Publications by authors named "Fengfeng Ping"

13 Publications

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Erratum: Fungal infection in lung transplant recipients in perioperative period from one lung transplant center.

J Thorac Dis 2019 Aug;11(8):E146-E147

Institute of Medical and Technology, Xuzhou Medical University, Xuzhou 221004, China.

[This corrects the article DOI: 10.21037/jtd.2019.03.18.].
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http://dx.doi.org/10.21037/jtd.2019.07.39DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6753449PMC
August 2019

Fungal infection in lung transplant recipients in perioperative period from one lung transplant center.

J Thorac Dis 2019 Apr;11(4):1554-1561

Institute of Medical and Technology, Xuzhou Medical University, Xuzhou 221004, China.

Background: This study aimed to analyze the distribution and prophylaxis strategy of pathogens causing fungal infection in lung transplant recipients from cardiac-brain dead donors in the perioperative period to provide evidence for antifungal prophylaxis and treatment in lung transplant recipients.

Methods: This retrospective study evaluated 194 lung transplant recipients from January 2015 to December 2016. Fungal pathogens were isolated and identified from respiratory tract cultures before and after transplantation in the perioperative period. The galactomannan (GM) testing of bronchoalveolar lavage fluid (BALF) might facilitate the diagnosis of infection. Data were statistically analyzed using SPSS 19.0.

Results: A total of 31 cases of fungal strains isolated from the 194 recipients were identified prior to lung transplantation, and the positive rate was 16.0% (31/194). A total of 27 cases of isolated fungal strains in the 194 recipients were identified, and the positive rate after lung transplantation was 13.9% (27/194) in the perioperative period. A total of 54 cases with positive fungal infection (27.8%) were detected before and after lung transplantation. Overall, 10.3% (20/194) of the lung transplant recipients developed fungal infection in the observation period. The most common fungal pathogens were filamentous fungi and .

Conclusions: Our data suggested that fungi were frequently isolated before and after transplantation from respiratory samples. However, the incidence of invasive fungal infection in lung transplant recipients in the perioperative period was relatively low. Targeted antifungal prophylaxis and treatment should be applied on the basis of the fungal distribution status of different individuals.
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http://dx.doi.org/10.21037/jtd.2019.03.18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6531749PMC
April 2019

IL-17 induces cellular stress microenvironment of melanocytes to promote autophagic cell apoptosis in vitiligo.

FASEB J 2018 09 3;32(9):4899-4916. Epub 2018 Apr 3.

State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.

Vitiligo is a depigmentary disorder that develops as a result of the progressive disappearance of epidermal melanocytes. Stress can precipitate or exacerbate a skin disease through psychosomatic mechanisms. Stress exposure induces vitiligo-like symptoms in mice, as cellular damage to melanocytes causes synthetic pigment loss. Stress also increases IL-17, IL-1β, and antimelanocyte IgG in model mouse serum. Up-regulation of the IL-1β transcript in patients suggests its possible role in autoimmune pathogenesis of vitiligo. We demonstrate that IL-17 promoted IL-1β secretion from keratinocytes. Mitochondrial dysfunction, which can induce the excessive production of reactive oxygen species (ROS), is emerging as a mechanism that underlies various inflammatory and autoimmune diseases. In this study, we demonstrate that IL-17 inhibits melanogenesis of zebrafish, normal human epidermal melanocytes, and B16F10 cells. IL-17 increased mitochondrial dysfunction and ROS accumulation, which was related to autophagy induction. Autophagy is needed for autophagic apoptosis of B16F10 cells induced by IL-17. To inhibit ROS generation, B16F10 cells were pretreated with N-acetyl-l-cysteine (NAC), which inhibited autophagy. 3-Methyladenine (3-MA) also had an inhibiting effect on autophagy. NAC or 3-MA pretreatments inhibited IL-17-mediated cell apoptosis. In summary, IL-17 induces the cellular stress microenvironment in melanocytes to promote autophagic cell apoptosis in vitiligo.-Zhou, J., An, X., Dong, J., Wang, Y., Zhong, H., Duan, L., Ling, J., Ping, F., Shang, J. IL-17 induces cellular stress microenvironment of melanocytes to promote autophagic cell apoptosis in vitiligo.
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http://dx.doi.org/10.1096/fj.201701242RRDOI Listing
September 2018

Neurokinin-1 receptor is a novel positive regulator of Wnt/ β-catenin signaling in melanogenesis.

Oncotarget 2016 Dec;7(49):81268-81280

Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi 214023, P.R. China.

