RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      KCI등재후보

      Mesenchymal Stem Cells Ameliorate Adriamycin Induced Proteinuric Nephropathy = Adriamycin 유발 신병증에서 중간엽 줄기세포의 완화 효과

      한글로보기

      https://www.riss.kr/link?id=A101470766

      • 0

        상세조회
      • 0

        다운로드
      서지정보 열기
      • 내보내기
      • 내책장담기
      • 공유하기
      • 오류접수

      부가정보

      다국어 초록 (Multilingual Abstract)

      Purpose : Glomerulonephropathy (GN) often manifests as proteinuria and progresses to chronic renal failure without specific therapy. Mesenchymal stem cell (MSC) has been tried as a therapeutic agent in experimental GN, and previous studies showed that administration of MSC concomitantly to the insult inducing GN or via intra-renal administration ameliorated proteinuria. The purpose of this study was to test the therapeutic potential of MSC administered via intravenous route at the time of clinically evident proteinuria. Methods : MSCs were administered intravenously via tail vain into the mice with adriamycin (ADR) induced nephropathy (ADR-GN), two weeks after ADR injection when massive proteinuria was evident. To test the capacity of MSC modulate the cytokine production in the inflammatory milieu, the concentrations of IFN-$\gamma$ and IL-10 were measured in the supernatant of in vitro mixed lymphocyte culture (MLC) with or without additional MSC. Results : MSCs administered intravenously into the proteinuric mice with ADR-GN accelerated the recovery of this experimental GN with disappearance of proteinuria in two weeks when the saline treated (control) mice still showed significant proteinuria. The mice treated with MSC also had a tendency of better survival. Addition of MSC decreased IFN-$\gamma$ and increased IL-10 in the supernatant of MLC. Conclusion : This study showed that MSC had a therapeutic potential even when administered in a more clinically relevant setting into a proteinuric glomerulonephropathy model. Further study to verify the mechanism and long-term safety of this phenomenon is required.
      번역하기

      Purpose : Glomerulonephropathy (GN) often manifests as proteinuria and progresses to chronic renal failure without specific therapy. Mesenchymal stem cell (MSC) has been tried as a therapeutic agent in experimental GN, and previous studies showed that...

      Purpose : Glomerulonephropathy (GN) often manifests as proteinuria and progresses to chronic renal failure without specific therapy. Mesenchymal stem cell (MSC) has been tried as a therapeutic agent in experimental GN, and previous studies showed that administration of MSC concomitantly to the insult inducing GN or via intra-renal administration ameliorated proteinuria. The purpose of this study was to test the therapeutic potential of MSC administered via intravenous route at the time of clinically evident proteinuria. Methods : MSCs were administered intravenously via tail vain into the mice with adriamycin (ADR) induced nephropathy (ADR-GN), two weeks after ADR injection when massive proteinuria was evident. To test the capacity of MSC modulate the cytokine production in the inflammatory milieu, the concentrations of IFN-$\gamma$ and IL-10 were measured in the supernatant of in vitro mixed lymphocyte culture (MLC) with or without additional MSC. Results : MSCs administered intravenously into the proteinuric mice with ADR-GN accelerated the recovery of this experimental GN with disappearance of proteinuria in two weeks when the saline treated (control) mice still showed significant proteinuria. The mice treated with MSC also had a tendency of better survival. Addition of MSC decreased IFN-$\gamma$ and increased IL-10 in the supernatant of MLC. Conclusion : This study showed that MSC had a therapeutic potential even when administered in a more clinically relevant setting into a proteinuric glomerulonephropathy model. Further study to verify the mechanism and long-term safety of this phenomenon is required.

      더보기

      참고문헌 (Reference)

      1 Kunter U, "Transplanted mesenchymal stem cells accelerate glomerular healing in experimental glomerulonephritis" 17 : 2202-2212, 2006

      2 Morigi M, "The regenerative potential of stem cells in acute renal failure" 15 (15): S111-117, 2006

      3 Gao J, "The dynamic in vivo distribution of bone marrow-derived mesenchymal stem cells after infusion" 169 : 12-20, 2001

      4 Barbash IM, "Systemic delivery of bone marrow-derived mesenchymal stem cells to the infarcted myocardium: Feasibility, cell migration, and body distribution" 108 : 863-868, 2003

      5 Fischer UM, "Pulmonary passage is a major obstacle for intravenous stem cell delivery: The pulmonary first-pass effect" 18 : 683-692, 2009

      6 Wang Y, "Partial depletion of macrophages by ed7 reduces renal injury in adriamycin nephropathy" 10 : 470-477, 2005

      7 Ninichuk V, "Multipotent mesenchymal stem cells reduce interstitial fibrosis but do not delay progression of chronic kidney disease in collagen 4a3-deficient mice" 70 : 121-129, 2006

      8 Magnasco A, "Mesenchymal stem cells protective effect in adriamycin model of nephropathy" 17 : 1157-1167, 2008

      9 Kunter U, "Mesenchymal stem cells prevent progressive experimental renal failure but maldifferentiate into glomerular adipocytes" 18 : 1754-1764, 2007

      10 Mangi AA, "Mesenchymal stem cells modified with akt prevent remodeling and restore performance of infarcted hearts" 9 : 1195-1201, 2003

      1 Kunter U, "Transplanted mesenchymal stem cells accelerate glomerular healing in experimental glomerulonephritis" 17 : 2202-2212, 2006

