title: Eryptosis as an Underlying Mechanism in Systemic Lupus Erythematosus-Related Anemia.
abstract: BACKGROUND
  The progression of systemic lupus erythematosus (SLE) leads to anemia in patients, adversely affecting prognosis. The diverse causes of anemia may include excessive eryptosis or premature suicidal erythrocyte death characterized by cell shrinkage and phosphatidylserine (PS) exposure on the cell surface. The present study explored if SLE enhances eryptosis and the underlying mechanisms.
  
  
  METHODS
  Eryptosis was assessed using flow cytometry in healthy volunteers (n = 20) and anemic patients hospitalized for SLE (n = 22), for parameters including PS exposure, cell volume, cytosolic calcium ion (Ca2+) levels and reactive oxygen species (ROS) and ceramide abundance. These indicators were measured in erythrocytes of experimental subjects and erythrocytes treated with plasma from healthy volunteers or SLE patients.
  
  
  RESULTS
  The hemoglobin and hematocrit levels were significantly lower in anemic SLE patients than in healthy volunteers (***p<0.001, p<0.001, respectively). The percentage of PS-exposing erythrocytes was significantly higher in SLE patients than in healthy volunteers (p<0.001), accompanied by an increase in cytosolic Ca2+ levels, oxidative stress. The measurements of PS and Ca2+ levels were significantly higher in the erythrocytes of healthy volunteers following incubation in plasma of SLE patients than in plasma of healthy volunteers for 24h (***p<0.001, *p<0.05 respectively).
  
  
  CONCLUSIONS
  Eryptosis is enhanced in SLE and may contribute to anemia. The probable underlying mechanisms may be an excessive formation of ROS in erythrocytes. Also, some plasma components may trigger eryptosis by increasing the cytosolic Ca2+ concentration.
authors.affiliation: Department of Blood Transfusion, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
authors.forename: Peipei
authors.initials: P
authors.lastname: Jiang
authors.forename: Maohong
authors.initials: M
authors.lastname: Bian
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Ma
authors.forename: Chunqiu
authors.initials: C
authors.lastname: Liu
authors.forename: Peng
authors.initials: P
authors.lastname: Yang
authors.forename: Bangqiang
authors.initials: B
authors.lastname: Zhu
authors.forename: Yuanhong
authors.initials: Y
authors.lastname: Xu
authors.forename: Meijuan
authors.initials: M
authors.lastname: Zheng
authors.forename: Jinpin
authors.initials: J
authors.lastname: Qiao
authors.forename: Zongwen
authors.initials: Z
authors.lastname: Shuai
authors.forename: Xueyong
authors.initials: X
authors.lastname: Zhou
authors.forename: Dake
authors.initials: D
authors.lastname: Huang
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000740:Anemia / Q000097:blood / Q000150:complications* / Q000473:pathology*; D000975:Antioxidants / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002518:Ceramides / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D000072817:Eryptosis; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D064368:Healthy Volunteers; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D010718:Phosphatidylserines / Q000378:metabolism; D010949:Plasma / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D055815:Young Adult
chemical_list: D000975:Antioxidants; D002518:Ceramides; D010718:Phosphatidylserines; D017382:Reactive Oxygen Species; D002118:Calcium