본문 바로가기
KERD
논문KCI 등재

25HydroxyethylStarch를 이용한 냉동적혈구의 제조와 해동

The Cryopreservation and Thawing of Red Blood Cells Using 25% Hydroxyethyl

0

조회

0

다운로드

2

인용

0

참고문헌

주제분류병리학

초록

배경 : AML의 병태생리는 복잡하여 DNA의 손상, 염색체의대칭 또는 비대칭 교환, 손실, 역전, 비정상적인 활성전사인자 및수용체 등 여러 가지 요인에 의한다. C/EBP 및 C/EBP 는 과립구분화에 중요한 역할을 하는 활성전사인자이다. C/EBP 또는 C/EBP 의 활성을 증가시켜 백혈병 골수아구를 억제시킬 수있는지 여부를 파악하기 위하여 시행하였다. 방법 : BOSC23세포에서 MIG, MIG-C/EBP -ER 및 MIG-C/EBP -ER 바이러스를 만들어 32Dcl3세포를 감염시켜 세포증식, 과립구표현인자 Gr-1 및 Mac-1발현정도, 세포분화를 조사하였다. MIG-C/EBP -ER 및 MIG-C/EBP -ER바이러스로 감염된 #1111세포는 4.5 Gy 방사선 조사된 20마리 FVB/N 생쥐에 각 주입하고 다시 5마리씩 위약군, 4HT (C/EBP), ATRA,및 4HT & ATRA 군으로 분류하고 이들의 환약을 #1111세포를 주입한지 14일에 생쥐의 피하조직에 넣고 병색이 완연할 때 안락사 시켰다. 결과 :MIG 바이러스로 감염된 32Dcl 3세포의 2, 4, 6일에 파악한 세포수는 각각 684,976개, 1,975,965개, 2,808,244개이었고,MIG-C/EBP -ER의 경우 77,354개, 53,180개, 39,460개이었고,MIG-C/EBP -ER의 경우 328,384개, 698,424개, 974,850개이었다. 대조군에서 Gr-1과 Mac-1은 발현이 되지 않았으나 MIG-C/EBP -ER의 경우 Gr-1은 56.1%, Mac-1은 55.6% 발현되었고 MIG-C/EBP -ER의 경우 Gr-1 31.3%, Mac-1 32.6%가 발현되었다. 세포분화정도로 분류된 미성숙, 중간, 성숙세포는 MIG바이러스로 감염된 32Dcl3에서 각 90.0%, 6.0%, 4.0%이었고,MIG-C/EBP -ER의 경우 4.3%, 33.7%, 62.0%, MIG-C/EBP -32Dcl3 생쥐 골수아구 및 #1111 급성전골수구성백혈병세포에서 C/EBP 및C/EBP 의 영 향 345ER의 경우 41.0%, 48.3%, 10.7%로 세포가 분화되었다. MIG-C/EBP -ER 바이러스로 감염된 #1111세포를 FVB/N 생쥐에 주입 후 관찰한 평균 생존기간은 위약군에서 30.5일, 4HT (C/EBP )군 41.8일, ATRA군에서 69.0일, 4HT (C/EBP ) 및 ATRA동시투여군에서 97.8일이었고 MIG-C/EBP -ER의 경우 각 군별로 26.4일, 33.0일, 49.6일, 52.5일로 생존하였다.

참고문헌 (37)

