Poly(ADP-Ribose) Polymerases in Aging - Friend or Foe?

Vida, András; Abdul‐Rahman, Omar; Mikó, Edit; Brunyánszki, Attila; Bai, Péter

doi:10.2174/1389203717666160419144959

Cited by 18 publications

(15 citation statements)

References 58 publications

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“…The phenotype we observed, on one hand, corresponds to the known cell death‐promoting features of PARP1 . While on the other, there are studies suggesting that PARP activation can limit the self‐renewal capacity of stem cells, which may also contribute to the phenotype we observed …”

Section: Discussionsupporting

confidence: 65%

Poly(ADP‐ribose) polymerase‐1 depletion enhances the severity of inflammation in an imiquimod‐induced model of psoriasis

Kiss

Szántó

Hegedűs

et al. 2019

Experimental Dermatology

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Poly(ADP‐ribose) polymerase‐1 (PARP1) is a pro‐inflammatory protein, whose pro‐inflammatory properties were demonstrated in human. The pro‐inflammatory properties of PARP1 were shown in Th1‐ and Th2‐mediated inflammatory pathologies, but not Th17‐mediated inflammation. Thus, we studied the role of PARP1 in the imiquimod‐induced model of psoriasis. To our surprise, in imiquimod‐induced psoriasis, PARP1 acted as an anti‐inflammatory factor and its genetic deletion exacerbated symptoms. We showed that in the absence of PARP1, the epidermis thickened and the number of TUNEL‐positive cells decreased in the epidermis. These data indicate programmed cell death is decreased in keratinocytes. Changes in involucrin expression suggest that keratinocyte differentiation is hampered. Furthermore, epidermal expression of IL6 increased in the psoriasiform lesions of PARP1 knockout mice, suggesting that the inflammatory response is also derailed in the absence of PARP1. Finally, we showed that PARP1 expression is reduced in human psoriatic lesions compared with control skin samples. In imiquimod‐treated HPV‐KER keratinocytes, PARP inhibition recapitulated the in vivo findings, namely keratinocyte hyperproliferation; furthermore, the mRNA expression of psoriasis‐associated cytokines (IL6, IL1β, IL8, IL17 and IL23A) was also induced. The inhibition of TRPV1 abrogated the effects of the combined imiquimod + PARP inhibitor treatment.

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Section: Discussionsupporting

confidence: 65%

Poly(ADP‐ribose) polymerase‐1 depletion enhances the severity of inflammation in an imiquimod‐induced model of psoriasis

Kiss

Szántó

Hegedűs

et al. 2019

Experimental Dermatology

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“…Early commitment and clonal expansion PARP1, PARP2, and PARP7 have pivotal roles in decision making between retaining stem cell properties and differentiation in nonadipogenic models (Yélamos et al 2006;Farrés et al 2013Farrés et al , 2015Nozaki et al 2013;Roper et al 2014;Vida et al 2016). Therefore, PARPs may be crucial in the early commitment of cells toward preadipocytes and adipose lineages (Fig.…”

Section: The Role Of Parp Enzymes In Adipogenesismentioning

confidence: 99%

The role of ADP-ribose metabolism in metabolic regulation, adipose tissue differentiation, and metabolism

Szántó

Bai

2020

Genes Dev.

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Poly(ADP-ribose) polymerases (PARPs or ARTDs), originally described as DNA repair factors, have metabolic regulatory roles. PARP1, PARP2, PARP7, PARP10, and PARP14 regulate central and peripheral carbohydrate and lipid metabolism and often channel pathological disruptive metabolic signals. PARP1 and PARP2 are crucial for adipocyte differentiation, including the commitment toward white, brown, or beige adipose tissue lineages, as well as the regulation of lipid accumulation. Through regulating adipocyte function and organismal energy balance, PARPs play a role in obesity and the consequences of obesity. These findings can be translated into humans, as evidenced by studies on identical twins and SNPs affecting PARP activity.

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“…In addition to repairing strand breaks in DNA, PARP activity may also be required for the maintenance of telomeres, the repetitive DNA structures found at the ends of chromosomes [ 154 , 155 , 156 , 157 ]. Telomere shortening occurs through life, has been shown to be the cause of the replication exhaustion of populations such as fibroblasts (first described by Hayflick and Moorhead in 1961) [ 158 ] and has been proposed as a risk factor for age related diseases [ 159 , 160 ].…”

Section: Biochemistry Of Mitochondrial Ageingmentioning

confidence: 99%

Intimate Relations—Mitochondria and Ageing

Webb¹,

Sideris²

2020

IJMS

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Mitochondrial dysfunction is associated with ageing, but the detailed causal relationship between the two is still unclear. We review the major phenomenological manifestations of mitochondrial age-related dysfunction including biochemical, regulatory and energetic features. We conclude that the complexity of these processes and their inter-relationships are still not fully understood and at this point it seems unlikely that a single linear cause and effect relationship between any specific aspect of mitochondrial biology and ageing can be established in either direction.

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Poly(ADP-Ribose) Polymerases in Aging - Friend or Foe?

Cited by 18 publications

References 58 publications

Poly(ADP‐ribose) polymerase‐1 depletion enhances the severity of inflammation in an imiquimod‐induced model of psoriasis

Poly(ADP‐ribose) polymerase‐1 depletion enhances the severity of inflammation in an imiquimod‐induced model of psoriasis

The role of ADP-ribose metabolism in metabolic regulation, adipose tissue differentiation, and metabolism

Intimate Relations—Mitochondria and Ageing

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