      2 Morigi M, "The regenerative potential of stem cells in acute renal failure" 15 (15): S111-117, 2006

      3 Gao J, "The dynamic in vivo distribution of bone marrow-derived mesenchymal stem cells after infusion" 169 : 12-20, 2001

      4 Barbash IM, "Systemic delivery of bone marrow-derived mesenchymal stem cells to the infarcted myocardium: Feasibility, cell migration, and body distribution" 108 : 863-868, 2003

      5 Fischer UM, "Pulmonary passage is a major obstacle for intravenous stem cell delivery: The pulmonary first-pass effect" 18 : 683-692, 2009

      6 Wang Y, "Partial depletion of macrophages by ed7 reduces renal injury in adriamycin nephropathy" 10 : 470-477, 2005

      7 Ninichuk V, "Multipotent mesenchymal stem cells reduce interstitial fibrosis but do not delay progression of chronic kidney disease in collagen 4a3-deficient mice" 70 : 121-129, 2006

      8 Magnasco A, "Mesenchymal stem cells protective effect in adriamycin model of nephropathy" 17 : 1157-1167, 2008

      9 Kunter U, "Mesenchymal stem cells prevent progressive experimental renal failure but maldifferentiate into glomerular adipocytes" 18 : 1754-1764, 2007

      10 Mangi AA, "Mesenchymal stem cells modified with akt prevent remodeling and restore performance of infarcted hearts" 9 : 1195-1201, 2003

      11 Le Blanc K, "Mesenchymal stem cells for treatment of steroid-resistant, severe, acute graft-versus-host disease: A phase ii study" 371 : 1579-1586, 2008

      12 Herrera MB, "Mesenchymal stem cells contribute to the renal repair of acute tubular epithelial injury" 14 : 1035-1041, 2004

      13 Remuzzi G, "Mechanisms of progression and regression of renal lesions of chronic nephropathies and diabetes" 116 : 288-296, 2006

      14 Eddy AA, "Interstitial nephritis induced by protein-overload proteinuria" 135 : 719-733, 1989

      15 Degauque N, "Immunostimulatory tim-1-specific antibody deprograms tregs and prevents transplant tolerance in mice" 118 : 735-741, 2008

      16 Frank MH, "Immunomodulatory functions of mesenchymal stem cells" 363 : 1411-1412, 2004

      17 Aggarwal S, "Human mesenchymal stem cells modulate allogeneic immune cell responses" 105 : 1815-1822, 2005

      18 Beyth S, "Human mesenchymal stem cells alter antigen-presenting cell maturation and induce t-cell unresponsiveness" 105 : 2214-2219, 2005

      19 Wells AD, "Following the fate of individual t cells throughout activation and clonal expansion. Signals from t cell receptor and cd28 differentially regulate the induction and duration of a proliferative response" 100 : 3173-3183, 1997

      20 Okuda S, "Elevated expression of transforming growth factor-beta and proteoglycan production in experimental glomerulonephritis. Possible role in expansion of the mesangial extracellular matrix" 86 : 453-462, 1990

      21 Wang Y, "Depletion of cd4(+) t cells aggravates glomerular and interstitial injury in murine adriamycin nephropathy" 59 : 975-984, 2001

      22 Rangan GK, "Cytokine gene expression in adriamycin nephropathy: Effects of antioxidant nuclear factor kappab inhibitors in established disease" 86 : 482-490, 2000

      23 Togel F, "Bioluminescence imaging to monitor the in vivo distribution of administered mesenchymal stem cells in acute kidney injury" 295 : F315-321, 2008

      24 Togel F, "Autologous and allogeneic marrow stromal cells are safe and effective for the treatment of acute kidney injury" 18 : 475-485, 2009

      25 Peister A, "Adult stem cells from bone marrow (mscs) isolated from different strains of inbred mice vary in surface epitopes, rates of proliferation, and differentiation potential" 1662-1668, 2004

      26 Togel F, "Administered mesenchymal stem cells protect against ischemic acute renal failure through differentiation- independent mechanisms" 289 : F31-42, 2005

      더보기

      동일학술지(권/호) 다른 논문

      동일학술지 더보기

      더보기

      분석정보

      View

      상세정보조회

      0

      Usage

      원문다운로드

      0

      대출신청

      0

      복사신청

      0

      EDDS신청

      0

      동일 주제 내 활용도 TOP

      더보기

      주제

      연도별 연구동향

      연도별 활용동향

      연관논문

      연구자 네트워크맵

      공동연구자 (7)

      유사연구자 (20) 활용도상위20명

      인용정보 인용지수 설명보기

      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2024 평가예정 계속평가 신청대상 (계속평가)
      2022-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      2021-12-01 평가 등재후보 탈락 (계속평가)
      2019-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      2018-12-01 평가 등재후보 탈락 (계속평가)
      2017-12-01 평가 등재후보로 하락 (계속평가) KCI등재후보
      2016-01-12 학술지명변경 한글명 : 대한소아신장학회지 -> Childhood Kidney Diseases
      외국어명 : Journal of the Korean Society of Pediatric Nephrology -> Childhood Kidney diseases
      KCI등재
      2013-01-01 평가 등재 1차 FAIL (등재유지) KCI등재
      2010-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2009-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2008-01-01 평가 신청제한 (등재후보1차) KCI등재
      2007-01-01 평가 등재후보 1차 FAIL (등재후보2차) KCI등재후보
      2006-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2004-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      더보기

      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.12 0.12 0.13
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.11 0.11 0.332 0
      더보기

      이 자료와 함께 이용한 RISS 자료

      나만을 위한 추천자료

      해외이동버튼