Wnt/β-catenin signaling is essential for melanogenesis in melanocytes. Neurokinin-1 receptor (NK-1R) has recently been demonstrated to be involved in melanin production. However, the cross talk between NK-1R and Wnt/β-catenin is poorly understood. Here, [Sar9, Met(O2)11] substance P (SMSP) was used to activate NK-1R, while L-733060 was used to inhibit it. The effects of NK-1R activation and inhibition on Wnt and its inhibitors were analyzed using western blot and real-time quantitative PCR. The results showed that SMSP positively regulated Wnt/β-catenin signaling by increasing the expression of β-catenin and p-GSK3β protein, which resulted from the weakened expression of the Wnt inhibitor Dickkopf-1 (DKK1). On the contrary, L-733060 lowered the expression of β-catenin and p-GSK3β protein through the up-regulation of DKK1 expression. Furthermore, in L-733060-treated mice, it was found that the pigmentation level as well as the melanogenic proteins and β-catenin protein expression were down-regulated, while the expression of DKK1 was up-regulated. These results showed the interaction between NK-1R and Wnt in human melanocytes in vitro and C57BL/6J mice in vivo, indicating that NK-1R may positively regulate melanogenesis through Wnt/β-catenin signaling pathway.
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http://dx.doi.org/10.18632/oncotarget.13222DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348391PMC
December 2016

Cross-talk between interferon-gamma and interleukin-18 in melanogenesis.

J Photochem Photobiol B 2016 Oct 21;163:133-43. Epub 2016 Aug 21.

Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi 214023, PR China. Electronic address:

Skin is the largest organ in our body and strategically placed to provide a metabolically active biological barrier against a range of noxious stressors. A lot of inflammatory cytokines, which are increased after ultraviolet (UV) irradiation produced by keratinocytes or other immunocytes, are closely related to pigmentary changes, including interleukin-18 (IL-18) and interferon-γ (IFN-γ). In this study, the effect of cross-talk between IL-18 and IFN-γ on melanogenesis was investigated. Treatment with IL-18 resulted in a dose-dependent increase of melanogenesis, while IFN-γ made an opposite effect. This influence of IL-18 and IFN-γ was mediated by regulations of microphthalmia-associated transcription factor (MITF) and its downstream enzymatic cascade expressions. Furthermore, IFN-γ inhibited basal and IL-18-induced melanogenesis. IFN-γ increased signal transducer and activator of transcription-1 (STAT-1) phosphorylation to play its position in regulating melanin pigmentation, and its inhibitory effect could be prevented by Janus Kinase 1 (JAK 1) inhibitor. IFN-γ could inhibit melanogenesis by decreasing melanocyte dendrite formation. In addition, IFN-γ inhibited the expressions of Rab Pases to suppress the mature and transport of melanosomes. IL-18 could rapidly induce Akt and PTEN phosphorylation and p65 expression in B16F10 cells. When treatment with IL-18 and IFN-γ together, the phosphorylation level of Protein Kinase B (Akt) and phosphatase and tensin homolog deleted on chromosome ten (PTEN) and expression of p65 NF-κB were inhibited, compared with treated with IL-18 only. Our studies indicated that IFN-γ could directly induce B16F10 cells apoptosis in vitro. Furthermore, we demonstrated that IFN-γ markedly up-regulated IL-18 binding protein (BP) production in normal human foreskin-derived epidermal keratinocytes in dose-dependent manner. UVB irradiation induced protease-activated receptor-2 (PAR-2) expression in NHEK, IFN-γ could inhibit this enhancement in a dose-dependent manner. These data suggest that IFN-γ plays a role in regulating inflammation- or UV-induced pigmentary changes, in direct/indirect manner.
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http://dx.doi.org/10.1016/j.jphotobiol.2016.08.024DOI Listing
October 2016

Interferon-γ Attenuates 5-Hydroxytryptamine-Induced Melanogenesis in Primary Melanocyte.

Biol Pharm Bull 2016 ;39(7):1091-9

School of Pharmaceutical Science, Jiangnan University.