  1. "Regulation of the myeloperoxidase enhancer binding proteinsPU1, C-EBP , - , and - during granulocyte-lineage specification", 93, pp.10838~10843 (1996)
  2. "A transcription factor party during bloodcell differentiation", 8, pp.545~551 (1998)
  3. "Transcriptional regulation of granulocyte and monocytedevelopment", 21, pp.3377~3390 (2002)
  4. "Regulation of granulopoiesis by transcription factors and cytokinesignals", 14, pp.973~990 (2000)
  5. "CCAAT-enhancer bindingprotein:A component of a differentiation switch", 251, pp.288~92 (1991)
  6. "Ras signaling enhances the activity of C", EBP alpha toinduce granulocytic differentiation by phosphorylation of serine248, 2002, pp.277, 26293~26299
  7. "Structural and Functional Studies ofCCAAT", Enhancer-binding Protein, 2001, pp.276, 17739~17746
  8. "CHOP,a novel developmentally regulatednuclear protein that dimerizes with transcription factor C", EBP andLAP functions as a dominant negative inhibitor of gene transcription, 1992, pp.6, 439~53
  9. "Ig", EBP(C, EBPfamily transcriptional activators, 1995[DOI]
  10. "The DNA bindingdomain of the rat liver protein C", EBP is bipartite, 1989, pp.243, 1681~8
  11. "The leucine zipper:ahypothetical structure common to a new class of DNA binding proteins", 240, pp.1759~64 (1988)
  12. "Molecular cloning, sequence,and expression patterns of the human gene encoding CCAAT", enhancer binding protein alpha (C, pp.1995, 215[DOI]
  13. "The role of C", EBP in the terminal stages ofgranulocyte differentiation, 2001, pp.19, 125~233
  14. "C", EBP interacts withretinoblastoma and E2F1 during granulopoiesis, 2004, pp.103, 828~835
  15. "Absence of granulocyte colony-stimulating factor signalingand neutrophil development in CCAAT enhancer bindingprotein -deficient mice", 94, pp.569~574 (1997)
  16. "Impaired granulopoiesis,myelodysplasia,andearly lethality in CCAAT", enhancer binding protein -deficientmice, 1997, pp.94, 13187~13192
  17. "Epidemiology of acute leukemia in childrenand adults", 24, pp.3~16 (1997)
  18. "Dominant-negative mutations of CEBPA, encoding CCAAT", enhancer binding protein- (C, pp.2001, 27[DOI]
  19. "AML1-ETO downregulates the granulocytic differentiationfactor C", EBP in t(8;21) myeloid leukemia, 2001, pp.7, 444~451
  20. "BCR-ABL suppresses C", EBP expression through inhibitoryaction of hnRNP E2, 2002, pp.30, 48~58
  21. "CCAAT", enhancer binding protein is a potential retinoidtarget gene in acute promyelocytic leukemia treatment, 1999, pp.103, 1399~1408
  22. "Demonstration of permanent factor-dependent multipotential(erythroid", neutrophil, pp.1983, 80[DOI]
  23. "The murinemyeloid cell line 32Dcl3 as a model system for studying neutrophilfunctions", 283, pp.195~204 (2003)
  24. "C", EBP bypassesgranulocyte colony-stimulating factor signals to rapidly inducePU.1 gene expression, stimulate granulocytic differentiation, andlimit proliferation in 32Dcl3 myeloblasts, 1999, pp.94, 560~571
  25. "A PMLRAR transgene initiates murine acute promyelocyticleukemia", 94, pp.2551~2556 (1997)
  26. "CCAAT", Enhancer binding proteins repress the leukemic phenotypeof acute myeloid leukemia, 2003, pp.101, 1141~1148
  27. "Differentiation or leukemia:Is C", EBP the answer?, 2001, pp.7, 407~408
  28. "Identificationof a rat liver nuclear protein that binds to the enhancer coreelement of three animal viruses", 1, pp.133~46 (1987)
  29. "Down-regulation and antiproliferative role of C", EBPalpha inlung cancer, 2002, pp.15(62), 528~534
  30. "C", EBPalpha is required to maintain postmitoticgrowth arrest in adipocytes, 2000, pp.19, 9~18
  31. "Down-regulated expression of the CCAAT", enhancer binding proteinalpha and beta genes in human hepatocellular carcinoma:apossible prognostic marker, 2003, pp.23, 351~354
  32. "The amino terminal and E2F interaction domains are criticalfor C", EBP -mediated induction of granulopoietic developmentof hematopoietic cells, 2003, pp.102, 3163~3171
  33. "c-Myc is a critical target for C", EBP in granulopoiesis, 2001, pp.21, 3789~3806
  34. "C", EBP arrests cell proliferation through direct inhibition of Cdk2and Cdk4, 2001, pp.8, 817~828
  35. "CCAAT", enhancer-binding protein-alpha cooperates with p21 to inhibit cyclin-dependentkinase-2 activity and induces growth arrest independent ofDNA binding, 2001, pp.276, 29200~29209
  36. "E2F repression by C", EBP is required for adipogenesis andgranulopoiesis in vivo, 2001, pp.107, 247~258
  37. "E2F", p107 and E2F, EBPalphain 3T3-L1 adipocytes, 1999[DOI]

관련 논문AI추천

이 간행물의 다른 논문 (2건)