Effects Of β₁ Integrin On The Proliferation,adhesion And Migration Of Cardiac Fibroblasts Induced By Argipressin And Their Relations With Cardiac Remodeling

With the development of biology, molecular biology and immunochemis- try, cardiac interstitial has been the research focus. Being a selfdevelopment process, the rearrangement of the individual component of the cardiac extracellular matrix (ECM), especially the collagens play a significant pathology role in the development of essential hypertension (EH). Numerous investigations have shown that both humoral factors and hemodynamic factors could affect the metabolism of ECM, and most of which are related with integrins family. Jntegrins are a family of transmembrane receptor composed of a and 13 subunit heterodimers. These receptors mediate adhesion of cells directly to ECM proteins. It has been approved that AVP is secreted by hypothalamo-neurohypophysial system, and it is a potent antidiuretic, vasoconstricting, and growth-stimulating neuropeptide. Argipressin (AVP) plays a vital role in the regulation of myocytes hypertrophy and cardiac fibroblasts (CFs) proliferation and excessive collagen synthesis in CFs. But whether AVP is involved in the modulating mechanism of adhesion, migration and the expression of 13 integrin in CFs is still unclear. To study the role of adhesion molecules in Eli and left ventricular hypertrophy, to certain the probably mechanism of using antisense olignucleoutide (ASOND) technology and the intervening effects of interleukin-1 13 (IL-i 13) on these aspects. We investigate the effects of AVP on adhesion and migration of CFs and the expression of f3 integrin in CFs, the interference of ASODN and IL-i f3 inCFs, so as to find an new way for precaution and reversing cardiac remodeling. Isolated and cultured CFs of neonatal Sprague-Dawley (SD) rats was used as experiment model. Collagen and DNA synthesis was measured by incorporation of 3H-proline and 3H-Thymiding (3H1-TdR), respectively. MTT techniques and enzyme linked immuno sorbent assay(ELISA)were also adopted to evaluate the number, the expression of 13 integrin in CFs. Collagen gel contraction was also calculated. We observed: (1)the effects of AVP on proliferation, extramicro structure, the expression of f3 1 integrin and the specialty of collagen gel contraction in CFs; (2)the effects of 131 integrin ASODN on the number, DNA and collagen synthesis of CFs; (3)the effects of 131 integrin ASODN on AVP induced proliferation, the expression of f3~ integrin, DNA and collagen synthesis ,collagen gel contraction in CFs; the number, DNA and collagen synthesis of CFs the effects of (4)the effects of IL-i 13 on AVP induced expression of f3 1 integrin and collagen gel contraction inCFs. The results showed that: (1)Pretreatment of CFs with 1O7M~?O6M AVP, enhanced cell proliferation. With the increasing of AVP the number of CFs was raised. 106M AVP increased MTT A value in CFs at 24 and 48 hours (P