Transforming Growth Factor-β (TGF-β) in Human Skin during Aging

Гунин, А. Г.; Golubtzova, N N

doi:10.1134/s2079057019030068

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…TGF-β, which belongs to the TGF cytokine superfamily, can regulate cell migration, cell adhesion, and extracellular matrix synthesis and promote the proliferation, differentiation, and apoptosis of a variety of cells. It plays an important role in bone reconstruction, wound repair, and embryonic development [32,33]. We have found that in terms of VEGF, HGF, and TGF-β secretion ability, ASCs derived from T2D mice are inferior to ASCs derived from normal mice especially in the ability to secrete HGF [10].…”

Section: Discussionmentioning

confidence: 99%

Knockdown of Adra2a Increases Secretion of Growth Factors and Wound Healing Ability in Diabetic Adipose-Derived Stem Cells

Zhao

Zhang

Zuo

et al. 2022

Stem Cells International

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Studies showed that compared to normal adipose-derived stem cells (ASCs), ASCs from type 2 diabetic (T2D) mice were less effective in treating diabetic cutaneous wounds. However, the mechanisms remain unclear. Our transcriptomic profiling comparison showed that the expression of α2A-adrenergic receptor (Adra2a) was significantly increased in ASCs from T2D mice (T2D ASCs). Therefore, the purpose of this study was to investigate whether the elevated Adra2a is involved in the diminished wound-healing capabilities of T2D ASCs. RNA-seq was used to compare the transcriptomic profiles of T2D and normal ASCs. The differential genes were verified by real-time RT-qPCR. Clonidine was used to active Adra2a, and lentivirus-mediated RNAi was used to knockdown Adra2a. The secretion and expression of growth factors were detected by enzyme-linked immunosorbent assay (ELISA) and real-time RT-qPCR, respectively. The cAMP and PKA activity were also detected. Wound healing abilities of various ASCs were assessed in T2D mouse excisional wound models. The results showed Adra2a agonist clonidine decreased the expression and secretion of growth factors, cAMP content, and activity of PKA in ASCs, while Adra2a knockdown T2D ASCs showed the opposite effects. Adra2a knockdown T2D ASCs also showed increased wound-healing capabilities compared to untreated T2D ASCs. Altogether, T2D increased Adra2a expression, which may subsequently decrease the expression and secretion of growth factors and eventually diminish the wound-healing capabilities of T2D ASCs. Adra2a knockdown can restore the secretion of growth factors in T2D ASCs and then accelerate the wound healing, which may provide a new possibility in the treatment of diabetic wounds.

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Section: Discussionmentioning

confidence: 99%

Knockdown of Adra2a Increases Secretion of Growth Factors and Wound Healing Ability in Diabetic Adipose-Derived Stem Cells

Zhao

Zhang

Zuo

et al. 2022

Stem Cells International

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“…Interestingly, the significant activation of the TGF-β/Smad pathway in mouse skin-derived precursor supernatant after ultraviolet B (UVB) irradiation could alleviate the UVB irradiation damage (Li et al, 2020). This indicates that TGF-β may be an aging skin marker (Gunin and Golubtzova, 2019). Activation of the TGF-β signaling pathway has been found to downregulate sebocyte differentiation markers, such as fatty acid desaturase 2 (FADS2) and PPARγ, inhibit sebum secretion, and maintain the undifferentiated state of sebocytes (McNairn et al, 2013).…”

Section: Transforming Growth Factor-βmentioning

confidence: 99%

“…Transforming growth factor- (TGF-β) levels increase in dermal fibroblasts with aging ( Gunin and Golubtzova, 2019 ). Interestingly, the significant activation of the TGF-β/Smad pathway in mouse skin-derived precursor supernatant after ultraviolet B (UVB) irradiation could alleviate the UVB irradiation damage ( Li et al, 2020 ).…”

Section: Molecular Variations Associated With Sebaceous Gland Agingmentioning

confidence: 99%

Aging in the sebaceous gland

Hou

Wei

Zouboulis

et al. 2022

Front. Cell Dev. Biol.

