Title : Parp1 protects against Aag-dependent alkylation-induced nephrotoxicity in a sex-dependent manner.

Pub. Date : 2016 Jul 19

PMID : 27391435






5 Functional Relationships(s)
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1 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate poly (ADP-ribose) polymerase family, member 1 Mus musculus
2 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate poly (ADP-ribose) polymerase family, member 1 Mus musculus
3 Here we report that Parp1-deficient mice expressing increased Aag (AagTg/Parp1-/-) develop sex-dependent kidney failure upon exposure to the alkylating agent, methyl methanesulfonate (MMS), and suffer increased whole-animal lethality compared to AagTg and wild-type mice. Methyl Methanesulfonate poly (ADP-ribose) polymerase family, member 1 Mus musculus
4 Pharmacological Parp inhibition in AagTg mice also resulted in sensitivity to MMS-induced nephrotoxicity. Methyl Methanesulfonate poly (ADP-ribose) polymerase family, member 1 Mus musculus
5 These findings provide in vivo evidence that Parp1 modulates Aag-dependent MMS-induced nephrotoxicity in a sex-dependent manner and highlight the critical roles that Aag-initiated BER and Parp1 may play in determining the side-effects of chemotherapeutic alkylating agents. Methyl Methanesulfonate poly (ADP-ribose) polymerase family, member 1 Mus musculus