kinase expression in the balloon-injured rat carotid artery
PDGF receptor protein tyrosine kinase expression in the balloon-injured rat carotid artery
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DOI：
10.1161/01.atv.17.7.1283
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发表时间：
1997-07-01
影响因子：
8.7
通讯作者：
Keiser, JA
中科院分区：
文献类型：
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作者：
Panek, RL;Dahring, TK;Keiser, JA
血小板源性生长因子（PDGF）受体基因表达先前已被证明在球囊损伤的大鼠颈动脉在颈动脉损伤的修复过程中进行调节。在本研究中，我们发现PDGF受体蛋白表达和磷酸化在颈动脉损伤后随着时间的推移而改变。在对照组和损伤后2天的血管中，PDGF α受体蛋白的表达很容易检测到，而PDGF β受体的表达似乎很低。在损伤后2 - 7天之间，先前显示的时间间隔对应于平滑肌细胞迁移，随后出现新生内膜，PDGF α受体表达仅略微增加，约为对照水平的35%，在损伤后7天达到最大值，而PDGF β受体表达增加了一倍。颈动脉损伤后7 - 14天，内膜面积显著增加，并与PDGF β受体蛋白表达和受体磷酸化的进一步增加相关，在第10 - 12天达到最大值。相比之下，PDGF α受体表达在此时间间隔内略有下降。此外，PDGF α受体的磷酸化几乎检测不到，并且在7月份的时间过程中没有变化。损伤后14 - 28天，内膜面积仅略有增加，而PDGF β受体蛋白和磷酸化水平下降至10天损伤值的大约一半。此外，随着损伤时间的推移观察到的PDGF β受体蛋白表达和酪氨酸磷酸化的增加也与磷脂酰肌醇3'激酶（PI-3激酶）与磷酸化PDGF β受体的相关性相应增加相关。这些结果表明，球囊损伤大鼠颈动脉的结果在时间相关的PDGF受体的表达和酪氨酸磷酸化的状态的变化。此外，体内球囊损伤大鼠颈动脉中PDGF β受体的酪氨酸磷酸化导致PI-3激酶的缔合。这些都是重要的新发现，增加了我们对PDGF受体在新生内膜形成中的作用和活性的认识。
Platelet-derived growth factor (PDGF) receptor gene expression has previously been demonstrated in balloon-injured rat carotid arteries to be regulated during repair of carotid injury. In the present study we showed that PDGF receptor protein expression and phosphorylation are changed over time after carotid artery injury. In control and 2-day-postinjury vessels, expression of PDGF alpha receptor protein was readily detectable, whereas PDGF beta receptor expression appeared very low. Between 2 and 7 days postinjury, a time interval previously shown to correspond with smooth muscle cell migration followed by the appearance of a neointima, PDGF alpha receptor expression had increased only slightly, to roughly 35% above control levels, and was maximal by day 7 postinjury, whereas PDGF beta receptor expression had doubled. From 7 to 14 days after carotid injury, intimal area was greatly increased and was associated with a further increase in PDGF beta receptor protein expression and receptor phosphorylation to a maximum between days 10 and 12. In contrast, PDGF alpha receptor expression had decreased slightly during this time interval. Moreover, phosphorylation of PDGF alpha receptors was barely detectable and did not change over the time course of in july. From 14 to 28 days after injury, intimal area was increased only slightly, whereas PDGF beta receptor protein and phosphorylation levels had diminished to roughly half of the 10-day injury values. In addition, the increases in PDGF beta receptor protein expression and tyrosine phosphorylation observed over the time of injury were also associated with a corresponding increase in the association of phosphatidylinositol 3' kinase (PI-3 kinase) with phosphorylated PDGF beta receptors. These findings show that balloon injury to rat carotid arteries results in temporally related changes in the expression of PDGF receptors and their state of tyrosine phosphorylation. Furthermore, tyrosine phosphorylation of PDGF beta receptors in the balloon-injured rat carotid artery in vivo resulted in the association of PI-3 kinase. These are important new findings, which add to our knowledge concerning the role and activity of PDGF receptors in the formation of a neointima.