Interferon-γ (IFN-γ) is an important cytokine which can be secreted by keratinocytes or macrophages induced by UVB irradiation in skin. Mammalian skin cells have the capability to produce and metabolize 5-hydroxytryptamine (5-HT) whose cutaneous effects are mediated by the interactions with 5-HT receptors. Treatment with 5-HT resulted in a dose-dependent increase of tyrosinase (TYR) activity and melanin contents in normal human foreskin-derived epidermal melanocytes (NHEM), while with IFN-γ a decreased effect resulted. These regulatory results were due to changes of the expression levels of microphthalmia-associated transcription factor (MITF) and its downstream TYR, tyrosinase-related protein 1 (TRP-1) and dopachrome tautomerase (DCT). We proved here that 5-HTR1A/2A participated in the regulation of melanogenesis. IFN-γ could offset the pro-melanogenesis effect of 5-HT in NHEM and the intensity of this neutralization was unanticipated below the baseline level. IFN-γ neutralized the up-regulation effect of 5-HT on MITF and downstream TYR, TRP-1 and DCT. Though functioning as 5-HT1A/2A receptor during the melanogenesis process, IFN-γ played no role in 5-HT1A/2A receptor expressions. Our results also demonstrated that the inhibition of IFN-γ was reversible after its removal. Confusingly, the effect of cross-talk between 5-HT and IFN-γ on NHEM melanogenesis was irreversible. Whether treated with 5-HT for 5 d or 12 d, the pigmentation level neither recovered after displacing the IFN-γ-containing medium. In addition, IFN-γ was able to inhibit the inductive effect of 5-HT on NHEM migration. Taken together, the suppression of IFN-γ on 5-HT-induced melanogenesis further suggests the negative role of IFN-γ in inflammation-associated pigmentary changes.
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http://dx.doi.org/10.1248/bpb.b15-00914DOI Listing
January 2017

Interleukin 10 protects primary melanocyte by activation of Stat-3 and PI3K/Akt/NF-κB signaling pathways.

Cytokine 2016 07 14;83:275-281. Epub 2016 May 14.

Department of Clinical Laboratory Science, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi 214023, PR China. Electronic address:

Vitiligo is a common melanocytopenic disorder of the skin, with acquired focal depigmentation. Normal human skin relies on melanocytes to provide photoprotection and thermoregulation by producing melanin. Interleukin 10 (IL-10) is a pleiotropic immunoregulatory cytokine drawing more and more researchers' attention. The present study was conducted to investigate the effects of IL-10 on melanocytes and elucidate the underlying mechanisms. We proved that IL-10 play no role in regulating melanogenesis of normal human foreskin-derived epidermal melanocytes (NHEM). IL-10 stimulation activated the JAK/Stat-3 and PI3K/Akt signaling pathways. Moreover, IL-10 treatment increased translocation of p65 NF-κB into the nuclear compartment, and up-regulated expression of the pro-survival proteins Bcl-2 and Bcl-xL. IL-10 restored anti-apoptotic proteins expression and suppressed cytochrome c release in H2O2-induced apoptosis. In conclusion, IL-10 may provide pro-survival cues to melanocytes and be applied in the treatment of vitiligo and other depigmenting disorders.
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http://dx.doi.org/10.1016/j.cyto.2016.05.013DOI Listing
July 2016

Differential Expression of Proteins Associated with the Hair Follicle Cycle - Proteomics and Bioinformatics Analyses.

PLoS One 2016 11;11(1):e0146791. Epub 2016 Jan 11.

Department of Dermatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

Hair follicle cycling can be divided into the following three stages: anagen, catagen, and telogen. The molecular signals that orchestrate the follicular transition between phases are still unknown. To better understand the detailed protein networks controlling this process, proteomics and bioinformatics analyses were performed to construct comparative protein profiles of mouse skin at specific time points (0, 8, and 20 days). Ninety-five differentially expressed protein spots were identified by MALDI-TOF/TOF as 44 proteins, which were found to change during hair follicle cycle transition. Proteomics analysis revealed that these changes in protein expression are involved in Ca2+-regulated biological processes, migration, and regulation of signal transduction, among other processes. Subsequently, three proteins were selected to validate the reliability of expression patterns using western blotting. Cluster analysis revealed three expression patterns, and each pattern correlated with specific cell processes that occur during the hair cycle. Furthermore, bioinformatics analysis indicated that the differentially expressed proteins impacted multiple biological networks, after which detailed functional analyses were performed. Taken together, the above data may provide insight into the three stages of mouse hair follicle morphogenesis and provide a solid basis for potential therapeutic molecular targets for this hair disease.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0146791PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709225PMC
July 2016

Enhancement of the p38 MAPK and PKA signaling pathways is associated with the pro-melanogenic activity of Interleukin 33 in primary melanocytes.

J Dermatol Sci 2014 Feb 25;73(2):110-6. Epub 2013 Sep 25.

Center for Drug Screening, China Pharmaceutical University, Nanjing 210009, China; State Key Laboratory of Natural Medicines, China Pharmaceutical University, China. Electronic address:

Background: Interleukin-33 (IL-33) was recently recognized as a member of the IL-1 cytokine family. The triggers no matter environmental or endogenous that provoke IL-33 cellular release may be associated with inflammation, infection or tissue damage. However, to date, the regulatory role of IL-33 in the control of melanogenesis has not been elucidated.

