Lamin B1 and lamin B2 in human skin in the process of aging

Golubtsova, N. N.; Filippov, F. N.; Гунин, А. Г.

doi:10.1134/s2079057016040068

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…Looking for a better senescence marker we quantified lamin B1, a protein of the NE that has been shown to be down-regulated in HGPS ( 89 ), cellular senescence ( 90 ) and normal aging ( 91 ). The down-regulation of lamin B1 occurs specifically in DM1 myoblasts and is independent of the repeat length (Figure 2B ).…”

Section: Discussionmentioning

confidence: 99%

Myotonic Dystrophy—A Progeroid Disease?

et al. 2018

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Myotonic dystrophies (DM) are slowly progressing multisystemic disorders caused by repeat expansions in the DMPK or CNBP genes. The multisystemic involvement in DM patients often reflects the appearance of accelerated aging. This is partly due to visible features such as cataracts, muscle weakness, and frontal baldness, but there are also less obvious features like cardiac arrhythmia, diabetes or hypogammaglobulinemia. These aging features suggest the hypothesis that DM could be a segmental progeroid disease. To identify the molecular cause of this characteristic appearance of accelerated aging we compare clinical features of DM to “typical” segmental progeroid disorders caused by mutations in DNA repair or nuclear envelope proteins. Furthermore, we characterize if this premature aging effect is also reflected on the cellular level in DM and investigate overlaps with “classical” progeroid disorders. To investigate the molecular similarities at the cellular level we use primary DM and control cell lines. This analysis reveals many similarities to progeroid syndromes linked to the nuclear envelope. Our comparison on both clinical and molecular levels argues for qualification of DM as a segmental progeroid disorder.

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Section: Discussionmentioning

confidence: 99%

Myotonic Dystrophy—A Progeroid Disease?

et al. 2018

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“…Lamin B1, Sirtuin-1, and Aging-Associated DNA Damage Given the complex, multi-level pathobiology of human skin aging (see Section 1), we next assessed whether melatonin non-discriminatively improves additional core skin-aging associated biomarkers across the board. To this end, we examined p16 INK4 protein expression, a key biomarker for senescent cells [28,32,60,77]; lamin B1, a nuclear lamina component whose abundance declines with age/senescence [36,78,79]; sirtuin-1 (SIRT-1), an NAD +dependent deacetylase enzyme that is crucially involved in cell and tissue aging [80][81][82][83]; and γH2A.x formation resulting from histone H2A.x phosphorylation as a marker of DNA damage [24,61,84,85].…”

Section: Melatonin Unfolds Differential Anti-aging Activities In Huma...mentioning

confidence: 99%

“…Moreover, melatonin is well tolerated, inexpensive [33], and has good skin penetration, thus being recommended for topical application [34,35]. Its amphiphilic nature enables it to penetrate biological membranes better than any other known endogenous antioxidant and to thereby effectively protect DNA, proteins, and lipids against oxidative damage, especially in the nucleus and mitochondria [36,37]. This property is important because topical application prevents the problems of rapid hepatic degradation and offtarget sedative effects of systemically administered melatonin and facilitates cutaneous accumulation in excess of the endogenous levels synthesized within human skin and its appendages [16,[21][22][23][24]38,39].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Exerts Prominent, Differential Epidermal and Dermal Anti-Aging Properties in Aged Human Eyelid Skin Ex Vivo

Samra,

Gomez-Gomez,

Linowiecka

et al. 2023

IJMS

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Human skin aging is associated with functional deterioration on multiple levels of physiology, necessitating the development of effective skin senotherapeutics. The well-tolerated neurohormone melatonin unfolds anti-aging properties in vitro and in vivo, but it remains unclear whether these effects translate to aged human skin ex vivo. We tested this in organ-cultured, full-thickness human eyelid skin (5–6 donors; 49–77 years) by adding melatonin to the culture medium, followed by the assessment of core aging biomarkers via quantitative immunohistochemistry. Over 6 days, 200 µM melatonin significantly downregulated the intraepidermal activity of the aging-promoting mTORC1 pathway (as visualized by reduced S6 phosphorylation) and MMP-1 protein expression in the epidermis compared to vehicle-treated control skin. Conversely, the transmembrane collagen 17A1, a key stem cell niche matrix molecule that declines with aging, and mitochondrial markers (e.g., TFAM, MTCO-1, and VDAC/porin) were significantly upregulated. Interestingly, 100 µM melatonin also significantly increased the epidermal expression of VEGF-A protein, which is required and sufficient for inducing human skin rejuvenation. In aged human dermis, melatonin significantly increased fibrillin-1 protein expression and improved fibrillin structural organization, indicating an improved collagen and elastic fiber network. In contrast, other key aging biomarkers (SIRT-1, lamin-B1, p16INK4, collagen I) remained unchanged. This ex vivo study provides proof of principle that melatonin indeed exerts long-suspected but never conclusively demonstrated and surprisingly differential anti-aging effects in aged human epidermis and dermis.

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“…Good examples are the Hutchinson-Gilford and the Néstor-Guillermo progeria syndromes, which were linked to mutations in lamin genes responsible for formation of the nuclear lamina (De Sandre-Giovannoli et al, 2003; Eriksson et al, 2003; Cabanillas et al, 2011). In addition, both the accumulation of progerin, which is an aberrant form of lamin A, and the reduced expression of lamin B1 were linked to aging (Freund et al, 2012; Golubtsova et al, 2016; Hilton et al, 2017), and lamins were also shown to regulate DNA damage response (Gonzalez-Suarez et al, 2009). Thus, the canine homologs of lamins could be promising targets in aging research.…”

Section: The Hallmarks Of Aging In Dogsmentioning

confidence: 99%

Genetic Pathways of Aging and Their Relevance in the Dog as a Natural Model of Human Aging

Sándor

Kubinyi

2019

Front. Genet.

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Aging research has experienced a burst of scientific efforts in the last decades as the growing ratio of elderly people has begun to pose an increased burden on the healthcare and pension systems of developed countries. Although many breakthroughs have been reported in understanding the cellular mechanisms of aging, the intrinsic and extrinsic factors that contribute to senescence on higher biological levels are still barely understood. The dog, Canis familiaris, has already served as a valuable model of human physiology and disease. The possible role the dog could play in aging research is still an open question, although utilization of dogs may hold great promises as they naturally develop age-related cognitive decline, with behavioral and histological characteristics very similar to those of humans. In this regard, family dogs may possess unmatched potentials as models for investigations on the complex interactions between environmental, behavioral, and genetic factors that determine the course of aging. In this review, we summarize the known genetic pathways in aging and their relevance in dogs, putting emphasis on the yet barely described nature of certain aging pathways in canines. Reasons for highlighting the dog as a future aging and gerontology model are also discussed, ranging from its unique evolutionary path shared with humans, its social skills, and the fact that family dogs live together with their owners, and are being exposed to the same environmental effects.

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Lamin B1 and lamin B2 in human skin in the process of aging

Cited by 4 publications

References 14 publications

Myotonic Dystrophy—A Progeroid Disease?

Myotonic Dystrophy—A Progeroid Disease?

Melatonin Exerts Prominent, Differential Epidermal and Dermal Anti-Aging Properties in Aged Human Eyelid Skin Ex Vivo

Genetic Pathways of Aging and Their Relevance in the Dog as a Natural Model of Human Aging

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