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  • RIPK1-RIPK3-MLKL-dependent necrosis promotes the aging of mouse male reproductive system.

RIPK1-RIPK3-MLKL-dependent necrosis promotes the aging of mouse male reproductive system.

eLife (2017-08-16)
Dianrong Li, Lingjun Meng, Tao Xu, Yaning Su, Xiao Liu, Zhiyuan Zhang, Xiaodong Wang
ABSTRACT

A pair of kinases, RIPK1 and RIPK3, as well as the RIPK3 substrate MLKL cause a form of programmed necrotic cell death in mammals termed necroptosis. We report here that male reproductive organs of both Ripk3- and Mlkl-knockout mice retain 'youthful' morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. The RIPK3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild-type mice. When the testes of young wild-type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
RIPA-56, ≥98% (HPLC)
Pricing and availability is not currently available.
Sigma-Aldrich
Anti-UTF-1 Antibody, clone 5G10.2, clone 5G10.2, Chemicon®, from mouse
Pricing and availability is not currently available.