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YKL-40, a newly found inflammatory marker, is belonged to the mammals′chitinase family.It showed that YKL-40 can participate in a variety of inflammatory diseases such as airway inflammatory diseases, cardiovascular and neurological inflamma-tory diseases, and arthritis etc.It could be used to diagnose and evaluate these inflammatory diseases.Since its specific receptor has not been identified, the exact biological role of YKL-40 in inflammatory response still remains unclear.This article reviews the function of YKL-40 in inflammatory response and its related signaling pathways.
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Objective To study the expression of interleukin-1β in aortic dissections and aneurysms. Methods Aortic specimens were obtained from patients with type Ⅰ thoracic aortic dissection (11 cases),ascending thoracic aortic aneurysms (10 cases),and healthy organ donors (7 cases).Expression of interleukin-1β,matrix metalloproteinase-9,and signal transduction factors phospho-p38 and phospho-JNK were detected by real time RT-PCR,Western blot,and immunohistochemistry,respectively.TUNEL staining was performed to detect apoptosis of media cells. Results Apoptosis in the media of thoracic aortic dissection and ascending thoracic aortic aneurysms was dramatically higher than control group.Expression of interleukin-1β gradually increased in an order of control group,thoracic aortic dissection to ascending thoracic aortic aneurysms ( P ＜ 0.01,respectively).Expression of matrix metalloproteinase-9significantly increased in the media of thoracic aortic dissection and ascending thoracic aortic aneurysms compared with control group (P ＜ 0.01,respectively).There were positive correlations between interleukin1 β and matrix metalloproteinase-9,interleukin-1β and phospho-p38 in thoracic aortic dissection ( P ＜ 0.01,respectively),interleukin-1β and apoptosis in ascending thoracic aortic aneurysms (P ＜ 0.01 ).Conclusions Interleukin-1β and interferon-γ might effect the formation of thoracic aortic dissection and ascending thoracic aortic aneurysms possibly through the up-regulation of matrix metalloproteinase-9 and apoptosis of media cells in humans.
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The actin depolymerizing factor/cofilin (ADF/cofilins) are a family of actin-binding proteins expressed in all eukaryotic cells. The ADF/cofilins appear to have multiple functions, and this is reflected in their very complex association with both monomeric and filamentous actin. Phosphorylation by some kinases and other factors such as LIM kinases 1 and 2, TESK 1 and TESK 2 kinase, Insulin, etc, prevents ADF/cofllins from binding actin. The serial researchs of ADF/cofilins are increasingly becoming study hot spots, especially on the relationship between homo-sapiens disease and mechanism of action of ADF/cofilins.Now in this domain wilderness details are still far from clear, such as the mechanism by which actin filaments are depolymerized by ADF/cofilins has been controversial.
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Objective:To construct an adenoviral vect or carrying human tissue inhibitor of metalloproteinase-2(TIMP-2)gene in order to mediate the expression of TIMP-2 gene in vascular smooth muscle cells(SMC)i n vitro. Methods:A recombinant adenovirus(AdhTIMP-2)containging human TIM P-2 cDNA fragment was generated by homologous recombination in BJ5183 bacteria. Recombinant plasmids were screened by alteration of antibiotics.The adenovirus v ector was then packaged and amplified in 293 cells.The SMC of rat aortic were is olated and cultured in vitro and been infected with AdhTIMP-2.The expression of TIMP-2 was detected by the techniques of Western blot and RT-PCR. Results:The recombinant adenoviral vector carrying human TI MP-2 was constructed. The titer was 4?1011efu/ml after purification.The AdhTIMP-2 could infect the cultured VSMC efficiently(MOI=100,infection ra te=94%).The expression of TIMP-2 gene in those infected cells was detected by R T-PCR.After the cells were infected with AdhTIMP-2 24hours,TIMP-2 protein cou ld be detected in the conditioned medium by Western blot. Conclusion:The recombinant adenoviral vector carrying human TIMP -2 is successfully constructed and AdhTIMP-2 can efficently mediate the expres sion of TIMP-2 gene in cultured VSMC,paving the way for further application in vascular disease gene therapy.
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Objective To investigate the effect of TIMP-2 gene that was transfected by adenovirus on extracellular matrix of abdominal aortic through assessing the changes of morphology and histopathology of the rat models with abdominal aortic aneurysm. Methods The rat models with abdominal aortic aneurysm were constructed by intraluminally perfusing porcine pancreatic elastase. Twenty-four SD rats with aneurysm were then randomly divided into 3 groups: AdTIMP-2 group (perfused locally with solution of TIMP-2 gene transfected by adenovirus vector to abdominal aorta), AdCMV group (transfected by non-viral vector), and PBS group. After 14 days, the concentrations of elastin and collagen that were collected from the samples of aortic wall were measured by image analysis system and the fixed aortic tissues were examined by light microscopy and some other specific staining methods. Results None of abdominal aortic aneurysm developed in TIMP-2 gene transfected group, with significantly higher rates of developed aneurysm in the other groups (P
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Objective To investigate expression of inducible nitric oxide synthase (iNOS) and production of nitric oxide(NO) in cultured vascular smooth muscle cells(SMCs)from human abdominal aortic aneurysm(AAA). Methods TypeⅠ collagenase enzyme digestion method was used to culture AAA SMC . Cell proliferation curves for AAA SMC proliferation ability were evaluated,? smooth muscle actin (? SMA) , iNOS protein expression of AAA SMC and nitrite and nitrate (NO 2 -+NO 3 -,NO X ) in cultured media were measured. Results AAA SMCs had a limited proliferation ability, with 45%?5 8% positive rate of ? SMA and 86 7%?4 6% of iNOS protein expression. High concentration of NO X existed in the cultured media. Conclusion AAA SMCs present abnormal but limited proliferation and changed phenotype; The expression of iNOS and high production of NO of AAA SMCs may play an important role in AAA pathogenesis.
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Nitric oxide (NO) and matrix metalloproteinases (MMPs) are important in vascular remolding, especially in abdominal aortic aneurysm. NO may be associated with aneurysms by modulating MMPs expression and activity. [
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Objective To construct an adenoviral vector carrying human tissue inhibitor of metalloproteinase-2 (TIMP-2) gene for gene therapy. Methods A recombinant adenovirus (AdhTIMP-2) containing human TIMP-2 cDNA fragment was generated by homologous recombination in BJ5183 bacteria. Recombinant plasmids were screened by alteration of antibiotic. The adenovirus vector was then packaged and amplified in 293 cells. The expression of TIMP-2 was detected by the techniques of Western blot and RT-PCR. Results The recombinant adenoviral vector carrying human TIMP-2 was constructed. The titer was 4?10 11pfu/ml after purification. The expression of TIMP-2 gene in 293 cells was detected by RT-PCR. After the 293 cells were transfected with AdhTIMP-2 24 hours, TIMP-2 protein could be detected in the medium by Western blot. Conclusions The recombinant adenoviral vector carrying human TIMP-2 is successfully constructed and paved the way for further application in vascular disease gene therapy.