Abstract: SA-PO996
Subsequent Impaction on Renal Tissue After Myocardial Infarction in Animal Models
Session Information
- Hypertension and CVD: Mechanisms - II
October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Su, Chi-Ting, National Taiwan University Hospital, Yun-Lin Branch, Taipei, Taiwan
- Liu, Yen-wen, Department of Internal Medicine, National Cheng Kung University Hospital, Taiwan, Tainan, Taiwan
- Huang, Jenq-wen, National Taiwan University Hospital, Taipei, Taiwan
Background
The interaction between kidney and heart has been an important entity for decades. Investigation of pathogenesis may optimize therapeutic strategies and modalities, which potentially leads patients with cardiac and renal impairments to better outcomes. The major goal for this research is to investigate the biological functions of the latent transforming growth factor-beta-binding proteins (LTBPs) and identify pathophysiological role in renal impairment after myocardial infarction.
Methods
We created myocardial infarction with ligation over left anterior descending artery in mice. Echocardiogarphy and picrosirius red/fast green-stained histology studies were used to demonstrate the cardiac dysfunction after myocardial infarction. Gene and protein expression have been studied one week, two weeks, and four weeks after the surgery.
Results
Echocardiography successfully demonstrated cardiac wall motion abnormalities after myocardial infarction and cardiac fibrosis had been shown in histology studies. Ltbp4, pSMAD2 and pERK had been up-regulated in cardiac tissue obviously two weeks after myocardial infarction. On the other hand, one week after myocardial infarction, interleukin 6 (IL- 6) and monocyte chemoattractant protein -1(MCP-1) in renal tissues had been up-regulated significantly (p<0.001). It is interesting that increasing expression of kidney injury molecule-1 (KIM-1), ltbp4 and transforming growth factor beta (TGF-β) in renal tissue had been detected until two weeks after the surgery. Moreover, renal platelet-derived growth factor receptor beta (Pdgfrb) was detected increasing steadily. In addition, increased ltbp4 expression in renal after kidney injury had been found as an essential regulatory factor in TGF-β pathways.
Conclusion
Cardiac fibrosis can enhance renal inflammation early and induce KIM-1 and Pdgfrb expression in renal tissue. Inflammation served as a prelude before the expression of fibrotic factors. Ltbp4 is an essential regulatory in TGF-β signaling and is one of the significant factors to manipulate the progress of renal injury and the crosstalk between kidney and heart, the cardiorenal syndrome.
Funding
- Government Support - Non-U.S.