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Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target
Ming-Shian Tsai,Po-Huang Lee,Cheuk-Kwan Sun,Ting-Chia Chiu,Yu-Chun Lin,I-Wei Chang,Po-Han Chen,Ying-Hsien Kao 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
This study investigated the regulatory role of nerve growth factor (NGF) in sirtuin 1 (SIRT1) expression in cholestatic livers. We evaluated the expression of NGF and its cognate receptors in human livers with hepatolithiasis and the effects of NGF therapy on liver injury and hepatic SIRT1 expression in a bile duct ligation (BDL) mouse model. Histopathological and molecular analyses showed that the hepatocytes of human diseased livers expressed NGF, proNGF (a precursor of NGF), TrkA and p75NTR, whereas only p75NTR was upregulated in hepatolithiasis, compared with non-hepatolithiasis livers. In the BDL model without NGF therapy, p75NTR, but not TrkA antagonism, significantly deteriorated BDL-induced liver injury. By contrast, the hepatoprotective effect of NGF was abrogated only by TrkA and not by p75NTR antagonism in animals receiving NGF therapy. Intriguingly, a positive correlation between hepatic SIRT1 and NGF expression was found in human livers. In vitro studies demonstrated that NGF upregulated SIRT1 expression in mouse livers and human Huh-7 and rodent hepatocytes. Both NGF and proNGF induced protective effects against hydrogen peroxide-induced cytotoxicity in Huh-7 cells, whereas inhibition of TrkA and p75NTR activity prevented oxidative cell death. Mechanistically, NGF, but not proNGF, upregulated SIRT1 expression in human Huh-7 and rodent hepatocytes via nuclear factor (NF)-κB activity, whereas NGF-induced phosphoinositide-3 kinase/Akt, extracellular signal–regulated kinase and NF-κB signaling and SIRT1 activity were involved in its hepatoprotective effects against oxidative injury. These findings suggest that pharmacological manipulation of the NGF/SIRT1 axis might serve as a novel approach for the treatment of cholestatic disease.
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Lam Phoebe Kar Wai,Fung Chi Pun,Lam James Yui,Luk Wang Lung,Lee Alvin Ka Wai,Lee Cheuk Hung,Tam Paul Man Kei,Lau Edwin Kwan Chark 대한미용의학회 2022 대한미용의학회지 Vol.6 No.1
Background: There was evidence of improvement in mid-face laxity using three pairs of suspension sutures in mid-face lifting in our early and mid-term follow-up. Objective: This 24-month prospective follow-up study aimed to determine the efficacy of mid-face lifting and lower jawline contouring using poly lactic-co-glycolic acid (PLGA) sutures in Asian patients. Methods: Ten healthy volunteers received three pairs of 8-cones bidirectional cones sutures at the mid-face. One of the ten volunteers lost to follow-up, and all remaining patients followed up for 24 months. Our primary outcome measure is the change in the facial laxity rating scale (FLRS), an “improvement” defined as at least “one-grade change” in FLRS. Other assessment parameters include the severity of the nasolabial fold (NLF), assessed on the wrinkle severity rating scale (WSRS). The secondary outcome measures were the self-satisfaction rating scale (SSRS) and global aesthetic improvement scale (GAIS), rated by participants at each follow-up interval. Results: A linear improvement in the mid-face was observed almost immediately after treatment, with progressive improvement up to at least 12 months following the intervention and no deterioration by 24 months. This improvement was significant (p<0.05), and the differences between before and after treatment at each follow-up interval were large (Cohen’s d>0.8). Contour improvement for the lower face followed a similar trend, except for a delay in the observable differences at three months (Cohen’s d=0.29, 0.8 at six weeks and three months, respectively). The differences in the level of patient satisfaction were significant (p<0.05) from 6 weeks to 24 months, peaking between 12 and 18 months, based on both the GAIS and SSRS ratings. No observed complications. Conclusion: Mid-facing lifting in Asian patients with mild-to-moderate laxity is safe and effective with PLGA bidirectional cone sutures, with concurrent improvement in the lower face contour and elevated patient satisfaction over the 24-month follow-up period.
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Kao Ying-Hsien,Lin Yu-Chun,Lee Po-Huang,Lin Chia-Wei,Chen Po-Han,Tai Tzong-Shyuan,Chang Yo-Chen,Chou Ming-Huei,Chang Chih-Yang,Sun Cheuk-Kwan 한국조직공학과 재생의학회 2020 조직공학과 재생의학 Vol.17 No.5
Background: This study investigated whether xenotransplantation of human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) reduces thioacetamide (TAA)-induced mouse liver fibrosis and the underlying molecular mechanism. Methods: Recipient NOD/SCID mice were injected intraperitoneally with TAA twice weekly for 6 weeks before initial administration of WJ-MSCs. Expression of regenerative and pro-fibrogenic markers in mouse fibrotic livers were monitored post cytotherapy. A hepatic stallate cell line HSC-T6 and isolated WJ-MSCs were used for in vitro adhesion, migration and mechanistic studies. Results: WJ-MSCs were isolated from human umbilical cords by an explant method and characterized by flow cytometry. A single infusion of WJ-MSCs to TAA-treated mice significantly reduced collagen deposition and ameliorated liver fibrosis after 2-week therapy. In addition to enhanced expression of hepatic regenerative factor, hepatocyte growth factor, and PCNA proliferative marker, WJ-MSC therapy significantly blunted pro-fibrogenic signals, including Smad2, RhoA, ERK. Intriguingly, reduction of plasma fibronectin (pFN) in fibrotic livers was noted in MSC-treated mice. In vitro studies further demonstrated that suspending MSCs triggered pFN degradation, soluble pFN conversely retarded adhesion of suspending MSCs onto type I collagen-coated surface, whereas pFN coating enhanced WJ-MSC migration across mimicked wound bed. Moreover, pretreatment with soluble pFN and conditioned medium from MSCs with pFN strikingly attenuated the response of HSC-T6 cells to TGF-β1-stimulation in Smad2 phosphorylation and RhoA upregulation. Conclusion: These findings suggest that cytotherapy using WJ-MSCs may modulate hepatic pFN deposition for a better regenerative niche in the fibrotic livers and may constitute a useful anti-fibrogenic intervention in chronic liver diseases.
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