Anti-Nitro tyrosine polyclonal antibody [HRP]

Parthanatos is a modality of regulated cell death initiated by poly(ADP-ribose) polymerase 1 (PARP-1) hyperactivation and characterized by apoptosis inducing factor (AIF)-dependent and microphage migration inhibitory factor (MIF)-dependent DNA degradation. It is a caspase-independent, mitochondrial-linked paradigm of cell death and has been demonstrated to be related to the pathogenesis of various nervous system diseases. An in-depth understanding of the role that parthanatos plays in the pathological processes of these diseases can provide new targets for nervous system diseases treatments. In this review, on the basis of parthanatos mechanism, the involvement of parthanatos in the pathogenesis of nervous system diseases including neurodegenerative disorders, cerebrovascular diseases, spinal cord injury and glioma will be summarized in detail. (C) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

Acute kidney injury (AKI), a critical syndrome characterized by a rapid decrease of kidney function, is a global health problem. Src family kinases (SFK) are proto-oncogenes that regulate diverse biological functions including mitochondrial function. Since mitochondrial dysfunction plays an important role in the development of AKI, and since unbalanced SFK activity causes mitochondrial dysfunction, the present study examined the role of SFK in AKI. Lipopolysaccharides (LPS) inhibited mitochondrial biogenesis and upregulated the expression of NGAL, a marker of tubular epithelial cell injury, in mouse proximal tubular epithelial (mProx) cells. These alterations were prevented by PP2, a pan SFK inhibitor. Importantly, PP2 pretreatment significantly ameliorated LPS-induced loss of kidney function and injury including inflammation and oxidative stress. The attenuation of LPS-induced AKI by PP2 was accompanied by the maintenance of mitochondrial biogenesis. LPS upregulated SFK, especially Fyn and Src, in mouse kidney as well as in mProx cells. These data suggest that Fyn and Src kinases are involved in the pathogenesis of LPS-induced AKI, and that inhibition of Fyn and Src kinases may have a potential therapeutic effect, possibly via improving mitochondrial biogenesis.