UVB damage response of dermal stem cells as melanocyte precursors compared to keratinocytes, melanocytes, and fibroblasts from human foreskin

Mhamdi-Ghodbani, Mouna; Starzonek, Christin; Degenhardt, Sarah; Bender, Marc; Said, Mohammed; Greinert, Rüdiger; Volkmer, Beate

doi:10.1016/j.jphotobiol.2021.112216

Cited by 10 publications

(11 citation statements)

References 72 publications

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“…e main target cells of UV-like fibroblasts and melanocytes can block and absorb UV [24,25]. In this study, after modeling by UVA combined with 8-MOP, the morphology of aged fibroblasts under the microscope showed larger size, reduced intercellular space, flat shape, excessive extension and flexion of cell synapses, and long branches at the ends.…”

Section: Discussionmentioning

confidence: 59%

“…As the ultraviolet light with the longest wavelength and strongest penetration, UVA can directly cross the ozone layer and atmosphere and damage the human skin dermis. The main target cells of UV-like fibroblasts and melanocytes can block and absorb UV [ 24 , 25 ]. In this study, after modeling by UVA combined with 8-MOP, the morphology of aged fibroblasts under the microscope showed larger size, reduced intercellular space, flat shape, excessive extension and flexion of cell synapses, and long branches at the ends.…”

Section: Discussionmentioning

confidence: 99%

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Protective Effects and Molecular Mechanism of Total Flavonoids from Lycium Barbarum Leaves on Photoaged Human Dermal Fibroblasts

Song

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate the effects and corresponding mechanisms of total flavonoids (TFL) from Lycium barbarum leaves on photoaged human dermal fibroblasts (HDFs). Methods. Crude TFL was extracted with 70% ethanol, and a Rutin standard curve was drawn using the sodium nitrite-aluminum nitrate-sodium hydroxide colorimetry method to calculate its yield and mass concentration. After that, the photoaging HDFs model was established by UVA combined with 8-MOP. CCK-8 was performed to assess the influence of TFL on the proliferation of HDFs and photoaging HDFs. β-galactosidase (SA-β-gal) staining and activity assays were performed to evaluate the activity of SA-β-gal and the rate of SA-β-gal-positive cells in HDFs cells. The level of skin ECM proteins and oxidative stress-related substances in HDFs cells of each group was determined by ELISA and biochemical detection, respectively. Apoptosis of HDFs in each group was assessed by flow cytometry. The expressions of MAPK signaling pathway-related proteins in HDFs were detected by western blot. Results. The yield rate of TFL extracted by 70% ethanol was 41.9%, and its purity rate was 34.6%. TFL at 25, 50, and 100 μg/mL was able to greatly promote the proliferation of HDFs. A photoaged HDFs model was successfully constructed by combining UVA irradiation at 9 J/cm2 and 8-MOP at 50 mg/L. TFL treatment could significantly inhibit apoptosis, SA-β-gal-positive cell staining rate, SA-β-gal activity, lactate dehydrogenase (LDH) leakage, and malondialdehyde (MDA) content in photoaged HDFs. Further, TFL increased the proliferative activity, superoxide dismutase (SOD) activity, catalase (CAT) activity, type I collagen (Col I), hydroxyproline (HYP), and hyaluronic acid (HA) level of photoaged HDFs in a dose-dependent manner. Additional experiments suggested that TFL played a protective role by downregulating MAPK signaling pathway activity in photoaged HDFs cells. Conclusion. TFL could inhibit oxidative stress and apoptosis, promote cell proliferation and the level of ECM-related component proteins, and participate in antiphotoaging in a concentration-dependent manner. The protective role of TFL in photoaged HDFs might be related to its inhibition of MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Protective Effects and Molecular Mechanism of Total Flavonoids from Lycium Barbarum Leaves on Photoaged Human Dermal Fibroblasts