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Sebaceous glands (SGs) originate from hair follicular stem cells and secrete lipids to lubricate the skin. The coordinated effects of intrinsic and extrinsic aging factors generate degradation of SGs at a late age. Senescence of SGs could be a mirror of the late aging of both the human body and skin. The procedure of SG aging goes over an initial SG hyperplasia at light-exposed skin areas to end with SG atrophy, decreased sebum secretion, and altered sebum composition, which is related to skin dryness, lack of brightness, xerosis, roughness, desquamation, and pruritus. During differentiation and aging of SGs, many signaling pathways, such as Wnt/β-catenin, c-Myc, aryl hydrocarbon receptor (AhR), and p53 pathways, are involved. Random processes lead to random cell and DNA damage due to the production of free radicals during the lifespan and neuroendocrine system alterations. Extrinsic factors include sunlight exposure (photoaging), environmental pollution, and cigarette smoking, which can directly activate signaling pathways, such as Wnt/β-catenin, Notch, AhR, and p53 pathways, and are probably associated with the de-differentiation and hyperplasia of SGs, or indirectly activate the abovementioned signaling pathways by elevating the inflammation level. The production of ROS during intrinsic SG aging is less, the signaling pathways are activated slowly and mildly, and sebocytes are still differentiated, yet terminal differentiation is not completed. With extrinsic factors, relevant signaling pathways are activated rapidly and fiercely, thus inhibiting the differentiation of progenitor sebocytes and even inducing the differentiation of progenitor sebocytes into keratinocytes. The management of SG aging is also mentioned.

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“…Poziom TGF-β w mikronaczyniach ulegał znacznemu obniżeniu od 41 roku życia, czemu towarzyszyło zależne od wieku zmniejszenie liczby tych naczyń w skórze właściwej. Ponadto, wzrost poziomu TGF-β w fibroblastach korelował ze związanym z wiekiem obniżeniem liczby fibroblastów i ich proliferacji [115]. Wzrost ekspresji genu TGF-β1 zaobserwowano w badaniu ludzkich fibroblastów, które charakteryzują się SASP po ekspozycji na stres oksydacyjny [116].…”

Section: Szlak Sygnałowy Notchunclassified

Zapalenie starcze - mechanizmy i szlaki sygnałowe

et al. 2021

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Starzenie się jest złożonym i wieloetapowym procesem, angażującym mechanizmy na poziomie molekularnym, komórkowym i tkankowym. Podczas procesu starzenia się obserwowany jest rozwój przewlekłego, sterylnego stanu zapalnego, który jest określany terminem inflammaging, czyli zapalenie starcze. Zapalenie starcze jest wymieniane jako czynnik ryzyka wystąpienia i progresji chorób przewlekłych, nie tylko tych związanych z wiekiem. Ponadto, zapalenie starcze sprzyja wzrostowi zachorowalności i śmiertelności oraz wpływa na jakość życia osób starszych. Do rozwoju zapalenia starczego przyczynia się starzenie komórkowe oraz zaburzenia w regulacji aktywacji inflamasomów, pracy mitochondriów, autofagii i mitofagii, działania systemu ubikwityna â proteasom i odpowiedzi na uszkodzenia DNA. Powyższe procesy wzajemnie na siebie oddziaływają oraz są modulowane poprzez komórkowe szlaki sygnałowe uczestniczące w regulacji odpowiedzi zapalnej tj.: szlak mTOR, RIG-I, Notch, TGF-b, Ras, oraz regulacja aktywności sirtuin. Szczególną uwagę przypisuje się czynnikowi transkrypcyjnemu NF-kB. Celem pracy jest przedstawienie procesów oraz szlaków sygnałowych leżących u podstaw zapalenia starczego z uwzględnieniem badań klinicznych i eksperymentalnych.

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Transforming Growth Factor-β (TGF-β) in Human Skin during Aging

Cited by 6 publications

References 12 publications

Knockdown of Adra2a Increases Secretion of Growth Factors and Wound Healing Ability in Diabetic Adipose-Derived Stem Cells

Knockdown of Adra2a Increases Secretion of Growth Factors and Wound Healing Ability in Diabetic Adipose-Derived Stem Cells

Aging in the sebaceous gland

Zapalenie starcze - mechanizmy i szlaki sygnałowe

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