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Deficiency of platelet adhesion molecule CD226 causes megakaryocyte development and platelet hyperactivity.

FASEB J. 2020 May;34(5):6871-6887. doi:10.1096/fj.201902142R. Epub 2020 Apr 05
Jinxue Zhang 1 , Yong Ding 1 , Dongxu Jiang 2 , Jiangang Xie 3 , Yongming Liu 1 , Jingchang Ma 2 , Yang Mu 2 , Xuexin Zhang 2 , Chaoping Yu 3 , Yun Zhang 2 , Xin Yi 1 , Ziqing Zhou 2 , Liang Fang 2 , Shen Shen 2 , Yixin Yang 2 , Kun Cheng 4 , Ran Zhuang 4 , Yuan Zhang 5
Jinxue Zhang 1 , Yong Ding 1 , Dongxu Jiang 2 , Jiangang Xie 3 , Yongming Liu 1 , Jingchang Ma 2 , Yang Mu 2 , Xuexin Zhang 2 , Chaoping Yu 3 , Yun Zhang 2 , Xin Yi 1 , Ziqing Zhou 2 , Liang Fang 2 , Shen Shen 2 , Yixin Yang 2 , Kun Cheng 4 , Ran Zhuang 4 , Yuan Zhang 5
+ et al

[No authors listed]

Author information
  • 1 Orthopedic Department of Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
  • 2 Department of Immunology, Fourth Military Medical University, Xi'an, China.
  • 3 Department of Emergency, Fourth Military Medical University, Xi'an, China.
  • 4 Transplant Immunology Laboratory, Fourth Military Medical University, Xi'an, China.
  • 5 Institute of Medical Research, Northwestern Polytechnical University, Xi'an, China.

摘要


This study used constitutive CD226 gene knockout (KO) mice as a model to investigate the functions and mechanisms of CD226 in megakaryocyte (MK) maturation and platelet activation. Although CD226 deficiency did not cause MK polyploidization or platelet granule abnormalities, increased MK counts were detected in the femora bone marrow (BM) and spleen of CD226 KO mice. Particularly, CD226 KO mice have a more extensive membrane system in MKs and platelets than wild-type (WT) mice. We also demonstrated that CD226 KO mice displayed increased platelet counts, shortened bleeding time, and enhanced platelet aggregation. CD226 KO platelets had an increased mature platelet ratio compared to the control platelets. In addition, the observed reduction in bleeding time may be due to decreased nitric oxide (NO) production in the platelets. Platelet-specific CD226-deficient mice showed similar increased MK counts, shortened bleeding time, enhanced platelet aggregation, and decreased NO production in platelets. Furthermore, we performed middle cerebral artery occlusion-reperfusion surgery on WT and CD226 KO mice to explore the potential effect of CD226 on acute ischemia-reperfusion injury; the results revealed that CD226 deficiency led to significantly increased infarct area. Thus, CD226 is a promising candidate for the treatment of thrombotic disorders.

KEYWORDS: CD226, activation, megakaryocyte, nitric oxide, platelet