Correlation between expression of two transforming growth factor-beta 1 receptors and microvascular density in a rat model of cerebral ischemia and reperfusion injury  

作　　者：Li Jiang Qingzhu Yue Lingzhi Yu Xudong Liu 

机构地区：[1]Department of Anesthesiology, Hebei Province People's Hospital, Shijiazhuang 050000, Hebei Province, China [2]Department of Anesthesiology, Fourth People's Hospital of Jinan, Jinan 250031, Shandong Province, China [3]Department of Analgesia, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, Shandong Province, China [4]Department of Analgesia, Qilu Hospital, Shandong University, Jinan 250012, Shandong Province, China

出　　处：《Neural Regeneration Research》2011年第11期850-854,共5页中国神经再生研究（英文版）

基　　金：a grant of Supportive Fund for Young Scientists from the Department of Science & Technology of Shandong Province, China, No. 2004BS03013

摘　　要：The effects of transforming growth factor-β1 （TGF-β1） are currently controversial. Whether TGF-β1 promotes or inhibits revascularization under different conditions remains poorly understood. Based on previous studies, the current experiment established rat models of cerebral ischemia and reperfusion injury （IRI）, and demonstrated that pathological and functional damage was also increased after IRI. The most serious damage was observed at 3 days after reperfusion, at which time microvascular density fell to its lowest level. Soon afterwards, microvascular density increased, new collateral circulation was gradually established at 4 to 7 days after reperfusion, and pathological damage and neurological deficits were improved. TGF-β1, activin receptor-like kinase 5 （ALK5） mRNA and protein expression levels increased gradually over time. In contrast, ALK1 mRNA and protein expression decreased over the same period. A significant negative correlation was detected between microvascular density and expression of the ALK5 gene transcript. There was no correlation between microvascular density and ALK1 gene transcriptional expression following cerebral IRI in a rat model. These findings suggest that ALK5, rather than ALK1, is the critical receptor in the TGF-β1 signal pathways after cerebral IRI.The effects of transforming growth factor-β1 （TGF-β1） are currently controversial. Whether TGF-β1 promotes or inhibits revascularization under different conditions remains poorly understood. Based on previous studies, the current experiment established rat models of cerebral ischemia and reperfusion injury （IRI）, and demonstrated that pathological and functional damage was also increased after IRI. The most serious damage was observed at 3 days after reperfusion, at which time microvascular density fell to its lowest level. Soon afterwards, microvascular density increased, new collateral circulation was gradually established at 4 to 7 days after reperfusion, and pathological damage and neurological deficits were improved. TGF-β1, activin receptor-like kinase 5 （ALK5） mRNA and protein expression levels increased gradually over time. In contrast, ALK1 mRNA and protein expression decreased over the same period. A significant negative correlation was detected between microvascular density and expression of the ALK5 gene transcript. There was no correlation between microvascular density and ALK1 gene transcriptional expression following cerebral IRI in a rat model. These findings suggest that ALK5, rather than ALK1, is the critical receptor in the TGF-β1 signal pathways after cerebral IRI.

关 键 词：cerebral ischemia and reperfusion injury transforming growth factor-β1 transforming growth factor-β1 receptor/activin receptor-like kinase 1 activin receptor-like kinase 5 microvascular density neural regeneration 

分 类 号：Q516[生物学—生物化学] Q95-33