PMID- 11641530
OWN - NLM
STAT- MEDLINE
DCOM- 20020103
LR  - 20171116
IS  - 1011-8934 (Print)
IS  - 1598-6357 (Electronic)
IS  - 1011-8934 (Linking)
VI  - 16
IP  - 5
DP  - 2001 Oct
TI  - alpha-Melanocyte stimulating hormone (MSH) decreases cyclosporine a induced 
      apoptosis in cultured human proximal tubular cells.
PG  - 603-9
AB  - The pathogenesis of chronic cyclosporine A (CsA) nephrotoxicity has not been 
      elucidated, but apoptosis is thought to play an important role in CsA induced 
      tubular atrophy. Recently Fas-Fas ligand system mediated apoptosis has been 
      frequently reported in many epithelial cells as well as in T lymphocytes. We 
      investigated the ability of CsA to induce apoptosis in cultured human proximal 
      tubular epithelial cells and also the effect of alpha-MSH on them. Fas, Fas 
      ligand, and an intracellular adaptor protein, Fas-associating protein with death 
      domain (FADD) expression, and poly-ADP ribose polymerase (PARP) cleavage were 
      also studied. CsA induced apoptosis in cultured tubular epithelial cells 
      demonstrated by increased number of TUNEL positive cells and it was accompanied 
      by a significant increase in Fas mRNA and Fas ligand protein expressions. FADD 
      and the cleavage product of PARP also increased, indicating the activation of 
      caspase. In alpha-MSH co-treated cells, apoptosis markedly decreased with 
      downregulation of Fas, Fas ligand and FADD expressions and also the cleavage 
      product of PARP. In conclusion, these data suggest that tubular cell apoptosis 
      mediated by Fas system may play a role in tubular atrophy in chronic CsA 
      nephrotoxicity and pretreatment of alpha-MSH may have a some inhibitory effect on 
      CsA induced tubular cell apoptosis.
FAU - Jo, S K
AU  - Jo SK
AD  - Department of Internal Medicine, Korea University College of Medicine, The 
      Institute of Renal Disease, Seoul, Korea. wonyong@korea.ac.kr
FAU - Lee, S Y
AU  - Lee SY
FAU - Han, S Y
AU  - Han SY
FAU - Cha, D R
AU  - Cha DR
FAU - Cho, W Y
AU  - Cho WY
FAU - Kim, H K
AU  - Kim HK
FAU - Won, N H
AU  - Won NH
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - J Korean Med Sci
JT  - Journal of Korean medical science
JID - 8703518
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Carrier Proteins)
RN  - 0 (FADD protein, human)
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Fas-Associated Death Domain Protein)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (fas Receptor)
RN  - 581-05-5 (alpha-MSH)
RN  - 83HN0GTJ6D (Cyclosporine)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Apoptosis/*drug effects
MH  - Carrier Proteins/biosynthesis
MH  - Caspases/physiology
MH  - Cells, Cultured
MH  - Cyclosporine/*toxicity
MH  - Fas Ligand Protein
MH  - Fas-Associated Death Domain Protein
MH  - Humans
MH  - Immunosuppressive Agents/*toxicity
MH  - Kidney Tubules, Proximal/cytology/*drug effects/metabolism
MH  - Membrane Glycoproteins/biosynthesis
MH  - Poly(ADP-ribose) Polymerases/metabolism
MH  - RNA, Messenger/analysis
MH  - alpha-MSH/*pharmacology
MH  - fas Receptor/genetics
PMC - PMC3057601
EDAT- 2001/10/20 10:00
MHDA- 2002/01/05 10:01
PMCR- 2001/10/01
CRDT- 2001/10/20 10:00
PHST- 2001/10/20 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/20 10:00 [entrez]
PHST- 2001/10/01 00:00 [pmc-release]
AID - 200110603 [pii]
AID - 10.3346/jkms.2001.16.5.603 [doi]
PST - ppublish
SO  - J Korean Med Sci. 2001 Oct;16(5):603-9. doi: 10.3346/jkms.2001.16.5.603.