Song

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…UVB penetrates and damages the epidermal layer of the skin, whereas UVA, while also damaging to the epidermis, penetrates deeper into the dermis. UVA leads to the DNA damage of epidermal cells, 15,16 collagen, elastin and blood vessels in dermis 17 …”

Section: Photoaging Under the Magnifying Glassmentioning

confidence: 99%

“…UVA leads to the DNA damage of epidermal cells, 15,16 collagen, elastin and blood vessels in dermis. 17 In terms of photoaging, UVA radiation is the more potent factor since it penetrates deep into the dermis and is associated with the production of reactive oxygen species (ROS) such as superoxide anion, peroxide and singlet oxygen.…”

Section: Molecular Changesmentioning

confidence: 99%

Hyaluronan: A key player or just a bystander in skin photoaging?

Šínová

Pavlík

Ondrej

et al. 2021

Experimental Dermatology

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Photoaged skin exhibits signs of inflammation, DNA damage and changes in morphology that are visible at the macroscopic and microscopic levels. Photoaging also affects the extracellular matrix (ECM) including hyaluronan (HA), the main polysaccharide component thereof. HA is a structurally simple but biologically complex molecule that serves as a water‐retaining component and provides both a scaffold for a number of the proteins of the ECM and the ligand for cellular receptors. The study provides an overview of the literature concerning the changes in HA amount, size and metabolism, and the potential role of HA in photoaging. We also suggest novel HA contributions to photoaging based on our knowledge of the role of HA in other pathological processes, including the senescence and inflammation‐triggered ECM reorganization. Moreover, we discuss potential direct or indirect intervention to mitigate photoaging that targets the hyaluronan metabolism, as well as supplementation.

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“…Cutaneous melanoma originates from the malignant transformation of cells of the neural-crest-derived melanocytic lineage, primarily melanocytes, cells of the basal layer of the epidermis that are responsible for producing the pigment known as melanin [ 4 , 5 , 6 ]. The involvement of other cells, such as melanocyte precursor and dermal stem cells, in the origin of melanoma has been proposed and is still under investigation [ 7 , 8 , 9 , 10 ]. Nevi such as common acquired nevi, dysplastic nevi and congenital nevi are considered precursor lesions of melanoma, although several melanomas may arise from clinically undetectable precursor lesions.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Autophagy as Key Targets in Melanoma Cell Fate

Catalani

Giovarelli

Zecchini

et al. 2021

Cancers

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Melanoma originates from the malignant transformation of melanocytes and is one of the most aggressive forms of cancer. The recent approval of several drugs has increased the chance of survival although a significant subset of patients with metastatic melanoma do not show a long-lasting response to these treatments. The complex cross-talk between oxidative stress and the catabolic process autophagy seems to play a central role in all aspects of melanoma pathophysiology, from initiation to progression and metastasis, including drug resistance. However, determining the fine role of autophagy in cancer death and in response to redox disruption is still a fundamental challenge in order to advance both basic and translational aspects of this field. In order to summarize the interactions among reactive oxygen and nitrogen species, autophagy machinery and proliferation/growth/death/apoptosis/survival, we provide here a narrative review of the preclinical evidence for drugs/treatments that modulate oxidative stress and autophagy in melanoma cells. The significance and the potential for pharmacological targeting (also through multiple and combination approaches) of these two different events, which can contribute independently or simultaneously to the fate of melanoma, may help to define new processes and their interconnections underlying skin cancer biology and unravel new reliable approaches.

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UVB damage response of dermal stem cells as melanocyte precursors compared to keratinocytes, melanocytes, and fibroblasts from human foreskin

Cited by 10 publications

References 72 publications

Protective Effects and Molecular Mechanism of Total Flavonoids from Lycium Barbarum Leaves on Photoaged Human Dermal Fibroblasts

Protective Effects and Molecular Mechanism of Total Flavonoids from Lycium Barbarum Leaves on Photoaged Human Dermal Fibroblasts

Hyaluronan: A key player or just a bystander in skin photoaging?

Oxidative Stress and Autophagy as Key Targets in Melanoma Cell Fate

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