Objective: The present study was designed to investigate the effect of IL-33 on melanogenesis and to explore its underlying mechanisms.

Methods: Melanocytes were exposed to IL-33. Then cell viabilities were measured by MTT assay. The improving activities of IL-33 were examined by melanin synthesis, tyrosinase (TYR) activity assay. The expressions of relative proteins were assessed by Western blotting.

Results: IL-33 increased the TYR activity and melanin content in a dosage-dependent manner at concentrations of 1-10ng/ml. Treatment with 10ng/ml of IL-33 enhanced the expression of microphthalmia-associated transcription factor (MITF), TYR, tyrosinase-related protein 1 (TRP-1) and dopachrome tautomerase (DCT) in normal human foreskin-derived epidermal melanocytes (NHEM). Furthermore, IL-33 could remarkably promote the phosphorylation levels of p38 mitogen-activated protein kinases (MAPKs) and cyclic AMP-responsive element-binding protein (CREB). This pro-melanogenic effect could be partially reversed by the pre-treatment with the special p38 MAPK inhibitor, SB203580, and protein kinase A (PKA) inhibitor, H89.

Conclusions: Our results collectively indicated that IL-33 improved melanin biosynthesis in NHEM. This function might be attributed to the fact that IL-33 stimulates the phosphorylation of p38 MAPK and CREB, increases the TYR, TRP-1 and DCT expression through MITF, finally resulting in the augment of melanogenesis.
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http://dx.doi.org/10.1016/j.jdermsci.2013.09.005DOI Listing
February 2014

Interleukin-18 augments growth ability of primary human melanocytes by PTEN inactivation through the AKT/NF-κB pathway.

Int J Biochem Cell Biol 2013 Feb 22;45(2):308-16. Epub 2012 Nov 22.

New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China.

Normal human skin relies on melanocytes to provide photoprotection and thermoregulation by producing melanin. The growth and behavior of melanocytes are controlled by many factors. Interleukin-18 (IL-18) is expressed in both immune and non-immune cells and participates in the adjustment of multitude cellular functions. Nonetheless, the regulative roles of IL-18 in melanogenesis and growth of melanocytes have not been explored. The present study was conducted to investigate the effects of IL-18 on melanocytes and elucidate the underlying mechanisms. We proved that IL-18 increased the tyrosinase activity and melanin content in normal human foreskin-derived epidermal melanocytes (NHEM). Treatment with IL-18 (20 ng/ml) enhanced the expression of c-Kit, microphtalmia-associated transcription factor (MITF) and its downstream tyrosinase-related protein 1 (TRP-1), and TRP-2. In addition, IL-18 induced NHEM migration at concentration of 20 ng/ml. These results indicated a promotive action of IL-18 on melanogenesis in NHEM. Our data revealed that IL-18 stimulated ERK1/2 and NF-κB activation, improved p-Akt, p70 S6K and anti-apoptotic Bcl-2 levels, and deactivated phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in NHEM. Besides, IL-18 increased level of PTEN phosphorylation to protect NHEM from damage induced by H(2)O(2). These results in vitro showed the accommodation of IL-18 in melanocytes growth. Therefore, we suggested an important regulating action of IL-18 to melanogenesis and cell growth ability of skin melanocytes.
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http://dx.doi.org/10.1016/j.biocel.2012.11.008DOI Listing
February 2013

Activation of neurokinin-1 receptor by substance P inhibits melanogenesis in B16-F10 melanoma cells.

Int J Biochem Cell Biol 2012 Dec 2;44(12):2342-8. Epub 2012 Oct 2.

Center for Drug Screening, China Pharmaceutical University, Nanjing 210009, PR China.

