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IMAGE: Activity of Neo™-L19 in F9 teratocarcinoma or WEHI-164 fibrosarcoma tumor bearing mice. (A) F9 teratocarcinoma. Left: Tumor bearing mice received 3 injections (?) of Neo™-L19, Neo™-KSF or saline (PBS) when. view more
Credit: Correspondence to - Michael R. Mortensen - michael.mortensen@pharma.ethz.ch
Oncotarget recently published Targeting an engineered cytokine with interleukin-2 and interleukin-15 activity to the neovasculature of solid tumors by Mortensen, et al. which reported that there is a growing interest in the antibody-based delivery of cytokines to the tumor environment as a means to boost the anti-cancer activity of tumor-resident T cells and NK cells.
The authors used the
C. elegans nematode model and fed the wildtype and 9 mutant strains ±sulforaphane.
Sulforaphane increased the lifespan and promoted a health-related phenotype by increasing mobility, appetite and food intake and reducing lipofuscin accumulation.
Mechanistically, sulforaphane inhibited DAF-2-mediated insulin/insulin-like growth factor signaling and its downstream targets AGE-1, AKT-1/AKT-2. This was associated with increased nuclear translocation of the FOXO transcription factor homolog DAF-16. In turn, the target genes sod-3, mtl-1 and gst-4, known to enhance stress resistance and lifespan, were upregulated.
The results in this
Aging-US research output, indicate that sulforaphane prolongs the lifespan and healthspan of
NMN administration significantly increased NAD levels, SIRT1 protein expression, and heme oxygenase-1 expression.
Delayed NMN administration still exerted protective effects after RD.
This
Aging-US article concludes that NMN administration exerts neuroprotective effects on photoreceptors after RD and oxidative injury, suggesting a therapeutic avenue to treating photoreceptor degeneration.
Major photoreceptor degenerative diseases are primarily age-related eye disorders, leading to severe vision impairment or irreversible vision loss.
Despite distinct differences between these diseases, the separation of photoreceptors from the underlying retinal pigment epithelium or a loss of functional RPE, and eventual photoreceptor death is common to all of them.
Since photoreceptors are highly metabolic, nutrient deprivation from the separated RPE induces the pathological responses that result in permanent neuronal loss.