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Mechanism of arterial remodeling in chronic allograft vasculopathy

Qichang Zheng, Shanglong Liu, Zifang Song

《医学前沿（英文）》 2011年第5卷第3期页码 248-253 doi: 10.1007/s11684-011-0149-3

摘要： Chronic allograft vasculopathy (CAV) remains a major obstacle for long-term survival of grafts even though therapeutic strategies have improved considerably in recent years. CAV is characterized by concentric and diffuse neointimal formation, medial apoptosis, infiltration of lymphocyte or inflammatory cells, and deposition of extracellular matrix both in arteries and veins. Recent studies have shown that stem cells derived from the recipient contribute to neointimal formation under the regulation of chemokines and cytokines. Arterial remodeling in allografts eventually causes ischemic graft failure. The pathogenesis is multi-factorial with both immunologic and non-immunological factors being involved. The immunological factors have been discussed extensively in other articles. This review focuses mainly on the arterial remodeling that occurs in 3 layers of vessel walls including intimal injury, accumulation of smooth muscle-like cells in the neointimal, medial smooth muscle cell apoptosis, adventitial fibrosis, and deposition of extracellular matrix.

关键词： transplantation chronic rejection neointimal immunology arterial remodeling allograft vasculopathy

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Relationship between Th17 cells and allograft rejection

Zhikun ZHENG MM, Jinsong LI MD, Ke JIANG MD,

《医学前沿（英文）》 2009年第3卷第4期页码 491-494 doi: 10.1007/s11684-009-0066-x

摘要： Thl7 cells, a special kind of auxiliary type T cells, can secrete IL-17A, IL-17F, IL-21, IL-22, etc., as a newly discovered T-cell subset in recent years. As a different subset from the Thl and Th2 cells, Th17 cells play an important role in the development of a variety of autoimmune diseases. A current study shows that the IL-6 inflammatory response of the organization in combination with the occurrence of TGF-β can induce the differentiation of Thl7 cells. IL-23 can promote the production of IL17, as well as participate in amplification and maintenance of the survival of IL-l7 generating cells. In this process, STAT3 and ROR-γt are key transcription factors for the growing of Thl7 cells. As our knowledge on Th17 family members is rapidly growing and changing, it will be important to specify their involvement in the induction and regulation of allograft rejection in animal models as well as in clinical settings. Herein, we review the key features of Th17 cells and discuss their potential relevance to transplantation immunity.

关键词： TH17 cells regulation allograft rejection

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Adenovirus-mediated antisense ERK2 gene therapy ameliorates chronic allograft nephropathy in a rat model

Zhao DING, Zhishui CHEN, Xilin CHEN, Ming CAI, Hui GUO, Nianqiao GONG

《医学前沿（英文）》 2009年第3卷第2期页码 204-210 doi: 10.1007/s11684-009-0039-0

摘要： To investigate the effect and underlying mechanism of adenovirus-mediated antisense ERK2 (Adanti-ERK2) gene therapy upon chronic allograft nephropathy (CAN) of rats, male Lewis (LEW, RT11) rats received male Fisher (F344, RT11v1) renal allografts. The recipients were divided into three groups: (1) empty control group; (2) vector control group; (3) gene therapy group. All recipients were sacrificed for the grafts and serum analysis at the 24th week after transplantation. Morphometric analysis was used to determine the fibrosis of grafts. Immunohistochemistry was used to detect the expression of E-Cadherin, Vimentin, TβR I and the infiltration of CD4 T lymphocyte, CD8 T lymphocyte and ED-1 monocytes. Enzyme linked immunosorbent assay (ELISA) was used to detect TGF-β1 in serum. The grafts in the control group and vector control group showed CAN. There was less E-Cadherin in renal tubular epithelial cells in the empty control group but more Vimentin and TβR I. In the gene therapy group, the fibrosis was ameliorated and fewer T lymphocytes and ED-1 monocytes infiltrated in the interstitium. There was no significant difference in the expression of E-Cadherin between the gene therapy group and normal rats. Compared with the empty control group, the expression of TGF-β1 in the gene therapy group was down-regulated. Adanti-ERK2 gene therapy protects the renal allograft and attenuates graft fibrosis, which may be correlated with a decreased renal tubular epithelial mesenchymal transition, a decreased infiltration of CD4 T lymphocyte, CD8 T lymphocytes and ED-1 monocytes in renal interstitium, and the down-regulated TGF-β1 expression.

关键词： anti-ERK2 renal transplantation epithelial mesenchymal transition chronic allograft nephropathy

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Construction of the vessel-collateral theory and its guidance for prevention and treatment of vasculopathy

Yiling Wu

《医学前沿（英文）》 2011年第5卷第2期页码 118-122 doi: 10.1007/s11684-011-0140-z

摘要： According to the self-discipline of traditional Chinese medicine, vessel-collateral theory was constructed systematically, which was important to improving prevention and treatment level of vasculopathy. The hypothesis of “homeostasis ( ), compensatory auto-adaptation ( ), regulation ( ) and equilibrium ( )” based on the “qi–yin-yang–five elements” coupled with the (nutrients)- (defense) theory, has become the core content of the vessel-collateral theory. Clinical and laboratory trials have been developed to further confirm the scientific connotations of the hypothesis, such as capsule, as the representative drugs of vessel collateral theory, showed good efficacy in protecting the vascular endothelium, stabilizing the vulnerable plaque and reducing the blood vessel spasm. “Sou, ti, shu, tong” was the characteristics of capsule in treating “microvascular damage” as the core mechanism of acute myocardial infarction, cerebral infarction and microvascular complications of diabetes. capsules in the treatment of arrhythmia have made integrated adjustment advantage. capsules have been made treating both manifestation and root cause of chronic heart failure. These research have improved prevention and treatment level of major vascular system diseases.

关键词： vessel-collateral theory vasculopathy prevention and treatment