PRMT3: New binding molecule to RhoGDI-α during mycophenolic acid-induced β-cell death

K. H. Huh, Y. Cho, B. S. Kim, D. J. Joo, M. S. Kim, Y. S. Kim

Research output: Contribution to journalArticle

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Abstract

Mycophenolic acid (MPA)-induced beta cell toxicity limits islet graft survival. However, the signal transduction mechanisms underlying MPA-induced β-cell toxicity have not been fully elucidated. Previously, we showed that MPA-induced pancreatic β-cell apoptosis proceeds via RhoGDI-α down-regulation linked to Rac1 activation. In the present study, we investigated factors affecting RhoGDI-α during MPA-induced β-cell apoptosis. The presence of RhoGDI-α-related protein was determined with the use of yeast 2-hybrid (Y2H) analysis. Y2H screening of RhoGDI-α was performed in yeast PBN204 strain containing 3 reporters (URA3, lacZ, and ADE2) under the control of different GAL promoters. INS-1E cells (an insulin-secreting pancreatic β-cell line) were treated with MPA for 12, 24, and 36 hours. Eighty-three real positives were obtained by Y2H analysis, and of these, arginine N-methyltransferase 3 (PRMT3) protein interacted with RhoGDI-α in INS-1E cells. PRMT3 gene expressions and its protein levels were significantly decreased during MPA-induced apoptosis. In summary, PRMT3 and RhoGDI-α were found to interact in INS-1E cells. Furthermore, MPA was found to regulate this interaction in INS-1E cells by down-regulating the gene expression of PRMT3. These findings suggest that control of the interaction between PRMT3 and RhoGDI-α could be used to prevent MPA-induced β-cell death.

Original languageEnglish
Pages (from-to)1229-1232
Number of pages4
JournalTransplantation Proceedings
Volume46
Issue number4
DOIs
Publication statusPublished - 2014 May

Fingerprint

Mycophenolic Acid
Cell Death
Yeasts
Apoptosis
Gene Expression
Proteins
Insulin-Secreting Cells
Graft Survival
Signal Transduction
Down-Regulation
Cell Line

All Science Journal Classification (ASJC) codes

  • Surgery
  • Transplantation

Cite this

Huh, K. H. ; Cho, Y. ; Kim, B. S. ; Joo, D. J. ; Kim, M. S. ; Kim, Y. S. / PRMT3 : New binding molecule to RhoGDI-α during mycophenolic acid-induced β-cell death. In: Transplantation Proceedings. 2014 ; Vol. 46, No. 4. pp. 1229-1232.
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PRMT3 : New binding molecule to RhoGDI-α during mycophenolic acid-induced β-cell death. / Huh, K. H.; Cho, Y.; Kim, B. S.; Joo, D. J.; Kim, M. S.; Kim, Y. S.

In: Transplantation Proceedings, Vol. 46, No. 4, 05.2014, p. 1229-1232.

Research output: Contribution to journalArticle

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T2 - New binding molecule to RhoGDI-α during mycophenolic acid-induced β-cell death

AU - Huh, K. H.

AU - Cho, Y.

AU - Kim, B. S.

AU - Joo, D. J.

AU - Kim, M. S.

AU - Kim, Y. S.

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AB - Mycophenolic acid (MPA)-induced beta cell toxicity limits islet graft survival. However, the signal transduction mechanisms underlying MPA-induced β-cell toxicity have not been fully elucidated. Previously, we showed that MPA-induced pancreatic β-cell apoptosis proceeds via RhoGDI-α down-regulation linked to Rac1 activation. In the present study, we investigated factors affecting RhoGDI-α during MPA-induced β-cell apoptosis. The presence of RhoGDI-α-related protein was determined with the use of yeast 2-hybrid (Y2H) analysis. Y2H screening of RhoGDI-α was performed in yeast PBN204 strain containing 3 reporters (URA3, lacZ, and ADE2) under the control of different GAL promoters. INS-1E cells (an insulin-secreting pancreatic β-cell line) were treated with MPA for 12, 24, and 36 hours. Eighty-three real positives were obtained by Y2H analysis, and of these, arginine N-methyltransferase 3 (PRMT3) protein interacted with RhoGDI-α in INS-1E cells. PRMT3 gene expressions and its protein levels were significantly decreased during MPA-induced apoptosis. In summary, PRMT3 and RhoGDI-α were found to interact in INS-1E cells. Furthermore, MPA was found to regulate this interaction in INS-1E cells by down-regulating the gene expression of PRMT3. These findings suggest that control of the interaction between PRMT3 and RhoGDI-α could be used to prevent MPA-induced β-cell death.

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