Changes of Platelet MKK3 Phosphorylation Level in Acute Respiratory Distress Syndrome Rats_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

 LIUHong ¹ , FANXiaozhi ^1,2 , TIANXinqiang ¹ , LIBing ¹

1. Research Institute of Respiratory and Occupational Diseases, Datong University, Datong, Shanxi 037009, P.R.China;
2. Department of Respiratory Medicine, The Central Hospital of Linfen, Linfen, Shanxi 041000, P.R.China;

Corresponding author：

LIUHong, Email: a-liuhong@163.com

Keywords：

Acute respiratory distress syndrome; Platelet; Mitogen activated protein kinase; Mitogen activated protein kinase kinase 3; Signal transduction pathway

DOI：

10.7507/1671-6205.201608019

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

Objective To explore the molecular mechanism of pathogenesis and signal pathway of platelet activation in acute respiratory distress syndrome (ARDS). Methods Thirty healthy Sprague-Dawley rats were randomly divided into 5 groups. Four groups were intravenously injected with oleic acid (OA, 0.25 ml/kg) to establish ARDS rat model. One group was intravenously injected with normal saline (NS) in same dose as control group. After injection of oleic acid for 2 h, 6 h, 24 h, 72 h in four OA groups, and injection of saline for 2 h in the control group, the rats were sacrificed. Blood was sampled from the abdominal aorta, then platelets were separated for abstracting platelet protein. The mitogen-activated protein kinase kinase 3 (MKK3) phosphorylation level in platelet was detected by Western blot method, to explore the changes of platelet mitogen activated protein kinase (MAPKs) signal transduction pathway in ARDS, and the relationship between the changes and the pathogenesis of ARDS. Results Platelet MKK3 phosphorylation level significantly increased 6-72 h after injection of oleic acid (P＜0.05). It was 2.4 times that of the control group in 6 h group (0.50±0.09vs. 0.21±0.05), peaked and 3.7 times that of the control group in 24 h group (0.78±0.06), then fell slightly but still significantly higher than the control group in 72 h group (0.75±0.13). Conclusion The activation process of platelets is related with MKK3-p38 MAPK signaling pathway in ARDS.

Citation： LIUHong, FANXiao zhi, TIANXin qiang, LIBing. Changes of Platelet MKK3 Phosphorylation Level in Acute Respiratory Distress Syndrome Rats. Chinese Journal of Respiratory and Critical Care Medicine, 2017, 16(1): 60-63. doi: 10.7507/1671-6205.201608019 Copy

1.	刘宏, 赵金垣, 王世俊, 等. 血小板激活在呼吸窘迫综合征中的发病学作用研究.中华结核和呼吸杂志, 1996, 19(4): 201.
2.	Avasarala S, Zhang FF, Liu G, et al. Curcumin modulates the inflammatory response and inhibits subsequent fibrosis in a mouse model of viral-induced acute respiratory distress syndrome. PLoS One , 2013, 8(2): e57285.
3.	Bozza FA, Shah AM, Weyrich AS, et al. Amicus or adversary: platelets in lung biology, acute injury, and inflammation. Am J Respir Cell Mol Biol, 2009, 40(2): 123-134.
4.	Rondina MT, Weyrich AS, Zimmerman GA. Platelets as cellular effectors of inflammation in vascular diseases. Circ Res, 2013, 112(11): 1506-1519.
5.	Jenne CN, Wong CHY, Petri B, et al. The use of spinning-disk confocal microscopy for the intravital analysis of platelet dynamics in response to systemic and local inflammation. PLoS One, 2011, 6(9): e25109.
6.	Li CL, Li J, Li Y, et al. Crosstalk between platelets and the immune system: old systems with new discoveries. Adv Hematol, 2012: 384685.
7.	Ware J, Corken A, Khetpal R. Platelet function beyond hemostasis and thrombosis. Curr Opin Hematol, 2013, 20(5): 451-456.
8.	Weyrich AS, Zimmerman GA. Platelets in lung biology. Annu Rev Physiol, 2013, 75: 569-591.
9.	Kroll MH, Afshar-Kharghan V. Platelets in pulmonary vascular physiology and pathology. Pulm Circ, 2012, 2(3): 291-308.
10.	Srivastava A, McGinniss J, Wong Y, et al. MKK3 deletion improves mitochondrial quality. Free Radic Biol Med, 2015, 87: 373-384.

1. 刘宏, 赵金垣, 王世俊, 等. 血小板激活在呼吸窘迫综合征中的发病学作用研究.中华结核和呼吸杂志, 1996, 19(4): 201.
2. Avasarala S, Zhang FF, Liu G, et al. Curcumin modulates the inflammatory response and inhibits subsequent fibrosis in a mouse model of viral-induced acute respiratory distress syndrome. PLoS One , 2013, 8(2): e57285.
3. Bozza FA, Shah AM, Weyrich AS, et al. Amicus or adversary: platelets in lung biology, acute injury, and inflammation. Am J Respir Cell Mol Biol, 2009, 40(2): 123-134.
4. Rondina MT, Weyrich AS, Zimmerman GA. Platelets as cellular effectors of inflammation in vascular diseases. Circ Res, 2013, 112(11): 1506-1519.
5. Jenne CN, Wong CHY, Petri B, et al. The use of spinning-disk confocal microscopy for the intravital analysis of platelet dynamics in response to systemic and local inflammation. PLoS One, 2011, 6(9): e25109.
6. Li CL, Li J, Li Y, et al. Crosstalk between platelets and the immune system: old systems with new discoveries. Adv Hematol, 2012: 384685.
7. Ware J, Corken A, Khetpal R. Platelet function beyond hemostasis and thrombosis. Curr Opin Hematol, 2013, 20(5): 451-456.
8. Weyrich AS, Zimmerman GA. Platelets in lung biology. Annu Rev Physiol, 2013, 75: 569-591.
9. Kroll MH, Afshar-Kharghan V. Platelets in pulmonary vascular physiology and pathology. Pulm Circ, 2012, 2(3): 291-308.
10. Srivastava A, McGinniss J, Wong Y, et al. MKK3 deletion improves mitochondrial quality. Free Radic Biol Med, 2015, 87: 373-384.

Previous Article
Measurement of Tracheal and Main Bronchial Dimensions by Bronchoscopy in Adults
Next Article
Protective Effects of Simvastatin on Monocrotaline-Induced Pulmonary Arteral Hypertension in Rats

Chinese Journal of Respiratory and Critical Care Medicine

Changes of Platelet MKK3 Phosphorylation Level in Acute Respiratory Distress Syndrome Rats

Abstract Full text Figures/Tables Video References Cited by

Previous Article

Next Article

Format

Content