Skin pigmentation plays a number of valuable roles and its regulation is a complex process that is controlled by different factors. Substance P (SP) regulates many biological functions, including neurogenic inflammation, pain, and stress. However, to date, the regulatory role of SP in the control of melanogenesis has not been elucidated. The present study was designed to investigate the effects of SP on melanogenesis and to elucidate its underlying mechanism(s). After treatment for 48 h in mouse B16-F10 melanoma cells, SP (1 and 10nM) significantly down-regulated tyrosinase activity and melanin content. Importantly, western blot analysis revealed the presence of neurokinin-1 receptor (NK-1 R) in B16-F10 cells and the activation of it after SP treatment. It was also found that preincubation with NK-1 receptor antagonist Spantide I could partially reversed SP-induced down-regulations of tyrosinase activity, melanin content and the expression of tyrosinase and tyrosinase-related protein 1. Furthermore, SP could remarkably inhibit the expressions of microphtalmia-associated transcription factor (MITF) and p-p38 MAPK and stimulated p-p70 S6K1. These effects could also be partially reversed by the pretreatment with Spantide I. These results collectively suggested that SP inhibited melanogenesis in B16-F10 cells, which might be attributed to the fact that SP induces the activation of NK-1 receptor, stimulates the phosphorylation of p70 S6K1 and inhibits that of p38 MAPK, decreases the tyrosinase and tyrosinase-related protein 1 expression through MITF, finally resulting in the suppression of melanogenesis. These observations in vitro indicated that the regulation of the SP/NK-1 receptor system might be a useful novel management for skin pigmentation.
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http://dx.doi.org/10.1016/j.biocel.2012.09.025DOI Listing
December 2012

Alcohol extract from Vernonia anthelmintica (L.) willd seed enhances melanin synthesis through activation of the p38 MAPK signaling pathway in B16F10 cells and primary melanocytes.

J Ethnopharmacol 2012 Sep 31;143(2):639-47. Epub 2012 Jul 31.

Center for Drug Screening, China Pharmaceutical University, Nanjing 210009, China.

Ethnopharmacological Relevance: Vernonia anthelmintica (L.) willd has been used in folk medicine to treat leukoderma in China for centuries. The promoting activities of its extract (AVE) in melanogenesis and possible signaling pathways were investigated in this article.

Materials And Methods: The improving activities of AVE were examined by melanin synthesis, tyrosinase activity assay and Western blot in B16F10 mouse melanoma cells and normal human primary melanocytes (NHMC).

Results: AVE increased the tyrosinase activity and melanin content in a dosage-dependent manner at concentrations of 1-40 μg/ml and treatment with 20 μg/ml AVE enhanced the expression of tyrosinase time-dependently in both B16F10 cells and NHMC. Whether AVE affects the expression of microphthalmia-associated transcription factor (MITF), which is required for tyrosinase expression, was investigated. Our results showed that AVE induced MITF protein expression up-regulation. Besides, Western blot analysis revealed that AVE promoted the level of phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) markedly at 0-6 h, while the level of phosphorylation of CREB at 0-2 h. The special p38 MAPK inhibitor, SB203580, and protein kinase A (PKA) inhibitor, H89, both attenuated the AVE-induced up-regulation of MITF and tyrosinase expression in B16F10 cells and NHMC. However, SB203580 could significantly decrease the melanin biosynthesis induced by AVE, but not H89.

Conclusion: AVE exerts its improving effect on melanogenesis mainly by p38 MAPK activation and MITF induction of tyrosinase.
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http://dx.doi.org/10.1016/j.jep.2012.07.030DOI Listing
September 2012

5-HT(1A) receptor and apoptosis contribute to interferon-α-induced "depressive-like" behavior in mice.

Neurosci Lett 2012 Apr 5;514(2):173-8. Epub 2012 Mar 5.

Center for Drug Screening, China Pharmaceutical University, Nanjing 210009, China.

Interferon-α (IFN-α)-induced "depressive-like" behavior is a major limitation for the treatment of hepatitis C virus (HCV), especially for patients with psychiatric disorders. Recently, serotonin 1A (5-HT(1A)) receptor and cellular apoptosis are involved in mechanism(s) contributing to depression. To gain insight into this mechanism(s), we used C57BL/6J mice to examine the impact of IFN-α on the modulation of 5-HT(1A) receptor and cellular apoptosis and their relationship. Our results showed that repeated administration of IFN-α (6 MIU/kg, s.c.) induced "depressive-like" behavior of mice in the forced swim test, tail suspension test and sucrose preference test. Besides, the depressive mice exhibited a notable downregulation of 5-HT(1A) receptor and upregulation of cleaved caspase-3 and Bax/Bcl-2 ratio. These changes could be blocked by the 5-HT(1A) receptor agonist 8-OH-DPAT (0.5 mg/kg, i.p., 30 min before IFN-α administration), but not by the standard antidepressant imipramine (10 mg/kg, i.p., 30 min before IFN-α administration) although both of them could ameliorate the depressive-like behavior of mice. These findings indicated that repeated injection with IFN-α provoked "depressive-like" behavior through cellular apoptosis, which could be ameliorated by the activation of 5-HT(1A) receptor.
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http://dx.doi.org/10.1016/j.neulet.2012.02.087DOI Listing
April 2012